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2DG
2-DeoxyGlucose
RD
Diagnostic agent used in PET, can determine glucose metabolism
<b>2-DeoxyGlucose</b> inhibits the production of glucose-6-phosphate from glucose at the phosphoglucoisomerase level. -an inhibitor of the glycolysis enzyme hexokinase<br> <br> <b>Key Pathways:</b> 1.Glycolysis Inhibition (blocking the glycolytic pathway.)<br> • blockade leads to energy deprivation—a mechanism of interest particularly in cancer cells that often depend on high glycolytic rates (the “Warburg effect”).<br> • 2DG is structurally similar to glucose and is taken up into cells via glucose transporters (GLUTs).<br> • “glycolytic blockade.” deprives the cell of ATP and glycolytic intermediates, crucial for biosynthetic functions in rapidly dividing cancer cells.<br> <br> 2.Impact on the Pentose Phosphate Pathway (PPP)<br> • The inhibition of glycolysis may indirectly affect the PPP and PPP is essential for reducing equivalents (NADPH), which are needed for cell survival and proliferation.<br> • Decreased flux through the PPP may reduce production of NADPH.<br> – NADPH is essential for countering oxidative stress by regenerating reduced glutathione (GSH).<br> • Reduced NADPH levels can compromise the cell’s ability to neutralize ROS, contributing to oxidative damage.<br> <br> 3.Interference with N-linked Glycosylation<br> • 2DG can disrupt N-linked glycosylation by competing with mannose in glycoprotein synthesis.<br> • This disruption can lead to endoplasmic reticulum (ER) stress and may trigger the unfolded protein response (UPR), contributing to cancer cell apoptosis or impaired growth.<br> • The process of ER stress itself is associated with increased ROS generation as cellular homeostatic mechanisms are overwhelmed.<br> <br> 4. Mitochondrial Dysfunction and ROS Generation<br> • While the primary action of 2DG is cytosolic (glycolysis), metabolic stress caused by energy deprivation indirectly affects mitochondrial function.<br> • Mitochondria may increase ROS production when the electron transport chain is perturbed due to altered cellular energy demands.<br> – Elevated ROS levels can damage mitochondrial DNA, proteins, and lipids.<br> • The resulting oxidative damage further impairs mitochondrial efficiency and may trigger intrinsic apoptotic pathways.<br> <br> 5. Cellular Redox Imbalance<br> • Inhibition of glycolysis and the subsequent reduction in PPP activity limit NADPH production, a key reducing agent.<br> • With decreased NADPH, the regeneration of antioxidants such as glutathione and thioredoxin is impaired.<br> – Accumulation of ROS leads to oxidative stress, damaging cellular components including lipids, proteins, and nucleic acids.<br> • Oxidative stress may sensitize cancer cells to further apoptotic signaling cascades.<br> <br> 6. Activation of Stress and Apoptotic Signaling Pathways<br> • 2DG-mediated metabolic stress and ROS accumulation can activate several stress-related kinases and transcription factors, including:<br> – AMP-activated protein kinase (AMPK): Activated by energy deprivation, AMPK may shift cellular metabolism and promote cell cycle arrest.<br> – c-Jun N-terminal kinase (JNK): Often activated by oxidative and ER stress, JNK can promote apoptotic signaling.<br> – p38 MAPK: Also is responsive to stress stimuli and can drive apoptosis or cell cycle changes.<br> • These stress responses can initiate apoptosis in cancer cells, particularly if homeostatic mechanisms for dealing with ROS are overwhelmed.<br> <br> Understanding these detailed pathways helps explain why 2DG can preferentially affect cancer cells that rely heavily on glycolysis (the Warburg effect) while also illuminating how ROS and oxidative damage contribute to its overall antitumor efficacy.<br> <br> some Phase I trials, doses in the range of 45–63 mg/kg/day (administered orally)<br> <br> do not combine with Caffeic acid phenethyl ester (CAPE) is one of the main active ingredients of <a href="https://pubmed.ncbi.nlm.nih.gov/37864895/">propolis</a>
20
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3BP
3-bromopyruvate
RD
<b>3BP</b>, a small molecule, results in a remarkable therapeutic effect when it comes to treating cancers exhibiting a <a href="https://pubmed.ncbi.nlm.nih.gov/22382780/">"Warburg effect."</a> <br> Overall, 3BP attacks cancer cells by “starving” them of energy, leading to energetic collapse, oxidative damage, and eventual cell death. <br> <br> - 3BP is known to inhibit enzymes involved in glycolysis, such as hexokinase II (HKII). Many cancer cells overexpress HKII and rely on glycolysis for ATP production. Inhibiting HKII leads to decreased ATP levels and energy depletion.<br> - Fermentation inhibitor:(inhibits conversion of pyruvate to lactate) NAD+ is compromised slowing Glycolysis leading to reduced ATP<br> - By depleting ATP, 3BP can impair mitochondrial functions indirectly.<br> - LDH converts pyruvate to lactate. In many cancers, lactate production is high (the Warburg effect). Inhibition of LDH disrupts lactate production and may contribute to an intracellular buildup of toxic metabolites.<br> - There is evidence indicating that, by interfering with glycolysis, 3BP might also indirectly affect the PPP. This reduces the production of NADPH, weakening the cancer cell’s ability to manage oxidative stress.<br> - Impairing energy metabolism, 3BP can indirectly affect mitochondrial function, potentially leading to an increase in ROS production. <br> <br> Although 3BP shows promise as a metabolic inhibitor with anticancer properties, its transition from preclinical studies to approved clinical therapy has not yet been realized. <br> <br> -Combining metabolic inhibitors like 3BP with agents that modulate ROS levels could represent a synergistic approach in cancer therapy. By simultaneously disrupting energy production and exacerbating oxidative stress, such combinations may more effectively induce cancer cell death while sparing normal cells.<br> <br> In advanced cancer it has been known to kill the cancer too fast, causing liver failure and death.<br>
332
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5-ALA
5-Aminolevulinic acid
NP
<b>Aminolevulinic acid </b>(5-ALA) is primarily known for its role as a biosynthetic precursor to heme<br> <br> -ALA is used in medical therapies such as photodynamic therapy (PDT) for certain types of cancer and skin conditions.<br> - Inside the cells, ALA enters the heme biosynthetic pathway and is converted to protoporphyrin IX (PpIX), a potent photosensitizer.<br> -The light activates the accumulated PpIX, leading to the production of reactive oxygen species (ROS).<br> -FDA approved June 2017 as a photo-imaging tool during neurosurgery for malignant glioma. The patient takes an oral dose of Gleolan 3 hours before surgery.<br> <br>
191
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5-FU
5-fluorouracil
D
<b>5-FU</b> is a chemotherapy medication used to treat various types of cancer, including colorectal, breast, stomach, and pancreatic cancer. It belongs to a class of drugs known as antimetabolites, which work by interfering with the growth and replication of cancer cells.<br> <b>Mechanisms:</b><br> - irreversibly inhibits Thymidylate Synthase (TS), thereby depleting the deoxythymidine monophosphate (dTMP) pool required for DNA synthesis. The resulting “thymineless death” prevents DNA replication and repair, particularly affecting rapidly proliferating tumor cells.<br> <br> 5-FU is a cornerstone in chemotherapy with a dual mechanism of action—primarily inhibiting thymidylate synthase (leading to disruption of DNA synthesis) and interfering with RNA processing by misincorporation. Its metabolism via activation (OPRT) and degradation (DPD) plays a crucial role in both its effectiveness and toxicity. Clinically, 5-FU is extensively used in treating a variety of cancers, most notably colorectal cancer, and remains a mainstay in multi-agent chemotherapeutic regimens due to its proven efficacy across diverse cancer types.<br> <br> 5-FU is one of the most common chemotherapeutic agents worldwide, particularly noted in gastrointestinal (GI) cancers.<br>
152
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5-HTP
5-Hydroxytryptophan
NP
<b>5-HTP</b> (5-Hydroxytryptophan) is a naturally occurring amino acid and chemical precursor in the biosynthesis of serotonin(5-HT).<br> -Serotonin (from 5-HTP) is further converted into melatonin in the pineal gland, regulating sleep-wake cycles<br> - 5-HTP freely crosses the blood–brain barrier.<br> -Serotonin Does not cross the blood-brain barrier well if excessively converted in the periphery, which is why it's often taken with carbidopa (a peripheral decarboxylase inhibitor) in clinical contexts.<br> -Doses over ~300–400 mg/day should be taken cautiously and under supervision.<br> -Alzheimer’s Disease (AD) patients show marked reductions in serotonin levels and serotonergic neurons, especially in the raphe nuclei and hippocampus. 5-HTP could help restore serotonin levels in the brain, potentially supporting cognition and mood.<br> -5-HTP may help reduce microglial activation and inflammatory cytokines (e.g. TNF-α, IL-6), both elevated in AD.<br> -Serotonin and melatonin (a downstream product of 5-HTP) have antioxidant properties, which might help reduce ROS-induced neuronal damage in AD.<br> -Many AD patients are on SSRIs or cholinesterase inhibitors, which could interact with 5-HTP.<br> <br>
275
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acet
acetaminophen
RD
<b>Acetaminophen:</b> The most common name in the United States.<br> Paracetamol: The name used in most of the world.<br> APAP: A common abbreviation used in biochemical and pharmacological studies.<br> <br> <b>Pathways:</b><br> -Cytochrome P450 Metabolism: NAPQI (N-acetyl-p-benzoquinone imine)<br> -Excess NAPQI depletes glutathione, a key antioxidant. The absence of sufficient glutathione leads to elevated oxidative stress.<br> -NF-κB Activation:<br> -Direct DNA Damage:<br> <br> Excess results in increased oxidative stress, mitochondrial dysfunction, and ultimately hepatocellular damage (liver injury)<br>
277
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acetaz
acetazolamide
RD
<b>Acetazolamide</b> is a synthetic small‐molecule drug primarily known as a carbonic anhydrase inhibitor. Although it is used mainly in treating glaucoma, altitude sickness, and certain neurological conditions, several studies have explored its potential in cancer treatment—mostly by targeting the tumor microenvironment. <br> <br> Acetazolamide might impact cancer biology:<br> <br> Carbonic Anhydrase Inhibition<br> • Acetazolamide inhibits several isoforms of carbonic anhydrase (especially CA IX and CA XII), enzymes that catalyze the reversible hydration of carbon dioxide to bicarbonate and protons.<br> • In many cancers, CA IX is overexpressed in response to hypoxia (mediated by HIF‐1α) and helps maintain an acidic extracellular environment while keeping the intracellular pH relatively neutral. This pH regulation supports cancer cell survival and invasion.<br> <br> Tumor pH Regulation<br> • By inhibiting carbonic anhydrases, acetazolamide can disrupt the acid–base balance in the tumor microenvironment.<br> • An altered pH gradient can impair cancer cell proliferation, migration, invasion, and can influence drug resistance. This disruption may also sensitize tumors to other therapeutic modalities.<br> <br> Hypoxia and HIF-1 Signaling<br> • Inhibiting CA IX may indirectly affect downstream targets of the HIF-1 pathway, potentially interfering with processes such as angiogenesis and metabolic adaptation.<br> <br> Impact on Tumor Metabolism<br> • The inhibition of carbonic anhydrases may affect the metabolic reprogramming seen in cancer cells.<br> • Alterations in bicarbonate and proton handling can influence metabolic pathways like glycolysis and oxidative phosphorylation, which are often altered in tumor cells.<br> <br> Potential Effects on Immune Response<br> • An acidic tumor microenvironment can contribute to immunosuppression.<br> • By modifying the pH environment through the inhibition of carbonic anhydrase, acetazolamide might help improve immune cell infiltration and function, although this area is still under investigation.<br> <br> In summary, while acetazolamide is a synthetic drug and not a natural product, its ability to alter key aspects of tumor biology—such as pH regulation, hypoxia response, and metabolic reprogramming—makes it an interesting candidate for adjuvant cancer therapies. However, its application in oncology remains investigational and would require further clinical validation.<br>
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Aco
Acoschimperoside P, 2’-acetate
NP
cardiac glycoside
<b>Acoschimperoside P, 2’-acetate</b> is isolated from the leaves of Vallaris glabra.<br> Acoschimperoside P, 2′-acetate is a natural glycoside with promising anticancer potential based on early-stage research that indicates possible induction of apoptosis, cell cycle arrest, and modulation of key signaling pathways (e.g., MAPK/ERK and PI3K/Akt). However, its pathways of action and overall clinical utility remain exploratory.<br> <br> Strong cytotoxicity against human pancreatic and human prostate cancer.<br> Acoschimperoside is a naturally occurring glycoside that has gained interest due to its potential therapeutic properties, including anticancer effects. Glycosides are compounds in which a sugar molecule (glycone) is linked to a non-sugar moiety (aglycone). In the case of acoschimperoside, the specific sugar–aglycone combination contributes to its bioactivity.<br> • As a glycoside, acoschimperoside consists of a sugar moiety attached to a non-carbohydrate component. This structural motif is common among many plant-derived compounds that exhibit various pharmacological activities.<br> The sugar portion can influence the solubility, bioavailability, and even the targeting mechanism of the molecule within biological systems. The aglycone, on the other hand, frequently contributes to the molecule’s direct bioactivity, such as modulating signaling pathways involved in cell survival, apoptosis, or inflammation.<br> Similar glycosides have been studied for their effects on pathways like apoptosis (programmed cell death), cell cycle regulation, and inhibition of survival pathways (such as PI3K/AKT/mTOR and NF‑κB signaling).<br>
254
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Adag
Adagrasib
D
<b>Adagrasib</b> is a small molecule inhibitor of the KRAS G12C mutation, which is a common driver mutation in various types of cancer, including non-small cell lung cancer (NSCLC), colorectal cancer (CRC), and pancreatic cancer.<br> <br> Mechanism of Action:<br> Adagrasib works by selectively inhibiting the activity of the KRAS G12C protein, which is a key player in the RAS/MAPK signaling pathway. By blocking the activity of KRAS G12C, adagrasib prevents the growth and proliferation of cancer cells, leading to tumor shrinkage and improved survival.<br> <br> Adagrasib is a promising treatment for patients with NSCLC and CRC who have the KRAS G12C mutation. Its ability to selectively inhibit KRAS G12C activity makes it a valuable option for patients who have limited treatment options. However, resistance to adagrasib can occur, and combination therapy may be necessary to overcome this resistance.<br> <br> Adagrasib is a novel KRAS G12C inhibitor that targets the mutant KRAS protein by covalently binding to its switch II pocket, thereby locking it in an inactive form. This inhibition blocks critical downstream signaling pathways, such as RAF/MEK/ERK and potentially PI3K/AKT/mTOR, which are essential for tumor growth and survival. Clinically, adagrasib is being developed and used primarily to treat NSCLC and other solid tumors with the KRAS G12C mutation, providing a targeted therapy option in a subset of cancers that historically have few effective targeted treatments.<br>
238
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TFdiG
Aflavin-3,3′-digallate
NP
<b>Aflavin-3,3′-digallate</b> (TFdiG) is a natural product. It is a flavonoid derivative that is found in certain plants, including tea plants (Camellia sinensis).<br> <br> TFdiG is a type of theaflavin, which is a class of flavonoids that are unique to tea plants. Theaflavins are formed during the fermentation process of tea production, and they are responsible for the characteristic astringent taste and dark color of black tea.<br> <br> TFdiG is one of the most abundant theaflavins found in black tea, and it has been shown to have a range of biological activities, including anti-inflammatory, antioxidant, and anti-cancer effects. Other natural sources of TFdiG include:<br> Black tea: TFdiG is found in high amounts in black tea, particularly in the leaves and buds of the tea plant.<br> Green tea: TFdiG is also found in green tea, although in lower amounts than in black tea.<br> Oolong tea: TFdiG is found in oolong tea, which is a type of tea that is partially fermented. <br> Aflavin-3,3′-digallate is a naturally derived polyphenolic compound that has shown promise in preclinical studies through its antioxidant, apoptosis-inducing, and cell cycle-arresting effects. Its potential modulation of key oncogenic signaling pathways is an additional point of interest. However, the compound is still in the early phases of research, lacking extensive in vivo validation and clinical trial data.<br>
251
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ATAGJ
Ai-Tong-An-Gao-Ji
NP
<b>Ai-Tong-An-Gao-Ji</b> is a traditional Chinese medicine (TCM) formula that has been studied for its potential anti-cancer properties. The formula is a combination of several herbs, including:<br> Ai ( Artemisia argyi or Artemisia annua)<br> Tong ( Polygonum multiflorum)<br> An ( Angelica sinensis)<br> Gao ( Glycyrrhiza uralensis)<br> Ji ( Astragalus membranaceus)<br> <br> Research has shown that Ai-Tong-An-Gao-Ji may have anti-tumor and anti-inflammatory effects, and may also have the ability to induce apoptosis (cell death) in cancer cells. However, more studies are needed to fully understand the effects of this formula on cancer.<br> <br> It's worth noting that traditional Chinese medicine formulas like Ai-Tong-An-Gao-Ji are often used in conjunction with conventional cancer treatments, and may be used to alleviate symptoms and improve quality of life for cancer patients.<br> <br> Ai-Tong-An-Gao-Ji is a traditional Chinese medicine formulation used primarily for alleviating pain, reducing inflammation, and supporting overall well-being. While some of its individual herbal components have been investigated for antioxidant, anti-inflammatory, and potential antiproliferative properties, the formulation as a whole is not established as a stand-alone anticancer treatment in modern clinical practice. Its usage remains largely within the TCM framework—often as an adjunct to other treatments—with mechanisms of action that may include modulation of inflammatory and immune pathways, pain relief, and antioxidant protection.<br>
196
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Ajoene
Ajoene (compound of Garlic)
NP
<b>Ajoene</b> is a compound found in garlic, specifically in the oil extracted from crushed garlic cloves. It has been studied for its potential anti-cancer properties. Research suggests that ajoene may have several mechanisms by which it can inhibit the growth of cancer cells and induce apoptosis (cell death).<br> <br> Approximate ajoene content values for different parts of the garlic plant:<br> Garlic bulbs: 1-5 mg of ajoene per clove<br> Garlic scapes (green shoots): 0.5-2 mg of ajoene per 100g<br> Garlic chives (leaves): 0.5-2 mg of ajoene per 100g<br> Garlic microgreens: 1-5 mg of ajoene per 100g<br> <br> μM concentrations of ajoene that have been reported to exhibit biological activity:<br> Antimicrobial activity: 1-10 μM<br> Antioxidant activity: 1-50 μM<br> Anti-inflammatory activity: 5-20 μM<br> Anticancer activity: 10-50 μM<br> Cardiovascular health: 5-20 μM<br> <br> Approximate μM concentrations of ajoene that can be achieved with different amounts of garlic or garlic chives:<br> 1 clove of garlic (3g): approximately 1-5 μM of ajoene<br> 1 tablespoon of minced garlic (15g): approximately 5-15 μM of ajoene<br> 1 cup of chopped garlic (100g): approximately 30-60 μM of ajoene<br> 1 tablespoon of chopped garlic chives (15g): approximately 0.5-2 μM of ajoene<br> 1 cup of chopped garlic chives (100g): approximately 5-10 μM of ajoene<br> 1 ounce (28g) of garlic microgreens: approximately 10-30 μM of ajoene<br> 1 cup of garlic microgreens (100g): approximately 30-60 μM of ajoene<br> 1 ounce (28g) of garlic chive microgreens: approximately 5-15 μM of ajoene<br> 1 cup of garlic chive microgreens (100g): approximately 15-30 μM of ajoene<br>
26
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Akk
Akkermansia
NP
Bacteria
<b>Akkermansia</b> improves cancer immunotherapy.<br> Gram-negative anaerobic bacterium of the phylum Verrucomicrobia.<br> Akkermansia muciniphila is a typical member of the human gut microbiome.<br> <br> Summary:<br> -Can significantly inhibit carcinogenesis and improve anti-tumor effects, thus increasing the effectiveness of cancer immunotherapy.<br> -Enhanced abundance of Akkermansia in the intestine of those who responded positively to the ICI(immune checkpoint inhibitors).<br> <br> -Eat fermented foods then fibre to maintain them. Fruits and vegs for fibre Chicory root for fibre (inulin which is main prebiotic).<br> <br> • Akkermansia muciniphila specializes in degrading mucin, the glycoprotein component of the mucus layer lining the gut.<br> <br> • Early clinical findings suggest that higher levels of Akkermansia correlate with improved responses to immune checkpoint inhibitors in cancer therapy.(e.g., anti-PD-1/PD-L1 therapy).<br> <br> Akkermansia, and in particular Akkermansia muciniphila, is a key gut bacterium implicated in supporting intestinal health, modulating immune responses, and influencing metabolic balance. Its roles in enhancing gut barrier integrity, reducing inflammation, and possibly improving responses to cancer immunotherapy make it an attractive target for probiotic development and microbiome-based interventions. Although not a drug in itself, Akkermansia’s potential as a biomarker and therapeutic adjunct offers promising avenues for integrative approaches in precision medicine and cancer care.<br>
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AL
Allicin (mainly Garlic)
NP
<b>Garlic</b> (Allium sativum L.) (active ingredient- Allicin, an active sulfer compound).<br> Summary:<br> - Four main organic sulfides in garlic, diallyl disulfide (DADS), diallyl trisulfide (DATS), S-allylmercaptocysteine (SAMC) and allicin.<br> - Reversible inhibitor of ACSS2.<br> - may inhibit NF-κB signaling<br> - induce oxidative stress in cancer cells by generating ROS<br> - might downregulate STAT3 activation<br> - Inconclusive evidence for cancer treatment.<br> - may inhibit <a href="tbResEdit.php?rid=2558">platelet aggregation</a><br> Allicin is a reactive sulfur species (RSS) [23] with oxidizing properties, and it is able to oxidize thiols in cells, e.g., glutathione and cysteine residues in proteins.<br> -Allicin is not present in intact garlic; rather, it is formed when garlic is chopped or crushed. -Using crushed or chopped raw garlic or adding garlic at the end of the cooking process (after the heat is reduced) can help preserve its potential allicin content.<br> <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC6073756/"> "Consumption of alliinase-inhibited cooked garlic was found to give higher than expected allicin bioequivalence, with AMS formation being about 30% (roasted garlic) or 16% (boiled garlic) that of crushed raw garlic."</a> <br> <br> -Note <a href="tbResList.php?qv=27&tsv=1109&wNotes=on&exSp=open">half-life</a> reports vary 2.5-90hrs?.<br> -low solubility of apigenin in water : <a href="tbResList.php?qv=27&tsv=792&wNotes=on&exSp=open">BioAv</a> <br><br> <br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - induce <a href="tbResList.php?qv=27&tsv=275&wNotes=on">ROS</a> production<br> - ROS↑ related: <a href="tbResList.php?&qv=27&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?&qv=27&tsv=103&wNotes=on">ER Stress↑</a>, <a href="tbResList.php?&qv=27&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>, <a href="tbResList.php?&qv=27&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?&qv=27&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?&qv=27&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?&qv=27&tsv=459&wNotes=on">UPR↑</a>, <a href="tbResList.php?&qv=27&tsv=239&wNotes=on">cl-PARP↑</a>, <a href="tbResList.php?&qv=27&wNotes=on&word=HSP">HSP↓</a> <br> <!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, --> - Lowers <a href="tbResList.php?&qv=27&tsv=1103&wNotes=on&word=antiOx↓">AntiOxidant</a> defense in Cancer Cells: <a href="tbResList.php?&qv=27&tsv=226&wNotes=on&word=NRF2↓">NRF2↓</a>, <a href="tbResList.php?&qv=27&tsv=137&wNotes=on&word=GSH↓">GSH↓</a> <br> - Raises <a href="tbResList.php?&qv=27&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?&qv=27&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?&qv=27&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?&qv=27&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?&qv=27&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?&qv=27&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?&qv=27&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?&qv=27&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, <a href="tbResList.php?&qv=27&tsv=235&wNotes=on&word=p38↓">p38↓</a>, Pro-Inflammatory Cytokines : <a href="tbResList.php?&qv=27&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, <a href="tbResList.php?&qv=27&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?&qv=27&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <a href="tbResList.php?&qv=27&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a> <br> - PI3K/AKT(Inhibition), JAK/STATs, Wnt/β-catenin, AMPK, MAPK/ERK, and JNK.<br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓--> - inhibit Growth/Metastases : <a href="tbResList.php?&qv=27&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?&qv=27&tsv=201&wNotes=on">MMP2↓</a>, <a href="tbResList.php?&qv=27&tsv=203&wNotes=on">MMP9↓</a>, <a href="tbResList.php?&qv=27&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?&qv=27&tsv=105&wNotes=on">ERK↓</a> <br> <!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, --> - reactivate genes thereby inhibiting cancer cell growth : <a href="tbResList.php?qv=27&tsv=140&wNotes=on">HDAC↓</a>(not commonly listed as inhibitor), <a href="tbResList.php?qv=27&tsv=85&wNotes=on">DNMT1↓</a>, <a href="tbResList.php?qv=27&tsv=236&wNotes=on">P53↑</a>, <a href="tbResList.php?&qv=27&wNotes=on&word=HSP">HSP↓</a> <br> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?&qv=27&tsv=322&wNotes=on">TumCCA↑</a>, <a href="tbResList.php?&qv=27&tsv=73&wNotes=on">cyclin D1↓</a>, <a href="tbResList.php?&qv=27&tsv=378&wNotes=on">cyclin E↓</a>, <a href="tbResList.php?&qv=27&tsv=467&wNotes=on">CDK2↓</a>, <a href="tbResList.php?&qv=27&tsv=894&wNotes=on">CDK4↓</a>, <a href="tbResList.php?&qv=27&tsv=895&wNotes=on">CDK6↓</a>, <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?&qv=27&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?&qv=27&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?&qv=27&tsv=105&wNotes=on">ERK↓</a>, <br> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - inhibits <a href="tbResList.php?qv=27&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=27&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?&qv=27&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?&qv=27&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, <br> <!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, --> - inhibits Cancer Stem Cells : <a href="tbResList.php?qv=27&tsv=795&wNotes=on">CSC↓</a>, <br> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=27&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=27&tsv=4&wNotes=on">AKT↓</a>, <a href="tbResList.php?qv=27&tsv=373&wNotes=on">STAT3</a>, <a href="tbResList.php?qv=27&tsv=377&wNotes=on">Wnt↓</a>, <a href="tbResList.php?qv=27&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=27&tsv=9&wNotes=on">AMPK↓</a>, <a href="tbResList.php?qv=27&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=27&tsv=168&wNotes=on">JNK</a>, <br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=27&tsv=1106&wNotes=on&exSp=open">chemo-sensitization</a>, <a href="tbResList.php?qv=27&tsv=1171&wNotes=on&exSp=open">chemoProtective</a>, <a href="tbResList.php?qv=27&tsv=1107&wNotes=on&exSp=open">RadioSensitizer</a>, <a href="tbResList.php?qv=27&tsv=1185&wNotes=on&exSp=open">RadioProtective</a>, <a href="tbResList.php?qv=27&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <a href="tbResList.php?qv=27&tsv=1105&wNotes=on">Neuroprotective</a>, <a href="tbResList.php?qv=27&tsv=557&wNotes=on">Cognitive</a>, <a href="tbResList.php?qv=27&tsv=1175&wNotes=on">Renoprotection</a>, <a href="tbResList.php?qv=27&tsv=1179&wNotes=on">Hepatoprotective</a>, <a href="tbResList.php?&qv=27&tsv=1188&wNotes=on">CardioProtective</a>, <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=27&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br> <br> Allicin has been reported to exhibit a range of effects, including:<br> Antimicrobial activity: 10-50 μM<br> Antioxidant activity: 10-100 μM<br> Anti-inflammatory activity: 20-50 μM <br> Anticancer activity: 50-100 μM or (50–300uM) (2–5 mg allicin per kilogram of body weight per day)<br> Cardiovascular health: 20-50 μM<br> <br> Approximate μM concentrations of allicin that can be achieved:<br> 1 clove of garlic (3g): approximately 10-50 μM of allicin<br> single clove of garlic may yield about 5–9 mg of allicin,<br> 1 tablespoon of minced garlic (15g): approximately 50-150 μM of allicin<br> 1 cup of chopped garlic (100g): approximately 200-500 μM of allicin<br> 1 tablespoon of chopped garlic chives (15g): approximately 5-20 μM of allicin<br> 1 cup of chopped garlic chives (100g): approximately 20-50 μM of allicin<br> 1 ounce (28g) of garlic microgreens: approximately 50-200 μM of allicin<br> 1 cup of garlic microgreens (100g): approximately 200-500 μM of allicin<br> 1 ounce (28g) of garlic chive microgreens: approximately 20-50 μM of allicin<br> 1 cup of garlic chive microgreens (100g): approximately 50-100 μM of allicin<br> <br> Allicin is a bioactive compound derived from garlic that has garnered significant interest for its potential anticancer properties through multiple mechanisms, including antioxidant activity, induction of apoptosis, cell cycle arrest, and modulation of key signaling pathways. While regular dietary intake of garlic is associated with cancer prevention benefits, allicin is also being explored as an adjunct to conventional cancer treatments. <br> <br> Available in supplement tablet/capsule form for example at 2000mg (fresh bulb equilvalent)<br> IC50 of normal cells it >160mg/mL (large selectivity).<br> IC50 might be about 12-30ug/ml (approximately 62-185 µM) (which is about 30-90 grams of garlic consumption).<br> This makes it difficult to consume enough supplements to achieve that level.<br> <br> Pathways:<br> <br> ROS Generation and Oxidative Stress (inducing)<br> • ROS generation is often considered a primary trigger that feeds into downstream pathways (e.g., MAPK activation, mitochondrial membrane permeabilization).<br> Mitochondrial (Intrinsic) Apoptotic Pathway<br> • ROS-induced mitochondrial damage can lead to the release of cytochrome c and subsequent activation of caspases (e.g., caspase-9 and caspase-3).<br> NF-κB Signaling Inhibition (block)<br> Modulation of MAPK Pathways (e.g., p38 MAPK and JNK)<br> • ROS generation by allicin can activate stress-responsive kinases such as p38 MAPK and c-Jun N-terminal kinase (JNK).<br> Inhibition of PI3K/Akt Pathway<br> ROS levels and PI3K/Akt signaling, with increased oxidative stress often correlating with reduced Akt phosphorylation and activity.<br> <br> At lower doses, allicin may lead to a modest increase in ROS levels that the cell’s antioxidant defenses (e.g., glutathione, superoxide dismutase) can manage<br>
278
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almon
almonertinib
D
<b>Almonertinib</b> is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI). It is chemically designed and manufactured.<br> <br> It is mainly used in the treatment of non-small cell lung cancer (NSCLC) with specific EGFR mutations. The drug is designed to overcome resistance to earlier-generation TKIs and to provide a more potent inhibition of EGFR signaling in tumors.<br>
28
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AV
Aloe vera
NP
<b>Aloe vera</b> Therapeutic properties include: anti-microbial, anti-viral, anti-cancer, anti-oxidant, anti-inflammatory, skin protection, wound healing, and regulation of blood glucose and cholesterol.<br> active constituents, such as aloe-emodin and acemannan.<br> <br> • Aloe vera extracts harbor antioxidant compounds that can scavenge free radicals, protecting cells from oxidative damage—a factor in aging and cancer development.<br> <br> Aloe vera’s blend of bioactive compounds offers a range of biological activities—including anti-inflammatory, antioxidant, immunomodulatory, and wound-healing effects—that have attracted interest for complementary roles in health maintenance and cancer supportive care. While it is not a primary anticancer agent, its potential to mitigate treatment side effects, enhance immune responses, and possibly contribute to chemoprevention makes it a subject of ongoing research. <br>
116
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aLinA
alpha Linolenic acid
NP
<b>Alpha Linolenic acid</b> naturally-occurring fatty acid. Found in vegetable oils, plant oils, nuts and meat.<br> • Alpha linolenic acid (ALA) is an essential omega-3 fatty acid commonly found in plant sources such as flaxseed, chia seeds, walnuts, and certain vegetable oils.<br> • As an essential fatty acid, ALA must be obtained from the diet and serves as a precursor to longer-chain omega-3 fatty acids, namely eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).<br> • While ALA itself is not a strong antioxidant, its downstream metabolites can indirectly support antioxidant defense systems.<br> • By reducing oxidative stress, ALA may help protect cellular DNA from damage that can trigger carcinogenesis.<br>
29
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ALA
Alpha-Lipoic-Acid
NP
antioxidant, energy production in cell mitochondria
<b>Alpha-Lipoic-Acid:</b> also known as lipoic acid or thioctic acid (reduced form is dihydrolipoic acid).<br> "Universal antioxidant" because it is both water- and fat-soluble and can neutralize free radicals.<br> -Treatment sometimes as ALA/N (alpha-lipoic acid/low-dose naltresone)<br> -Also done in IV<br> -Decreases ROS production, but also has pro-oxidant role.<br> Normal adult can take 300 milligrams twice a day with food, but they should always take a B-complex vitamin with it. Because B complex vitamins, especially thiamine, and biotin, and riboflavin, are depleted during this metabolic process.<br> α-Lipoic acid acts as a chelating agent for metal ions, a quenching agent for reactive oxygen species, and a reducing agent for the oxidized form of glutathione and vitamins C and E.<br> -It seems a paradox that LA functions as both antioxidant and prooxidant. LA functions the pro-oxidant only in special cancer cells, such as A549 and PC9 cells which should show high-level NRF2 expression and high glycolytic level. Through inhibiting PDK1 to further prohibit NRF2; LA functions as anticancer prooxidant.<br> <br> α-lipoic acid possesses excellent silver chelating properties.<br> <br> - ALA acts as pro-Oxidant only in <a href="tbResEdit.php?rid=278">cancer cells:#278</a> - Pro-Oxidant Dose <a href="tbResEdit.php?rid=304">margin >100uM:#304 </a><br> <br> - Bioavailability: 80-90%, but conversion to EPA/DHA is 5-10% (and takes longer time).<br> - AI (Adequate Intake): 1.1-1.6g/day. <br> - human studies have shown that ALA levels decline significantly with age <br> - 1g of ALA might achieve 500uM in the blood. <br> - ALA is poorly soluble, lecithin has been used as an amphiphilic matrix to enhance its bioavailability. <br> - Pilot studies or observational interventions have used flaxseed supplementation (rich in ALA) in doses providing roughly 3–4 g of ALA daily.<br> - Flaxseed oil is even more concentrated in ALA – typical 50–60% ALA by weight.<br> - single walnut may contain 300mg of ALA<br> - chia oil contains 55-65% ALA.<br> - α-LA can also be obtained from the diet through the consumption of dark green leafy vegetables and meats<br> - ALA is more stable in chia seeds, (2grams of ALA per tablespoon)<br> - ALA degrades when exposed to heat, light, and air. (prone to oxidation)<br> <br> -Note <a href="tbResList.php?qv=29&tsv=1109&wNotes=on&exSp=open">half-life</a> 1-2 hrs.<br> <a href="tbResList.php?qv=29&tsv=792&wNotes=on&exSp=open">BioAv</a> 30-40% from walnuts, 60-80% from supplements. Co-ingestion with fat improves absorption. Both fat and water soluble <br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - induce <a href="tbResList.php?qv=29&tsv=275&wNotes=on">ROS</a> production<br> - ROS↑ related: <a href="tbResList.php?qv=29&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?qv=29&tsv=103&wNotes=on">ER Stress↑</a>, <a href="tbResList.php?qv=29&tsv=459&wNotes=on">UPR↑</a>, <a href="tbResList.php?qv=29&tsv=356&wNotes=on">GRP78↑</a>, <!-- <a href="tbResList.php?qv=29&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>, --> <a href="tbResList.php?qv=29&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?qv=29&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?qv=29&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <!-- <a href="tbResList.php?qv=29&tsv=239&wNotes=on">cl-PARP↑</a>, --> <!-- <a href="tbResList.php?qv=29&wNotes=on&word=HSP">HSP↓</a>, --> <!-- <a href="tbResList.php?qv=29&wNotes=on&word=Prx">Prx</a>, --><!-- mitochondrial antioxidant enzyme--> <br> <!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, --> - Lowers AntiOxidant defense in Cancer Cells: <a href="tbResList.php?qv=29&tsv=226&wNotes=on&word=NRF2↓">NRF2↓</a>, <!-- <a href="tbResList.php?qv=29&word=Trx&wNotes=on">TrxR↓**</a>, --><!-- major antioxidant system --> <a href="tbResList.php?qv=29&tsv=298&wNotes=on&word=SOD↓">SOD↓</a>, <a href="tbResList.php?qv=29&tsv=137&wNotes=on&word=GSH↓">GSH↓</a> <a href="tbResList.php?qv=29&tsv=46&wNotes=on">Catalase↓</a> <a href="tbResList.php?qv=29&tsv=597&wNotes=on">HO1↓</a> <a href="tbResList.php?qv=29&wNotes=on&word=GPx">GPx↓</a> <br> - Raises <a href="tbResList.php?qv=29&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?qv=29&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>, <a href="tbResList.php?qv=29&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?qv=29&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?qv=29&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?qv=29&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <!-- genes involved in the oxidative stress-antioxidant defense system PRNP, NQO1, and GCLM --> <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?qv=29&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?qv=29&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?qv=29&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, <!-- <a href="tbResList.php?qv=29&tsv=235&wNotes=on&word=p38↓">p38↓</a>, --> Pro-Inflammatory Cytokines : <!-- <a href="tbResList.php?qv=29&tsv=908&wNotes=on&word=NLRP3↓">NLRP3↓</a>, --> <a href="tbResList.php?qv=29&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, <a href="tbResList.php?qv=29&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?qv=29&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <a href="tbResList.php?qv=29&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a> <br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓ inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.--> - inhibit Growth/Metastases : <a href="tbResList.php?qv=29&tsv=604&wNotes=on">TumMeta↓</a>, <a href="tbResList.php?qv=29&tsv=323&wNotes=on">TumCG↓</a>, <a href="tbResList.php?qv=29&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=29&tsv=204&wNotes=on">MMPs↓</a>, <a href="tbResList.php?qv=29&tsv=201&wNotes=on">MMP2↓</a>, <a href="tbResList.php?qv=29&tsv=203&wNotes=on">MMP9↓</a>, <!-- <a href="tbResList.php?qv=29&tsv=308&wNotes=on">TIMP2</a>, --> <a href="tbResList.php?qv=29&wNotes=on&word=IGF">IGF-1↓</a>, <!-- <a href="tbResList.php?qv=29&tsv=428&wNotes=on">uPA↓</a>, --> <a href="tbResList.php?qv=29&tsv=334&wNotes=on">VEGF↓</a>, <!-- <a href="tbResList.php?qv=29&tsv=1284&wNotes=on">ROCK1↓</a>, --> <a href="tbResList.php?qv=29&tsv=110&wNotes=on">FAK↓</a>, <!-- <a href="tbResList.php?qv=29&tsv=273&wNotes=on">RhoA↓</a>, --> <a href="tbResList.php?qv=29&tsv=214&wNotes=on">NF-κB↓</a>, <!-- <a href="tbResList.php?qv=29&tsv=79&wNotes=on">CXCR4↓</a>, --> <!-- <a href="tbResList.php?qv=29&tsv=1247&wNotes=on">SDF1↓</a>, --> <a href="tbResList.php?qv=29&tsv=304&wNotes=on">TGF-β↓</a>, <a href="tbResList.php?qv=29&tsv=719&wNotes=on">α-SMA↓</a>, <a href="tbResList.php?qv=29&tsv=105&wNotes=on">ERK↓</a> <!-- <a href="tbResList.php?qv=29&tsv=1178&wNotes=on">MARK4↓</a> --> <!-- contributing to tumor growth, invasion, and metastasis--> <br> <!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, --> <!-- - reactivate genes thereby inhibiting cancer cell growth : <a href="tbResList.php?qv=29&tsv=140&wNotes=on">HDAC↓</a>, <a href="tbResList.php?qv=29&wNotes=on&word=DNMT">DNMTs↓</a>, <a href="tbResList.php?qv=29&tsv=108&wNotes=on">EZH2↓</a>, <a href="tbResList.php?qv=29&tsv=236&wNotes=on">P53↑</a>, <a href="tbResList.php?qv=29&wNotes=on&word=HSP">HSP↓</a>, <a href="tbResList.php?qv=29&tsv=506&wNotes=on">Sp proteins↓</a>, <a href="tbResList.php?qv=29&wNotes=on&word=TET">TET↑</a> <br> --> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?qv=29&tsv=322&wNotes=on">TumCCA↑</a>, <a href="tbResList.php?qv=29&tsv=73&wNotes=on">cyclin D1↓</a>, <!-- <a href="tbResList.php?qv=29&tsv=378&wNotes=on">cyclin E↓</a>, --> <!-- <a href="tbResList.php?qv=29&tsv=467&wNotes=on">CDK2↓</a>, --> <!-- <a href="tbResList.php?qv=29&tsv=894&wNotes=on">CDK4↓</a>, --> <!-- <a href="tbResList.php?qv=29&tsv=895&wNotes=on">CDK6↓</a>, --> <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?qv=29&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?qv=29&tsv=324&wNotes=on">TumCI↓</a>, <a href="tbResList.php?qv=29&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <!-- encourages invasion, proliferation, EMT, and angiogenesis --> <a href="tbResList.php?qv=29&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?qv=29&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=29&tsv=96&wNotes=on">EMT↓</a>, <!-- <a href="tbResList.php?qv=29&wNotes=on&word=TOP">TOP1↓</a>, --> <!-- <a href="tbResList.php?qv=29&tsv=657&wNotes=on">TET1</a>, --> <br> <!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS --> - inhibits <a href="tbResList.php?qv=29&tsv=129&wNotes=on">glycolysis</a> <!-- /<a href="tbResList.php?qv=29&tsv=947&wNotes=on">Warburg Effect</a> --> and <a href="tbResList.php?qv=29&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> : <a href="tbResList.php?qv=29&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=29&tsv=772&wNotes=on">PKM2↓</a>, <!-- <a href="tbResList.php?qv=29&tsv=35&wNotes=on">cMyc↓</a>, --> <a href="tbResList.php?qv=29&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>, <!-- <a href="tbResList.php?qv=29&tsv=906&wNotes=on">LDH↓</a>, --> <a href="tbResList.php?qv=29&tsv=175&wNotes=on&word=LDH">LDHA↓</a>, <a href="tbResList.php?qv=29&tsv=773&wNotes=on">HK2↓</a>, <a href="tbResList.php?qv=29&wNotes=on&word=PFK">PFKs↓</a>, <a href="tbResList.php?qv=29&wNotes=on&word=PDK">PDKs↓</a>, <a href="tbResList.php?qv=29&tsv=847&wNotes=on">ECAR↓</a>, <a href="tbResList.php?qv=29&tsv=230&wNotes=on">OXPHOS↓</a>, <a href="tbResList.php?qv=29&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=29&tsv=1278&wNotes=on">Glucose↓</a>, <a href="tbResList.php?qv=29&tsv=623&wNotes=on">GlucoseCon↓</a> <br> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - inhibits <a href="tbResList.php?qv=29&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=29&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=29&tsv=143&wNotes=on">HIF-1α↓</a>, <!-- <a href="tbResList.php?qv=29&wNotes=on&word=NOTCH">Notch↓</a>, --> <!-- <a href="tbResList.php?qv=29&wNotes=on&word=FGF">FGF↓</a>, --> <!-- <a href="tbResList.php?qv=29&wNotes=on&word=PDGF">PDGF↓</a>, --> <a href="tbResList.php?qv=29&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, <a href="tbResList.php?qv=29&&wNotes=on&word=ITG">Integrins↓</a>, <br> <!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, --> - small indication of inhibiting Cancer Stem Cells : <a href="tbResList.php?qv=29&tsv=795&wNotes=on">CSC↓</a>, <!-- <a href="tbResList.php?qv=29&tsv=524&wNotes=on">CK2↓</a>, --> <!-- <a href="tbResList.php?qv=29&tsv=141&wNotes=on">Hh↓</a>, --> <!-- <a href="tbResList.php?qv=29&tsv=434&wNotes=on">GLi↓</a>, --> <!-- <a href="tbResList.php?qv=29&tsv=124&wNotes=on">GLi1↓</a>, --> <!-- <a href="tbResList.php?qv=29&tsv=677&wNotes=on">CD133↓</a>, --> <a href="tbResList.php?qv=29&tsv=655&wNotes=on">CD24↓</a>, <a href="tbResList.php?qv=29&tsv=342&wNotes=on">β-catenin↓</a>, <!-- <a href="tbResList.php?qv=29&tsv=357&wNotes=on">n-myc↓</a>, --> <!-- <a href="tbResList.php?qv=29&tsv=656&wNotes=on">sox2↓</a>, --> <!-- <a href="tbResList.php?qv=29&wNotes=on&word=NOTCH">Notch2↓</a>, --> <!-- <a href="tbResList.php?qv=29&tsv=1024&wNotes=on">nestin↓</a>, --> <!-- <a href="tbResList.php?qv=29&tsv=508&wNotes=on">OCT4↓</a>, --> <br> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=29&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=29&tsv=4&wNotes=on">AKT↓</a>, <a href="tbResList.php?qv=29&wNotes=on&word=JAK">JAK↓</a>, <a href="tbResList.php?qv=29&wNotes=on&word=STAT">STAT↓</a>, <!-- <a href="tbResList.php?qv=29&tsv=377&wNotes=on">Wnt↓</a>, --> <a href="tbResList.php?qv=29&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=29&tsv=9&wNotes=on">AMPK</a>, <!-- <a href="tbResList.php?qv=29&tsv=475&wNotes=on">α↓</a>, --> <a href="tbResList.php?qv=29&tsv=105&wNotes=on">ERK↓</a>, <!-- <a href="tbResList.php?qv=29&tsv=1014&wNotes=on">5↓</a>, --> <a href="tbResList.php?qv=29&tsv=168&wNotes=on">JNK</a>, <!-- - <a href="tbResList.php?qv=29&wNotes=on&word=SREBP">SREBP</a> (related to cholesterol). --><br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=29&tsv=1106&wNotes=on">chemo-sensitization</a>, <a href="tbResList.php?qv=29&tsv=1171&wNotes=on">chemoProtective</a>, <a href="tbResList.php?qv=29&tsv=1107&wNotes=on">RadioSensitizer</a>, <a href="tbResList.php?qv=29&tsv=1185&wNotes=on">RadioProtective</a>, <a href="tbResList.php?qv=29&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <a href="tbResList.php?qv=29&tsv=1105&wNotes=on">Neuroprotective</a>, <a href="tbResList.php?qv=29&tsv=557&wNotes=on">Cognitive</a>, <a href="tbResList.php?qv=29&tsv=1175&wNotes=on">Renoprotection</a>, <a href="tbResList.php?qv=29&tsv=1179&wNotes=on">Hepatoprotective</a>, <a href="tbResList.php?&qv=29&tsv=1188&wNotes=on">CardioProtective</a>, <br> <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=29&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br>
272
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AMQ
Amodiaquine
RD
<b>Amodiaquine</b> is a synthetic 4-aminoquinoline compound initially developed as an antimalarial agent. Like chloroquine, it is based on the quinoline scaffold and was chemically synthesized rather than being directly extracted from natural products.<br> <br> Pathways:<br> -Autophagy Inhibition:<br> Inhibition of autophagy and lysosomal dysfunction can lead to cellular stress through accumulation of damaged proteins and organelles, triggering pathways such as the unfolded protein response (UPR) and increasing reactive oxygen species (ROS).<br>
30
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And
Andrographis
NP
<b>Andrographis</b> (typically referring to Andrographis paniculata).<br> Bitter tasting annual plant prevalent in much of Asia.<br> <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC4032030/">"used traditionally for the treatment of array of diseases such as cancer, diabetes, high blood pressure, ulcer, leprosy, bronchitis, skin diseases, flatulence, colic, influenza, dysentery, dyspepsia and malaria for centuries in Asia, America and Africa continents."</a><br> <br> Andrographolide:<br> – Is a specific diterpenoid lactone and the major active constituent extracted from Andrographis paniculata.<br> – It is responsible for many of the therapeutic effects attributed to the plant, including anti-inflammatory and antioxidant properties.<br> <br> A. Anti-Inflammatory Effects.<br> • Andrographolide has been shown to inhibit the NF-κB pathway, leading to a reduction in the transcription of inflammatory cytokines (e.g., TNF-α, IL-6).<br> • Andrographolide has been reported to cause cell cycle arrest at critical checkpoints (such as G0/G1 or G2/M phase) in some cancer cell models.<br> <br> Andrographis, primarily through its active constituent andrographolide, offers compelling anti-inflammatory, immunomodulatory, pro-apoptotic, and antiproliferative properties. While not a standard anticancer agent, its capacity to modulate key pathways in cellular stress response and inflammation makes it an attractive candidate for complementary research in oncology.<br> <br> Andrographis paniculata, also known as the "King of Bitters," is a plant native to India and Southeast Asia. Its aqueous extract, Andrographis paniculata aqueous extract (APAE), has been studied for its potential anti-cancer properties.<br> • Inhibition of cancer cell growth: APAE has been shown to inhibit the growth of various cancer cell lines, including breast, lung, colon, and prostate cancer cells.<br> • Induction of apoptosis: APAE has been found to induce apoptosis (programmed cell death) in cancer cells, which may help to prevent tumor growth and progression.<br> • Anti-inflammatory effects: APAE has anti-inflammatory properties, which may help to reduce the risk of cancer development and progression.<br> • Antioxidant activity: APAE has antioxidant activity, which may help to protect against oxidative stress and DNA damage.<br> <br> Key compounds:Andrographolide, Neoandrographolide<br> APAE may interact with certain medications, including blood thinners and diabetes medications, and may not be suitable for individuals with certain medical conditions, such as autoimmune disorders.<br>
31
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ACNs
Anthocyanins
NP
<a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC5429338/"> <b>"Anthocyanins</b> are a class of water‐soluble flavonoids, which show a range of pharmacological effects, such as prevention of cardiovascular disease, obesity control and antitumour activity. Their potential antitumour effects are reported to be based on a wide variety of biological activities including antioxidant; anti‐inflammation; anti‐mutagenesis; induction of differentiation; inhibiting proliferation by modulating signal transduction pathways, inducing cell cycle arrest and stimulating apoptosis or autophagy of cancer cells; anti‐invasion; anti‐metastasis; reversing drug resistance of cancer cells and increasing their sensitivity to chemotherapy." </a> <br> • Anthocyanins are a class of water-soluble flavonoid pigments responsible for the red, purple, and blue hues in many fruits, vegetables, and flowers (e.g., berries, red grapes, and eggplants). <br> • Anthocyanins can effectively scavenge free radicals and reduce oxidative stress, thereby protecting cellular components like DNA, lipids, and proteins from oxidative damage—a factor linked to carcinogenesis. <br> • Their antioxidant capacity helps in neutralizing reactive oxygen species (ROS), which can otherwise promote mutations and tumor initiation. <br> • Anthocyanins have been shown to inhibit pro-inflammatory cytokines (e.g., TNF-α, IL-6) and enzymes (e.g., COX-2), reducing the inflammatory signals associated with cancer progression. <br> • They may modulate pathways such as NF-κB, MAPK, and PI3K/Akt, contributing to the downregulation of genes involved in survival and proliferation of cancer cells. <br> • Anthocyanins have been found to inhibit the formation of new blood vessels (angiogenesis) essential for tumor growth and metastatic spread. <br>
266
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antiOx
Anti-oxidants
NP
<b>"Antioxidants</b> are compounds that inhibit oxidation (usually occurring as autoxidation), a chemical reaction that can produce free radicals." <br> For example Vitamin C (normally Antioxidant), Vitamin e, and Trolox are anti-oxidants. <br> Berries: Blueberries, Strawberries, Raspberries, Blackberries <br> Fruits: Grapes, Pomegranates, Oranges, Apples <br> Vegetables: Spinach and other leafy greens, Kale, Broccoli, Brussels sprouts <br> Nuts and Seeds: Walnuts, Almonds, Flaxseeds, Chia seeds <br> Beverages: Green tea, Black tea <br> Spices and Herbs: curcumin, Ginger, Garlic, Cinnamon <br> Other: Dark chocolate (with high cocoa content), Beans and legumes, Tomatoes (rich in lycopene) <br> <br> Antioxidants are compounds that help neutralize free radicals—unstable molecules that can damage cells and contribute to the development of chronic diseases including cancer. <br> <br> Cancer Prevention: <br> Mechanism: Antioxidants protect cells from oxidative damage caused by free radicals, which can lead to mutations in DNA. Over time, these mutations might initiate or promote the growth of cancer cells. <br> Dietary Role: Eating a diet rich in antioxidants (fruits, vegetables, and other plant-based foods) has been associated with a lower risk of some cancers. Many epidemiological studies suggest that diets high in natural antioxidants are linked to a reduced risk of cancer. <br> <br> During Cancer Treatment: <br> Controversy: There is debate about whether taking antioxidant supplements during chemotherapy or radiation therapy is beneficial or harmful. Many therapies such as Chemotherapy raise the ROS(Reactive oxygen Species) intentionally to kill cancer cells. Some theory applies that antioxidants might prevent the ROS from being raised, and hence reduce treatment effectiveness. Some laboratory and clinical studies indicate that antioxidants might protect not only healthy cells but also cancer cells against the oxidative damage intentionally induced by these treatments. This could potentially reduce the effectiveness of cancer therapies. Another theory is there is a differential effect from taking antioxidants. Meaning the antioxidants help protect normal cells, but not the cancer cells. <br> Recommendation: Many oncologists recommend caution with high-dose antioxidant supplements during active cancer treatment. Instead, a balanced diet with naturally occurring antioxidants is typically advised. <br> <br> thiol-containing antioxidants: -Contain a functional –SH (sulfhydryl) group <br> -Can undergo oxidation to form disulfide bonds. This reversible redox behavior allows these molecules to neutralize reactive oxygen species (ROS). <br> -Thiol antioxidants (like N‑acetylcysteine or glutathione) are potent because the –SH group can directly scavenge ROS. <br> -There is concern that supplementation with thiol antioxidants during chemotherapy could neutralize some of the ROS generated by the treatment, potentially reducing the intended cytotoxic effects on cancer cells. <br> Examples: <br> -NAC <br> -GSH <br> -NMPG <br> -dihydrolipoic acid (reduced form of ALA) <br> -Cysteamine <br> -Methionine <br> -Ergothioneine <br> -Thioredoxin <br> <br> Non-thiol ROS scavengers: <br> -Act by donating electrons or hydrogen atoms to free radicals, thereby stabilizing them or converting them into less reactive species. <br> -Non‑thiol antioxidants (like vitamin C, vitamin E, flavonoids, etc.) have different mechanisms of action and may not interact as directly with ROS in the specific context of chemotherapy-induced cell death. <br> -That said, even non‑thiol antioxidants could potentially interfere with chemotherapy in some cases. For example, high doses of vitamin C or vitamin E might also diminish the oxidative stress essential for the efficacy of some chemotherapeutics. <br> Examples <br> -Ascorbic Acid(VitC) <br> -Vitamin E <br> -Flavoniods (Quercetin) <br> -Carotenoids(beta-carotene) <br> -Resveratrol <br> -Coenzyme Q10 (ubiquinone) <br> -Curcumin <br> -Selenium‑Dependent Enzymes (e.g., Glutathione Peroxidase) <br> -Polyphenols (ferulic acid and caffeic acid) <br> -manganese(III) <br> -tetrakis( (4-benzoic acid) <br> -porphyrin chloride (MnTBAP) <br> -SOD <br> <br> *** NOTE: <br> Thiol AntiOxidants could block ROS generation caused by Gambogic Acid, but not NON-Thiol AntiOxidants. <br> Question: does this mean NON-thiol AntiOxidants, might not interfere with therapies that raise ROS? <br> -It is a common notion that non‑thiol antioxidants might be less likely to interfere with chemotherapy compared to thiol antioxidants, both classes have the potential to impact treatment efficacy under the right (or wrong) circumstances. <br> <br> OTHER CLASSES of antioxidants <br> 1. Enzymatics Antioxidants (SOD, Catalase, GPXs) <br> -proteins that catalyze reactions to detoxify reactive oxygen species (ROS). <br> 2. Non-Enzymatic (Small-Molecule) Antioxidants. <br> Further divided to Thiol-Based Antioxidants, vs Non-Thiol Based Antioxidants. <br> 3. Metal-Binding Proteins and Chelators (Ferritin, Transferrin) <br> These compounds limit oxidative damage indirectly by sequestering transition metals (like iron and copper) that catalyze reactive oxygen species formation via the Fenton reaction. <br> 4. Indirect Antioxidants (Nrf2 Activators): (Sulforaphane, Curcumin) enhance the body’s own antioxidant defenses by upregulating the expression of antioxidant enzymes. <br>
32
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Api
Apigenin (mainly Parsley)
NP
<b> Apigenin</b> present in parsley, celery, chamomile, oranges and beverages such as tea, beer and wine.<br> <a href="https://pubmed.ncbi.nlm.nih.gov/32059077/">"It exhibits cell growth arrest and apoptosis in different types of tumors such as breast, lung, liver, skin, blood, colon, prostate, pancreatic, cervical, oral, and stomach, by modulating several signaling pathways." </a> <br> -Note <a href="tbResList.php?qv=32&tsv=1109&wNotes=on&exSp=open">half-life</a> reports vary 2.5-90hrs?.<br> -low solubility of apigenin in water : <a href="tbResList.php?qv=32&tsv=792&wNotes=on&exSp=open">BioAv</a> (improves when mixed with oil/dietary fat or <a href="https://www.mcsformulas.com/vitamins-supplements/apigenin-pro-liposomal/">lipid based formulations</a>)<br> -best oil might be <a href="tbResList.php?&qv=333&wNotes=onn&exSp=open&word=MCT">MCT</a> oils (medium-chain fatty acids)<br> <br> <br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - Often considered an antioxidant, in cancer cells it can paradoxically induce <a href="tbResList.php?qv=32&tsv=275&wNotes=on">ROS</a> production<br> (one report that goes against most others, by <a href="tbResEdit.php?rid=2638">lowering ROS</a> in cancer cells but still effective)<br> - ROS↑ related: <a href="tbResList.php?&qv=32&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?&qv=32&tsv=103&wNotes=on">ER Stress↑</a>, <a href="tbResList.php?&qv=32&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>, <a href="tbResList.php?&qv=32&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?&qv=32&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?&qv=32&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?&qv=32&tsv=459&wNotes=on">UPR↑</a>, <a href="tbResList.php?&qv=32&tsv=239&wNotes=on">cl-PARP↑</a>, <a href="tbResList.php?&qv=32&wNotes=on&word=HSP">HSP↓</a> <br> <!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, --> - Lowers AntiOxidant defense in Cancer Cells: <a href="tbResList.php?&qv=32&tsv=226&wNotes=on&word=NRF2↓">NRF2↓</a>, <a href="tbResList.php?&qv=32&tsv=137&wNotes=on&word=GSH↓">GSH↓</a> (<a href="https://www.mdpi.com/2076-3921/9/10/973">Conflicting evidence </a>about Nrf2) <br> - Combined with <a href="tbResList.php?&qv=32&qv2=11&wNotes=on">Metformin</a> (reduces Nrf2) amplifies ROS production in cancer cells while sparing normal cells.<br> - Raises <a href="tbResList.php?&qv=32&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?&qv=32&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?&qv=32&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?&qv=32&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?&qv=32&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?&qv=32&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?&qv=32&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?&qv=32&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, <a href="tbResList.php?&qv=32&tsv=235&wNotes=on&word=p38↓">p38↓</a>, Pro-Inflammatory Cytokines : <a href="tbResList.php?&qv=32&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, <a href="tbResList.php?&qv=32&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?&qv=32&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <a href="tbResList.php?&qv=32&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a> <br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓--> - inhibit Growth/Metastases : <a href="tbResList.php?&qv=32&tsv=96&wNotes=on"EMT↓</a>, <a href="tbResList.php?&qv=32&tsv=204&wNotes=on">MMPs↓</a>, <a href="tbResList.php?&qv=32&tsv=201&wNotes=on">MMP2↓</a>, <a href="tbResList.php?&qv=32&tsv=203&wNotes=on">MMP9↓</a>, <a href="tbResList.php?&qv=32&tsv=415&wNotes=on">IGF-1↓</a>, <a href="tbResList.php?&qv=32&tsv=428&wNotes=on">uPA↓</a>, <a href="tbResList.php?&qv=32&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?&qv=32&tsv=105&wNotes=on">ERK↓</a> <br> <!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, --> - reactivate genes thereby inhibiting cancer cell growth : <a href="tbResList.php?qv=32&tsv=140&wNotes=on">HDAC↓</a>, <a href="tbResList.php?qv=32&tsv=85&wNotes=on">DNMT1↓</a>, <a href="tbResList.php?qv=32&tsv=86&wNotes=on">DNMT3A↓</a>, <a href="tbResList.php?qv=32&tsv=108&wNotes=on">EZH2↓</a>, <a href="tbResList.php?qv=32&tsv=236&wNotes=on">P53↑</a>, <a href="tbResList.php?&qv=32&wNotes=on&word=HSP">HSP↓</a> <br> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?&qv=32&tsv=322&wNotes=on">TumCCA↑</a>, <a href="tbResList.php?&qv=32&tsv=73&wNotes=on">cyclin D1↓</a>, <a href="tbResList.php?&qv=32&tsv=378&wNotes=on">cyclin E↓</a>, <a href="tbResList.php?&qv=32&tsv=467&wNotes=on">CDK2↓</a>, <a href="tbResList.php?&qv=32&tsv=894&wNotes=on">CDK4↓</a>, <a href="tbResList.php?&qv=32&tsv=895&wNotes=on">CDK6↓</a>, <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?&qv=32&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?&qv=32&tsv=324&wNotes=on">TumCI↓</a>, <a href="tbResList.php?&qv=32&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?&qv=32&tsv=105&wNotes=on">ERK↓</a>, <br> <!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS --> - inhibits <a href="tbResList.php?qv=32&tsv=129&wNotes=on&exSp=open">glycolysis</a> and <a href="tbResList.php?qv=32&tsv=21&wNotes=on&exSp=open&word=ATP↓">ATP depletion</a> : <a href="tbResList.php?&qv=32&tsv=143&wNotes=on&exSp=open">HIF-1α↓</a>, <a href="tbResList.php?&qv=32&tsv=772&wNotes=on&exSp=open">PKM2↓</a>, <a href="tbResList.php?&qv=32&tsv=35&wNotes=on&exSp=open">cMyc↓</a>, <a href="tbResList.php?&qv=32&tsv=246&wNotes=on&exSp=open">PDK1↓</a>, <a href="tbResList.php?&qv=32&tsv=566&wNotes=on&exSp=open&word=GLUT">GLUT1↓</a>, <a href="tbResList.php?&qv=32&tsv=175&wNotes=on&exSp=open&word=LDH">LDHA↓</a>, <a href="tbResList.php?&qv=32&tsv=773&wNotes=on&exSp=open">HK2↓</a>, <a href="tbResList.php?&qv=32&tsv=1278&wNotes=on&exSp=open">Glucose↓</a>, <a href="tbResList.php?&qv=32&tsv=623&wNotes=on&exSp=open">GlucoseCon↓</a> <br> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - inhibits <a href="tbResList.php?qv=32&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=32&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?&qv=32&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?&qv=32&tsv=361&wNotes=on">PDGF↓</a>, <a href="tbResList.php?&qv=32&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, <a href="tbResList.php?&qv=32&&wNotes=on&word=ITG">Integrins↓</a>, <br> <!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, --> - inhibits Cancer Stem Cells : <a href="tbResList.php?qv=32&tsv=795&wNotes=on">CSC↓</a>, <a href="tbResList.php?qv=32&tsv=524&wNotes=on">CK2↓</a>, <a href="tbResList.php?qv=32&tsv=141&wNotes=on">Hh↓</a>, <a href="tbResList.php?qv=32&tsv=434&wNotes=on">GLi↓</a>, <a href="tbResList.php?qv=32&tsv=124&wNotes=on">GLi1↓</a>, <br> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=32&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=32&tsv=4&wNotes=on">AKT↓</a>, <a href="tbResList.php?qv=32&tsv=162&wNotes=on">JAK↓</a>, <a href="tbResList.php?qv=32&tsv=163&wNotes=on">1</a>, <a href="tbResList.php?qv=32&tsv=164&wNotes=on">2</a>, <a href="tbResList.php?qv=32&tsv=165&wNotes=on">3</a>, <a href="tbResList.php?qv=32&tsv=294&wNotes=on">STAT↓</a>, <a href="tbResList.php?qv=32&tsv=270&wNotes=on">1</a>, <a href="tbResList.php?qv=32&tsv=738&wNotes=on">2</a>, <a href="tbResList.php?qv=32&tsv=373&wNotes=on">3</a>, <a href="tbResList.php?qv=32&tsv=371&wNotes=on">4</a>, <a href="tbResList.php?qv=32&tsv=372&wNotes=on">5</a>, <a href="tbResList.php?qv=32&tsv=1157&wNotes=on">6</a>, <a href="tbResList.php?qv=32&tsv=377&wNotes=on">Wnt↓</a>, <a href="tbResList.php?qv=32&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=32&tsv=9&wNotes=on">AMPK↓</a>,, <a href="tbResList.php?qv=32&tsv=475&wNotes=on">α↓</a>,, <a href="tbResList.php?qv=32&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=32&tsv=1014&wNotes=on">5↓</a>, <a href="tbResList.php?qv=32&tsv=168&wNotes=on">JNK↓</a>, <br> - Shown to modulate the nuclear translocation of <a href="tbResList.php?&qv=32&tsv=1132&wNotes=on&exSp=open&word=SREBP2">SREBP-2</a> (related to cholesterol).<br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=32&tsv=1106&wNotes=on&exSp=open">chemo-sensitization</a>, <a href="tbResList.php?qv=32&tsv=1171&wNotes=on&exSp=open">chemoProtective</a>, <a href="tbResList.php?qv=32&tsv=1107&wNotes=on&exSp=open">RadioSensitizer</a>, <a href="tbResList.php?qv=32&tsv=1185&wNotes=on&exSp=open">RadioProtective</a>, <a href="tbResList.php?qv=32&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a><br> -Ex: other flavonoids(chrysin, Luteolin, querectin) curcumin, metformin, sulforaphane, ASA<br> <a href="tbResList.php?qv=32&tsv=1105&wNotes=on">Neuroprotective</a>, <a href="tbResList.php?qv=32&tsv=1175&wNotes=on">Renoprotection</a>, <a href="tbResList.php?qv=32&tsv=1179&wNotes=on">Hepatoprotective</a>, <a href="tbResList.php?&qv=32&tsv=1188&wNotes=on">CardioProtective</a>, <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=32&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br> <br> Apigenin exhibits biological effects (anticancer, anti-inflammatory, antioxidant, neuroprotective, etc.) typically at concentrations roughly in the range of 1–50 µM.<br> <br> Parsley microgreens can contain up to 2-3 times more apigenin than mature parsley.<br> Apigenin is typically measured in the range of 1-10 μM for biological activity. Assuming a molecular weight of 270 g/mol for apigenin, we can estimate the following μM concentrations:<br> 10uM*5L(blood)*270g/mol=13.5mg apigenin (assumes 100% bioavailability)<br> then an estimated 10-20 mg of apigenin per 100 g of fresh weight parlsey<br> 2.2mg/g of apigenin fresh parsley<br> 45mg/g of apigenin in dried parsley (wikipedia)<br> so 100g of parsley might acheive 10uM blood serum level (100% bioavailability)<br> BUT bioavailability is only 1-5%<br> (Supplements available in 75mg liposomal)( <a href="https://www.mcsformulas.com/vitamins-supplements/apigenin-pro-liposomal/">Apigenin Pro Liposomal</a>, 200 mg from mcsformulas.com)<br> <br> <a href="https://pubmed.ncbi.nlm.nih.gov/16407641/"> A study</a> had 2g/kg bw (meaning 160g for 80kg person) delivered a maximum 0.13uM of plasma concentration @ 7.2hrs.<br> Assuming parsley is 90-95% water, then that would be ~16g of dried parsley<br> Conclusion: to reach 10uM would seem very difficult by oral ingestion of parsley.<br> Other quotes:<br> “4g of dried parsley will be enough for 50kg adult”<br> 5mg/kg BW yields 16uM, so 80Kg person means 400mg (if dried parsley is 130mg/g, then would need 3g/d) <br> In many cancer cell lines, concentrations in the range of approximately 20–40 µM have been reported to shift apigenin’s activity from mild antioxidant effects (or negligible ROS changes) toward a clear pro-oxidant effect with measurable ROS increases.<br> <br> Low doses: At lower concentrations, apigenin is more likely to exhibit its antioxidant properties, scavenging ROS and protecting cells from oxidative stress. <br> In normal cells with robust antioxidant systems, apigenin’s antioxidant effects might prevail, whereas cancer cells—often characterized by an already high level of basal ROS—can be pushed over the oxidative threshold by increased ROS production induced by apigenin.<br> In environments with lower free copper levels, this pro-oxidant activity is less pronounced, and apigenin may tilt the balance toward its antioxidant function.<br>
33
-
AG
Arctigenin
NP
<b>Arctigenin</b> is a lignan found in certain plants of the Asteraceae, including the greater burdock (Arctium lappa) and Saussurea heteromalla. It has shown antiviral[1] and anticancer[2] effects in vitro. It is the aglycone of arctiin.<br>
337
-
ATO
Arsenic trioxide
NP
<b>Arsenic</b> has been known for centuries for its toxic and medicinal properties. Although once infamously used as a poison, ongoing research has repurposed arsenic derivatives for medicinal use.</br>
34
-
ART/DHA
Artemisinin
NP
<b>Artemisinin</b> a compound in a Chinese herb that may inhibit tumor growth and metastasis Artemisinin (antimalarial drugs)<br> Artesunic acid (Artesunate) , Dihydroartemisinin (DHA), artesunate, arteether, and artemether, SM735, SM905, SM933, SM934, and SM1044 <br> <br> The induction of OS in tumor cells via the production of ROS is the key mechanism of ART against cancer.<br> combination of ART and Nrf2 inhibitors to promote ferroptosis may have more efficient anticancer effects without damaging normal cells.<br> <br> Summary:<br> - Pro-oxidant, mechanism related with iron (hence avoid supplements containing iron? Or perhaps take with iron?)<br> -<a href="tbResList.php?qv=34&tsv=275&wNotes=on">ROS</a> seems to affect both cancer and normal cells<br> - Delivery of <a href="tbResEdit.php?rid=2577"> artemisinin in conjugate form with transferrin</a> or holotransferrin (serum iron transport proteins) have been shown to greatly improve its effectiveness.<br> - Potential direct inhibitor of <a href="tbResList.php?qv=34&tsv=373&wNotes=on&exSp=open">STAT3 </a><br> - <a href="tbResList.php?qv=34&qv2=19&wNotes=on&exSp=open"> Artemisinin synergized with the glycolysis inhibitor 2DG</a> (2-deoxy- D -glucose)<br> ART Combined Therapy: <a href="tbResList.php?qv=34&qv2=27&wNotes=on&exSp=open">Allicin</a>, <a href="tbResList.php?qv=34&qv2=141&wNotes=on&exSp=open">Resveratrol</a>, <a href="tbResList.php?qv=34&qv2=65&wNotes=on&exSp=open">Curcumin</a>, <a href="tbResList.php?qv=34&qv2=166&wNotes=on&exSp=open">VitC</a> (but not orally at same time), <a href="tbResList.php?qv=34&qv2=15&wNotes=on&exSp=open">Butyrate </a>, <a href="tbResList.php?qv=34&qv2=19&wNotes=on&exSp=open">2-DG</a>, <a href="tbResList.php?qv=34&qv2=332&wNotes=on&exSp=open">Aminolevulinic AcidG</a> <br> -possible problems with <a href="tbResEdit.php?rid=2571">liver toxicity??</a><br> <br> -Artesunate (ART), an artemisinin compound, is known for lysosomal degradation of ferritin, inducing oxidative stress and promoting cancer cell death.<br> <br> Pathways:<br> - Increasing reactive oxygen species (ROS) production. This oxidative stress can cause the loss of mitochondrial membrane potential, leading to cytochrome c release and subsequent activation of caspase cascades.<br> - Downregulate HIF-1α<br> - By impairing glycolysis, artemisinin might force cells to rely on oxidative phosphorylation (OXPHOS) for energy production.<br> - Inhibit GLUT1 (glucose uptake), HK2, PKM2 (slow the glycolytic flux, thereby reducing the energy supply)<br> <br> -Artemisinin has a <a href="tbResList.php?qv=34&&tsv=1109&wNotes=on&exSp=open">half-life </a> of about 3-4 hours, Artesunate 40 minutes and Artemether 12 hours. Peak plasma levels occur in 1-2 hour.<br> <a href="tbResList.php?qv=34&tsv=792&wNotes=on&exSp=open">BioAv</a> 21%, poor-good solubility. Artesunate (ART), a water soluble derivative of artemisinin. concentrations higher in blood, colon, liver, kidney (highly perfused organs) <br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - induce <a href="tbResList.php?qv=34&tsv=275&wNotes=on">ROS</a> production, iron dependent (affect both cancer and normal cells)<br> - ROS↑ related: <a href="tbResList.php?qv=34&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?qv=34&tsv=103&wNotes=on">ER Stress↑</a>, <a href="tbResList.php?qv=34&tsv=459&wNotes=on">UPR↑</a>, <a href="tbResList.php?qv=34&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=34&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>, <a href="tbResList.php?qv=34&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?qv=34&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?qv=34&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?qv=34&tsv=239&wNotes=on">cl-PARP↑</a>, <a href="tbResList.php?qv=34&wNotes=on&word=HSP">HSP↓</a>, <!-- <a href="tbResList.php?qv=34&wNotes=on&word=Prx">Prx</a>,--><!-- mitochondrial antioxidant enzyme--> <br> <!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, --> - Both Lowers (and raises) AntiOxidant defense in Cancer Cells: <a href="tbResList.php?qv=34&tsv=226&wNotes=on&word=NRF2">NRF2↓</a>(contary), <!-- <a href="tbResList.php?qv=34&word=Trx&wNotes=on">TrxR↓**</a>, --><!-- major antioxidant system --> <a href="tbResList.php?qv=34&tsv=298&wNotes=on&word=SOD↓">SOD↓</a>, <a href="tbResList.php?qv=34&tsv=137&wNotes=on&word=GSH↓">GSH↓</a> <a href="tbResList.php?qv=34&tsv=46&wNotes=on">Catalase↓</a> <!-- <a href="tbResList.php?qv=34&tsv=597&wNotes=on">HO1↓</a> --> <a href="tbResList.php?qv=34&wNotes=on&word=GPx">GPx↓</a> <br> - Small evidence of Raising <a href="tbResList.php?qv=34&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?qv=34&tsv=275&wNotes=on&word=ROS">ROS↓</a>(contary), <a href="tbResList.php?qv=34&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?qv=34&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>(contary), <a href="tbResList.php?qv=34&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?qv=34&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?qv=34&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?qv=34&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?qv=34&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, <a href="tbResList.php?qv=34&tsv=235&wNotes=on&word=p38↓">p38↓</a>, Pro-Inflammatory Cytokines : <a href="tbResList.php?qv=34&tsv=908&wNotes=on&word=NLRP3↓">NLRP3↓</a>, <!-- <a href="tbResList.php?qv=34&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, --> <a href="tbResList.php?qv=34&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?qv=34&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <a href="tbResList.php?qv=34&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a> <br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓ inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.--> - inhibit Growth/Metastases : <a href="tbResList.php?qv=34&tsv=604&wNotes=on">TumMeta↓</a>, <a href="tbResList.php?qv=34&tsv=323&wNotes=on">TumCG↓</a>, <a href="tbResList.php?qv=34&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=34&tsv=204&wNotes=on">MMPs↓</a>, <a href="tbResList.php?qv=34&tsv=201&wNotes=on">MMP2↓</a>, <a href="tbResList.php?qv=34&tsv=203&wNotes=on">MMP9↓</a>, <a href="tbResList.php?qv=34&tsv=308&wNotes=on">TIMP2</a>, <a href="tbResList.php?qv=34&wNotes=on&word=IGF">IGF-1↓</a>, <a href="tbResList.php?qv=34&tsv=428&wNotes=on">uPA↓</a>, <a href="tbResList.php?qv=34&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=34&tsv=1284&wNotes=on">ROCK1↓</a>, <!-- <a href="tbResList.php?qv=34&tsv=110&wNotes=on">FAK↓</a>, --> <!-- <a href="tbResList.php?qv=34&tsv=273&wNotes=on">RhoA↓</a>, --> <a href="tbResList.php?qv=34&tsv=214&wNotes=on">NF-κB↓</a>, <!-- <a href="tbResList.php?qv=34&tsv=79&wNotes=on">CXCR4↓</a>, --> <!-- <a href="tbResList.php?qv=34&tsv=1247&wNotes=on">SDF1↓</a>, --> <a href="tbResList.php?qv=34&tsv=304&wNotes=on">TGF-β↓</a>, <!-- <a href="tbResList.php?qv=34&tsv=719&wNotes=on">α-SMA↓</a>, --> <a href="tbResList.php?qv=34&tsv=105&wNotes=on">ERK↓</a> <!-- <a href="tbResList.php?qv=34&tsv=1178&wNotes=on">MARK4↓</a> --><!-- contributing to tumor growth, invasion, and metastasis--> <br> <!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, --> <!-- - reactivate genes thereby inhibiting cancer cell growth : <a href="tbResList.php?qv=34&tsv=140&wNotes=on">HDAC↓</a>, <a href="tbResList.php?qv=34&wNotes=on&word=DNMT">DNMTs↓</a>, <a href="tbResList.php?qv=34&tsv=108&wNotes=on">EZH2↓</a>, <a href="tbResList.php?qv=34&tsv=236&wNotes=on">P53↑</a>, <a href="tbResList.php?qv=34&wNotes=on&word=HSP">HSP↓</a>, <a href="tbResList.php?qv=34&tsv=506&wNotes=on">Sp proteins↓</a>, <a href="tbResList.php?qv=34&wNotes=on&word=TET">TET↑</a> <br> --> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?qv=34&tsv=322&wNotes=on">TumCCA↑</a>, <a href="tbResList.php?qv=34&tsv=73&wNotes=on">cyclin D1↓</a>, <a href="tbResList.php?qv=34&tsv=378&wNotes=on">cyclin E↓</a>, <a href="tbResList.php?qv=34&tsv=467&wNotes=on">CDK2↓</a>, <a href="tbResList.php?qv=34&tsv=894&wNotes=on">CDK4↓</a>, <a href="tbResList.php?qv=34&tsv=895&wNotes=on">CDK6↓</a>, <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?qv=34&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?qv=34&tsv=324&wNotes=on">TumCI↓</a>, <a href="tbResList.php?qv=34&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <!-- encourages invasion, proliferation, EMT, and angiogenesis --> <!-- <a href="tbResList.php?qv=34&tsv=110&wNotes=on">FAK↓</a>, --> <a href="tbResList.php?qv=34&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=34&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=34&wNotes=on&word=TOP">TOP1↓</a>, <!-- <a href="tbResList.php?qv=34&tsv=657&wNotes=on">TET1</a>, --> <br> <!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS --> - inhibits <a href="tbResList.php?qv=34&tsv=129&wNotes=on">glycolysis</a> /<a href="tbResList.php?qv=34&tsv=947&wNotes=on">Warburg Effect</a> and <a href="tbResList.php?qv=34&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> : <a href="tbResList.php?qv=34&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=34&tsv=772&wNotes=on">PKM2↓</a>, <a href="tbResList.php?qv=34&tsv=35&wNotes=on">cMyc↓</a>, <a href="tbResList.php?qv=34&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>, <a href="tbResList.php?qv=34&tsv=906&wNotes=on">LDH↓</a>, <a href="tbResList.php?qv=34&tsv=175&wNotes=on&word=LDH">LDHA↓</a>, <a href="tbResList.php?qv=34&tsv=773&wNotes=on">HK2↓</a>, <!-- <a href="tbResList.php?qv=34&wNotes=on&word=PFK">PFKs↓</a>, --> <!-- <a href="tbResList.php?qv=34&wNotes=on&word=PDK">PDKs↓</a>, --> <a href="tbResList.php?qv=34&tsv=847&wNotes=on">ECAR↓</a>, <!-- <a href="tbResList.php?qv=34&tsv=230&wNotes=on">OXPHOS↓</a>, --> <a href="tbResList.php?qv=34&tsv=356&wNotes=on">GRP78↑</a>, <!-- <a href="tbResList.php?qv=34&tsv=1278&wNotes=on">Glucose↓</a>, --> <a href="tbResList.php?qv=34&tsv=623&wNotes=on">GlucoseCon↓</a> <br> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - inhibits <a href="tbResList.php?qv=34&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=34&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=34&tsv=143&wNotes=on">HIF-1α↓</a>, <!-- <a href="tbResList.php?qv=34&wNotes=on&word=NOTCH">Notch↓</a>, --> <!-- <a href="tbResList.php?qv=34&wNotes=on&word=FGF">FGF↓</a>, --> <!-- <a href="tbResList.php?qv=34&wNotes=on&word=PDGF">PDGF↓</a>, --> <a href="tbResList.php?qv=34&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, <a href="tbResList.php?qv=34&&wNotes=on&word=ITG">Integrins↓</a>, <br> <!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, --> - some small indication of inhibiting Cancer Stem Cells : <a href="tbResList.php?qv=34&tsv=795&wNotes=on">CSC↓</a>, <!-- <a href="tbResList.php?qv=34&tsv=524&wNotes=on">CK2↓</a>, --> <a href="tbResList.php?qv=34&tsv=141&wNotes=on">Hh↓</a>, <!-- <a href="tbResList.php?qv=34&tsv=434&wNotes=on">GLi↓</a>, --> <!-- <a href="tbResList.php?qv=34&tsv=124&wNotes=on">GLi1↓</a>, --> <!-- <a href="tbResList.php?qv=34&tsv=677&wNotes=on">CD133↓</a>, --> <!-- <a href="tbResList.php?qv=34&tsv=655&wNotes=on">CD24↓</a>, --> <a href="tbResList.php?qv=34&tsv=342&wNotes=on">β-catenin↓</a>, <!-- <a href="tbResList.php?qv=34&tsv=357&wNotes=on">n-myc↓</a>, --> <a href="tbResList.php?qv=34&tsv=656&wNotes=on">sox2↓</a>, <!-- <a href="tbResList.php?qv=34&wNotes=on&word=NOTCH">Notch2↓</a>, --> <!-- <a href="tbResList.php?qv=34&tsv=1024&wNotes=on">nestin↓</a>, --> <a href="tbResList.php?qv=34&tsv=508&wNotes=on">OCT4↓</a>, <br> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=34&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=34&tsv=4&wNotes=on">AKT↓</a>, <a href="tbResList.php?qv=34&wNotes=on&word=JAK">JAK↓</a>, <a href="tbResList.php?qv=34&wNotes=on&word=STAT">STAT↓</a>, <a href="tbResList.php?qv=34&tsv=377&wNotes=on">Wnt↓</a>, <a href="tbResList.php?qv=34&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=34&tsv=9&wNotes=on">AMPK</a>, <!-- <a href="tbResList.php?qv=34&tsv=475&wNotes=on">α↓</a>, --> <a href="tbResList.php?qv=34&tsv=105&wNotes=on">ERK↓</a>, <!-- <a href="tbResList.php?qv=34&tsv=1014&wNotes=on">5↓</a>, --> <a href="tbResList.php?qv=34&tsv=168&wNotes=on">JNK</a>, <!-- - <a href="tbResList.php?qv=34&wNotes=on&word=SREBP">SREBP</a> (related to cholesterol). --> <br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=34&tsv=1106&wNotes=on">chemo-sensitization</a>, <!-- <a href="tbResList.php?qv=34&tsv=1171&wNotes=on">chemoProtective</a>, --> <a href="tbResList.php?qv=34&tsv=1107&wNotes=on">RadioSensitizer</a>, <!-- <a href="tbResList.php?qv=34&tsv=1185&wNotes=on">RadioProtective</a>, --> <a href="tbResList.php?qv=34&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <!-- <a href="tbResList.php?qv=34&tsv=1105&wNotes=on">Neuroprotective</a>, --> <!-- <a href="tbResList.php?qv=34&tsv=557&wNotes=on">Cognitive</a>, --> <!-- <a href="tbResList.php?qv=34&tsv=1175&wNotes=on">Renoprotection</a>, --> <!-- <a href="tbResList.php?qv=34&tsv=1179&wNotes=on">Hepatoprotective</a>, --> <!-- <a href="tbResList.php?&qv=34&tsv=1188&wNotes=on">CardioProtective</a>, --> <br> <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=34&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br>
35
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AP
Ascorbyl Palmitate
NP
<b>Ascorbyl palmitate</b> is an ester formed from ascorbic acid and palmitic acid creating a fat-soluble form of vitamin C.<br>
36
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Ash
Ashwagandha
NP
<b>Withaferin A</b> is a steroidal lactone derived from the medicinal plant Withania somnifera (commonly known as Ashwagandha).<br> The main active constituents of Ashwagandha leaves are alkaloids and steroidal lactones (commonly known as Withanolides).<br> -The main constituents of ashwagandha are withanolides such as withaferin A, alkaloids, steroidal lactones, tropine, and cuscohygrine.<br> Ashwagandha is an herb that may reduce stress, anxiety, and insomnia.<br> *-Ashwagandha is often characterized as an antioxidant.<br> -Some studies suggest that while ashwagandha may protect normal cells from oxidative damage, it can simultaneously stress cancer cells by tipping their redox balance toward cytotoxicity.<br> Pathways:<br> -Induction of Apoptosis and ROS Generation<br> -Hsp90 Inhibition and Proteasomal Degradation<br> <br> Cell culture studies vary widely, typically ranging from low micromolar (e.g., 1–10 µM).<br> In animal models (commonly mice), Withaferin A has been administered in doses ranging from approximately 2 to 10 mg/kg body weight.<br> - General wellness, Ashwagandha supplements are sometimes taken in doses ranging from 300 mg to 600 mg of an extract (often standardized to contain a certain percentage of withanolides) once or twice daily.<br> - 400mg of WS extract was given 3X/day to schizophrenia patients. report#2001.<br> - Ashwagandha Pure 400mg/capsule is available from mcsformulas.com.<br> <br> -Note <a href="tbResList.php?qv=36&tsv=1109&wNotes=on&exSp=open">half-life</a> 4-6 hrs?.<br> <a href="tbResList.php?qv=36&tsv=792&wNotes=on&exSp=open">BioAv</a> <br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - well-recognized for promoting <a href="tbResList.php?qv=36&tsv=275&wNotes=on">ROS</a> in cancer cells, while no effect(or reduction) on normal cells.<br> - ROS↑ related: <a href="tbResList.php?qv=36&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?qv=36&tsv=103&wNotes=on">ER Stress↑</a>, <a href="tbResList.php?qv=36&tsv=459&wNotes=on">UPR↑</a>, <a href="tbResList.php?qv=36&tsv=356&wNotes=on">GRP78↑</a>, <!-- <a href="tbResList.php?qv=36&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>, --> <a href="tbResList.php?qv=36&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?qv=36&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?qv=36&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?qv=36&tsv=239&wNotes=on">cl-PARP↑</a>, <a href="tbResList.php?qv=36&wNotes=on&word=HSP">HSP↓</a>, <a href="tbResList.php?qv=36&wNotes=on&word=Prx">Prx</a>,<!-- mitochondrial antioxidant enzyme--> <br> <!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, --> - Confusing results about Lowering AntiOxidant defense in Cancer Cells: <a href="tbResList.php?qv=36&tsv=226&wNotes=on&word=NRF2↓">NRF2↓</a>, <a href="tbResList.php?qv=36&word=Trx&wNotes=on">TrxR↓**</a>,<!-- major antioxidant system --> <a href="tbResList.php?qv=36&tsv=298&wNotes=on&word=SOD↓">SOD↓</a>, <a href="tbResList.php?qv=36&tsv=137&wNotes=on&word=GSH↓">GSH↓</a> <a href="tbResList.php?qv=36&tsv=46&wNotes=on">Catalase↓</a> <a href="tbResList.php?qv=36&tsv=597&wNotes=on">HO1↓</a> <a href="tbResList.php?qv=36&wNotes=on&word=GPx">GPx↓</a> <br> - Raises <a href="tbResList.php?qv=36&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?qv=36&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>, <a href="tbResList.php?qv=36&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?qv=36&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?qv=36&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?qv=36&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?qv=36&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?qv=36&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?qv=36&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, <a href="tbResList.php?qv=36&tsv=235&wNotes=on&word=p38↓">p38↓</a>, Pro-Inflammatory Cytokines : <a href="tbResList.php?qv=36&tsv=908&wNotes=on&word=NLRP3↓">NLRP3↓</a>, <a href="tbResList.php?qv=36&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, <a href="tbResList.php?qv=36&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?qv=36&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <a href="tbResList.php?qv=36&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a> <br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓ inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.--> - inhibit Growth/Metastases : <a href="tbResList.php?qv=36&tsv=604&wNotes=on">TumMeta↓</a>, <a href="tbResList.php?qv=36&tsv=323&wNotes=on">TumCG↓</a>, <a href="tbResList.php?qv=36&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=36&tsv=204&wNotes=on">MMPs↓</a>, <a href="tbResList.php?qv=36&tsv=201&wNotes=on">MMP2↓</a>, <a href="tbResList.php?qv=36&tsv=203&wNotes=on">MMP9↓</a>, <a href="tbResList.php?qv=36&tsv=308&wNotes=on">TIMP2</a>, <!-- <a href="tbResList.php?qv=36&tsv=415&wNotes=on">IGF-1↓</a>, --> <a href="tbResList.php?qv=36&tsv=428&wNotes=on">uPA↓</a>, <a href="tbResList.php?qv=36&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=36&tsv=1284&wNotes=on">ROCK1↓</a>, <!-- <a href="tbResList.php?qv=36&tsv=110&wNotes=on">FAK↓</a>, --> <!-- <a href="tbResList.php?qv=36&tsv=273&wNotes=on">RhoA↓</a>, --> <a href="tbResList.php?qv=36&tsv=214&wNotes=on">NF-κB↓</a>, <a href="tbResList.php?qv=36&tsv=79&wNotes=on">CXCR4↓</a>, <a href="tbResList.php?qv=36&tsv=1247&wNotes=on">SDF1↓</a>, <a href="tbResList.php?qv=36&tsv=304&wNotes=on">TGF-β↓</a>, <a href="tbResList.php?qv=36&tsv=719&wNotes=on">α-SMA↓</a>, <a href="tbResList.php?qv=36&tsv=105&wNotes=on">ERK↓</a> <!-- <a href="tbResList.php?qv=36&tsv=1178&wNotes=on">MARK4↓</a> --> <!-- contributing to tumor growth, invasion, and metastasis--> <br> <!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, --> - reactivate genes thereby inhibiting cancer cell growth : <a href="tbResList.php?qv=36&tsv=140&wNotes=on">HDAC↓</a>(combined with sulfor), <a href="tbResList.php?qv=36&tsv=85&wNotes=on">DNMT1↓</a>, <a href="tbResList.php?qv=36&tsv=86&wNotes=on">DNMT3A↓</a>, <!-- <a href="tbResList.php?qv=36&tsv=108&wNotes=on">EZH2↓</a>, --> <a href="tbResList.php?qv=36&tsv=236&wNotes=on">P53↑</a>, <a href="tbResList.php?qv=36&wNotes=on&word=HSP">HSP↓</a>, <a href="tbResList.php?qv=36&tsv=506&wNotes=on">Sp proteins↓</a>, <a href="tbResList.php?qv=36&wNotes=on&word=TET">TET↑</a> <br> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?qv=36&tsv=322&wNotes=on">TumCCA↑</a>, <!-- <a href="tbResList.php?qv=36&tsv=73&wNotes=on">cyclin D1↓</a>, --> <a href="tbResList.php?qv=36&tsv=378&wNotes=on">cyclin E↓</a>, <a href="tbResList.php?qv=36&tsv=467&wNotes=on">CDK2↓</a>, <a href="tbResList.php?qv=36&tsv=894&wNotes=on">CDK4↓</a>, <!-- <a href="tbResList.php?qv=36&tsv=895&wNotes=on">CDK6↓</a>, --> <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?qv=36&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?qv=36&tsv=324&wNotes=on">TumCI↓</a>, <a href="tbResList.php?qv=36&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <!-- encourages invasion, proliferation, EMT, and angiogenesis --> <!-- <a href="tbResList.php?qv=36&tsv=110&wNotes=on">FAK↓</a>, --> <a href="tbResList.php?qv=36&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=36&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=36&tsv=1117&wNotes=on">TOP1↓</a>, <!-- <a href="tbResList.php?qv=36&tsv=657&wNotes=on">TET1↓</a>, --> <br> <!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS --> - inhibits <a href="tbResList.php?qv=36&tsv=129&wNotes=on">glycolysis</a> /<a href="tbResList.php?qv=36&tsv=947&wNotes=on">Warburg Effect</a> and <a href="tbResList.php?qv=36&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> : <a href="tbResList.php?qv=36&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=36&tsv=772&wNotes=on">PKM2↓</a>, <a href="tbResList.php?qv=36&tsv=35&wNotes=on">cMyc↓</a>, <a href="tbResList.php?qv=36&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>, <a href="tbResList.php?qv=36&tsv=906&wNotes=on">LDH↓</a>, <a href="tbResList.php?qv=36&tsv=175&wNotes=on&word=LDH">LDHA↓</a>, <a href="tbResList.php?qv=36&tsv=773&wNotes=on">HK2↓</a>, <!-- <a href="tbResList.php?qv=36&wNotes=on&word=PFK">PFKs↓</a>, --> <!-- <a href="tbResList.php?qv=36&wNotes=on&word=PDK">PDKs↓</a>, --> <!-- <a href="tbResList.php?qv=36&tsv=847&wNotes=on">ECAR↓</a>, --> <a href="tbResList.php?qv=36&tsv=230&wNotes=on">OXPHOS↓</a>, <a href="tbResList.php?qv=36&tsv=356&wNotes=on">GRP78↑</a>, <!-- <a href="tbResList.php?qv=36&tsv=1278&wNotes=on">Glucose↓</a>, --> <a href="tbResList.php?qv=36&tsv=623&wNotes=on">GlucoseCon↓</a> <br> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - inhibits <a href="tbResList.php?qv=36&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=36&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=36&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=36&wNotes=on&word=NOTCH">Notch↓</a>, <!-- <a href="tbResList.php?qv=36&wNotes=on&word=FGF">FGF↓</a>, --> <a href="tbResList.php?qv=36&wNotes=on&word=PDGF">PDGF↓</a>, <a href="tbResList.php?qv=36&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, <a href="tbResList.php?qv=36&&wNotes=on&word=ITG">Integrins↓</a>, <br> <!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, --> - inhibits Cancer Stem Cells : <a href="tbResList.php?qv=36&tsv=795&wNotes=on">CSC↓</a>, <!-- <a href="tbResList.php?qv=36&tsv=524&wNotes=on">CK2↓</a>, --> <!-- <a href="tbResList.php?qv=36&tsv=141&wNotes=on">Hh↓</a>, --> <!-- <a href="tbResList.php?qv=36&tsv=434&wNotes=on">GLi↓</a>, --> <!-- <a href="tbResList.php?qv=36&tsv=124&wNotes=on">GLi1↓</a>, --> <!-- <a href="tbResList.php?qv=36&tsv=677&wNotes=on">CD133↓</a>, --> <!-- <a href="tbResList.php?qv=36&tsv=655&wNotes=on">CD24↓</a>, --> <a href="tbResList.php?qv=36&tsv=342&wNotes=on">β-catenin↓</a>, <!--<a href="tbResList.php?qv=36&tsv=357&wNotes=on">n-myc↓</a>, --> <a href="tbResList.php?qv=36&tsv=656&wNotes=on">sox2↓</a>, <!--<a href="tbResList.php?qv=36&tsv=222&wNotes=on">notch2↓</a>, --> <!-- <a href="tbResList.php?qv=36&tsv=1024&wNotes=on">nestin↓</a>, --> <!-- <a href="tbResList.php?qv=36&tsv=508&wNotes=on">OCT4↓</a>, --> <br> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=36&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=36&tsv=4&wNotes=on">AKT↓</a>, <a href="tbResList.php?qv=36&wNotes=on&word=JAK">JAK↓</a>, <a href="tbResList.php?qv=36&wNotes=on&word=STAT">STAT↓</a>, <a href="tbResList.php?qv=36&tsv=377&wNotes=on">Wnt↓</a>, <a href="tbResList.php?qv=36&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=36&tsv=9&wNotes=on">AMPK</a>, <a href="tbResList.php?qv=36&tsv=475&wNotes=on">α↓</a>, <a href="tbResList.php?qv=36&tsv=105&wNotes=on">ERK↓</a>, <!-- <a href="tbResList.php?qv=36&tsv=1014&wNotes=on">5↓</a>, --> <a href="tbResList.php?qv=36&tsv=168&wNotes=on">JNK</a>, <br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=36&tsv=1106&wNotes=on">chemo-sensitization</a>, <a href="tbResList.php?qv=36&tsv=1171&wNotes=on">chemoProtective</a>, <a href="tbResList.php?qv=36&tsv=1107&wNotes=on">RadioSensitizer</a>, <a href="tbResList.php?qv=36&tsv=1185&wNotes=on">RadioProtective</a>, <a href="tbResList.php?qv=36&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <a href="tbResList.php?qv=36&tsv=1105&wNotes=on">Neuroprotective</a>, <a href="tbResList.php?qv=36&tsv=557&wNotes=on">Cognitive</a>, <a href="tbResList.php?qv=36&tsv=1175&wNotes=on">Renoprotection</a>, <a href="tbResList.php?qv=36&tsv=1179&wNotes=on">Hepatoprotective</a>, <a href="tbResList.php?&qv=36&tsv=1188&wNotes=on">CardioProtective</a>, <br> <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=36&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br>
1
-
ASA
Aspirin -acetylsalicylic acid
D
nonsteroidal anti-inflammatory drug (NSAID)
<b>Aspirin</b> irreversibly inhibits COX-1 and modifies the enzymatic activity of COX-2. COX-2 normally produces prostanoids, most of which are proinflammatory.<br> <br> -Aspirin irreversibly inhibits the enzyme cyclooxygenase-1 (COX-1). This inhibition reduces the production of thromboxane A₂, a potent promoter of platelet aggregation.<br> -low-dose aspirin is frequently used for the prevention of cardiovascular events such as heart attacks and strokes in individuals at risk.<br> <br>
37
-
AS
Astragalus
NP
<a href="https://www.healthline.com/nutrition/astragalus"> <b>Astragalus<b></a> is an herb that has been used in traditional Chinese medicine for centuries.It has many purported health benefits, including immune-boosting, anti-aging and anti-inflammatory effects. <br>
2
-
ATV
Atorvastatin
D
Statin
<b>Atorvastatin</b> is a statin used to lower the level of cholesterol in the blood.<br>
273
-
Aur
Auranofin
RD
<b>Auranofin</b> is a synthetic gold(I) complex originally developed for the treatment of rheumatoid arthritis. Its structure features a gold atom coordinated with triethylphosphine and a thiolate ligand derived from a sugar (often referred to as a thiosugar).<br> <br> Pathways:<br> 1.Thioredoxin Reductase (TrxR) Inhibition.<br> - Most widely recognized for potently inhibiting TrxR.<br> 2.Induction of Reactive Oxygen Species (ROS) and Oxidative Stress.<br> 3.MMP depolarization, release of cytochrome c <br> 4.Endoplasmic Reticulum (ER) Stress and Unfolded Protein Response (UPR)<br> 5.Inhibition of Pro-survival Pathways (e.g., NF-κB Signaling)<br> <br> -ic50 for cancer typically 1-3uM, normal cell 5-10uM or higher.<br> -Several studies animal testing antitumor efficacy have used doses in the region of 5–8 mg/kg via intraperitoneal injection or oral administration.<br> <br> -Auranofin’s anticancer activity is often linked to its inhibition of thioredoxin reductase, leading to increased oxidative stress.<br>
38
-
Ba
Baicalein
NP
<b>Baicalein</b> is a flavone, a type of flavonoid, originally isolated from the roots of Scutellaria baicalensis and Scutellaria lateriflora. It is also a constituent of Oroxylum indicum and thyme.<br> Baicalein, a flavonoid found in several medicinal plants (notably Scutellaria baicalensis), has been investigated for its anticancer properties. Its activities involve modulation of multiple cellular pathways, including those that regulate cell proliferation, apoptosis, metastasis, and oxidative stress. Here are some of the key pathways and mechanisms implicated in its anticancer effects:<br> -Apoptosis and Cell Cycle Regulation<br> -Reactive Oxygen Species <a href="tbResList.php?&qv=38&tsv=275&wNotes=on&word=ROS↑">ROS↑ </a> Generation and Oxidative Stress<br> - ROS↑ related: <a href="tbResList.php?&qv=38&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?&qv=38&tsv=103&wNotes=on&word=ER Stress">ER Stress↑</a>, <a href="tbResList.php?&qv=38&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>, <a href="tbResList.php?&qv=38&tsv=77&wNotes=on&word=Cyt‑c">Cyt‑c↑</a>, <a href="tbResList.php?&qv=38&tsv=42&wNotes=on&word=Casp3↑">Caspase-3↑</a>, <a href="tbResList.php?&qv=38&tsv=45&wNotes=on&word=Casp9↑">Caspase-9↑</a>, <a href="tbResList.php?&qv=38&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <br> -Baicalein’s effects on ROS are context-dependent. In some cancer cells, it promotes ROS production to a degree that overwhelms the antioxidant defenses. Elevated ROS levels can damage cellular components and promote apoptosis, essentially tipping the balance toward cell death.<br> -Conversely, in normal cells, baicalein may exhibit antioxidant properties and reduce <a href="tbResList.php?&qv=38&tsv=275&wNotes=on&word=ROS↓">ROS↓ </a> under conditions of oxidative stress, highlighting its dual role.<br> - Lowers AntiOxidant defense in Cancer Cells: <a href="tbResList.php?&qv=38&tsv=226&wNotes=on&word=NRF2↓">NRF2↓</a>, <a href="tbResList.php?&qv=38&tsv=137&wNotes=on&word=GSH↓">GSH↓</a>, <a href="tbResList.php?&qv=38&tsv=597&wNotes=on&word=HO-1↓">HO-1↓</a>, <br> - Raises <a href="tbResList.php?&qv=38&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?&qv=38&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?&qv=38&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?&qv=38&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?&qv=38&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <a href="tbResList.php?&qv=38&tsv=597&wNotes=on&word=HO-1↑">HO-1↑</a>, <br> -<a href="tbResList.php?&qv=38&tsv=181&wNotes=on&exSp=open&word=MAPK">MAPK, </a> <a href="tbResList.php?&qv=38&tsv=105&wNotes=on&exSp=open&word=ERK">ERK </a> Pathway: <br> -PI3K/Akt Pathway: Inhibition of the <a href="tbResList.php?&qv=38&tsv=252&wNotes=on&exSp=open&word=PI3K">PI3K, </a> <a href="tbResList.php?&qv=38&tsv=4&wNotes=on&exSp=open&word=Akt">Akt </a> pathway by baicalein.<br> -<a href="tbResList.php?&qv=38&tsv=214&wNotes=on&exSp=open&word=NF-kB">NF-κB </a> Pathway: Baicalein can inhibit <br> -Inhibition of Metastasis and Invasion: Baicalein can downregulate <a href="tbResList.php?&qv=38&tsv=204&wNotes=on&exSp=open&word=MMPs">MMPs, </a> <a href="tbResList.php?&qv=38&tsv=201&wNotes=on&exSp=open&word=MMP2">MMP2, </a> <a href="tbResList.php?&qv=38&tsv=203&wNotes=on&exSp=open&word=MMP9">MMP9 </a><br> -Angiogenesis Suppression: <a href="tbResList.php?&qv=38&tsv=334&wNotes=on&exSp=open&word=VEGF">VEGF</a><br> -Baicalein is a well-known inhibitor of <a href="tbResList.php?&qv=38&tsv=1126&wNotes=on&exSp=open&word=12LOX">12-lipoxygenase</a><br> -inhibitor of <a href="tbResList.php?&qv=38&tsv=129&wNotes=on&exSp=open&word=Glycolysis">Glycolysis↓</a> and <a href="tbResList.php?&qv=38&tsv=143&wNotes=on&exSp=open&word=Hif1a">HIF-1α↓</a>, <a href="tbResList.php?&qv=38&tsv=772&wNotes=on&exSp=open&word=PKM2">PKM2↓</a>, <a href="tbResList.php?&qv=38&tsv=35&wNotes=on&exSp=open&word=cMyc">cMyc↓</a>, <a href="tbResList.php?&qv=38&tsv=246&wNotes=on&exSp=open&word=PDK1">PDK1↓</a>, <a href="tbResList.php?&qv=38&tsv=566&wNotes=on&exSp=open&word=GLUT">GLUT1↓</a>, <a href="tbResList.php?&qv=38&tsv=175&wNotes=on&exSp=open&word=LDH">LDHA↓</a>, <a href="tbResList.php?&qv=38&tsv=773&wNotes=on&exSp=open&word=HK2">HK2↓</a> <br> - promoting <a href="tbResList.php?&qv=38&tsv=267&wNotes=on&exSp=open&word=PTEN">PTEN</a><br> -<a href="tbResList.php?&qv=38&tsv=1106&wNotes=on">chemo-sensitization</a>, <a href="tbResList.php?qv=38&tsv=1171&wNotes=on">chemoProtective</a>, <a href="tbResList.php?&qv=38&tsv=1107&wNotes=onS">RadioSensitizer</a>, <a href="tbResList.php?qv=38&tsv=1185&wNotes=on">RadioProtective</a>, <a href="tbResList.php?&qv=38&tsv=1105&wNotes=on">neuroprotective</a>, <a href="tbResList.php?qv=38&tsv=557&wNotes=on">Cognitive</a>, <a href="tbResList.php?qv=38&tsv=1175&wNotes=on">Renoprotection</a>, <a href="tbResList.php?qv=38&tsv=1179&wNotes=on">Hepatoprotective</a>, <a href="tbResList.php?&qv=38&tsv=1188&wNotes=on&exSp=open&word=cardioP">cardioProtective</a>, <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=38&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br> -low <a href="tbResList.php?&qv=38&tsv=792&wNotes=on&exSp=open&word= BioAv">bioavailability</a> but <a href="https://www.mcsformulas.com/vitamins-supplements/baicalein-pro-liposomal/">liposomal</a> highly improves bioavailability<br> <br> In summary, baicalein affects cancer cells by modulating multiple pathways—promoting apoptosis, causing cell cycle arrest, generating or modulating ROS levels, inhibiting survival and proliferative signaling (such as MAPK, PI3K/Akt, and NF-κB pathways), and reducing angiogenesis and metastasis.<br> <br> Many animal studies, doses have been reported in the range of approximately 10 to 200 mg/kg body weight.<br> For example, some studies exploring anticancer or anti-inflammatory effects in rodent models have used doses around 50–100 mg/kg.<br> However, these doses do not directly translate to human dosages.<br> Some human studies or formulations (where they are used as nutraceuticals or supplements) may suggest dosing in the range of a few hundred milligrams per day of the extract, but it is often not standardized to a specific amount of baicalein or baicalin.<br> -mix with oil?<br> <br> -ic50 cancer cells 10-30uM, normal cells 50-100uM<br> -Animal studies, 10 to 100 mg/kg.<br> -Reported to induce apoptosis, cause cell cycle arrest, inhibit angiogenesis, and modulate various signaling pathways (e.g., STAT3, NF-κB, MAPK).<br>
39
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BA
Baicalin
NP
<b>Baicalin</b> is a flavone glycoside, it is a flavonoid. It is the glucuronide of baicalein. Baicalin is a flavonoid glycoside derived from plants in the genus Scutellaria. It has anxiolytic, anti-cancer and anti-viral properties, and is used in traditional Chinese medicine.<br> <br> Baicalein and baicalin are chemically related, with baicalin being essentially a conjugated (sugar-attached) form of baicalein. This conjugation can modify their biological functions and impacts, making them distinct in certain aspects even though they share several pharmacological properties.<br> <br> Baicalein appears to be antioxidant in normal cells (low Cu), but prooxidant in Cancer cells (higher Cu levels) (Applies to other plant polyphenols as well: Ex apigenin, luteolin, EGCG, and resveratrol).<br> <br> Pathways:<br> Apoptosis Pathways (Intrinsic/Mitochondrial):<br> NF-κB Inhibition :<br> PI3K/Akt/mTOR Signaling Pathway downregulate :<br> MAPK/ERK and JNK Signaling Pathways:<br> STAT3 Signaling: (inhibit)<br> Wnt/β-Catenin Signaling Pathway: (suppress)<br> Other Pathways and Effects:<br> • Cell Cycle Arrests (commonly G0/G1 or G2/M)<br> • Anti-angiogenic Effects: By inhibitins VEGF<br> • Modulation of Oxidative Stress: Balancing reactive oxygen species (ROS) levels in cancer cells can also contribute to its antitumor effects.<br> <br> • In normal cells or under conditions of oxidative stress, baicalin has been shown to act as an antioxidant.<br> • In cancer cells, baicalin may increase ROS levels, triggering apoptosis. Lower doses of baicalin might favor antioxidant responses, whereas higher concentrations could lead to ROS accumulation in cancer cells.<br> <br> • If copper levels are elevated in a cancer cell, the additional ROS generated via copper-mediated reactions may synergize with baicalin’s pro-oxidant effects (if observed at higher doses) to exceed the threshold for cancer cell survival.<br> • Conversely, in normal cells with tightly regulated copper levels, baicalin’s antioxidant properties may help in quenching excess ROS or maintaining redox balance.<br> <br> -IC50 in cancer cell lines: Approximately 50–200 µM (with some variability depending on the cell type).<br> <br> • IC50 in normal cell lines: Generally higher, often exceeding 200 µM, though values will vary with experimental conditions.<br>
63
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bemp
bempedoic acid
RD
<b>Bempedoic acid></b> is a synthetic small‐molecule drug developed to lower low‐density lipoprotein cholesterol (LDL-C) by targeting lipid metabolism in the liver. Its design and development were based on a detailed understanding of cholesterol biosynthetic pathways rather than on a natural product scaffold.<br> <br> Key Pathways:<br> -ATP Citrate Lyase (ACLY) Inhibition<br> -Fatty Acid Synthesis and Lipogenesis<br> • With reduced acetyl-CoA, de novo fatty acid synthesis is also curtailed.<br>
181
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BaP
benzo(a)pyrene
NP
<b>benzo(a)pyrene</b> formula C20H12. Significant carcinogen, found in foods, tobacco smoke, automobiles exhaust(especially diesel), coal tar, grilled meats. The result of incomplete combustion of organic matter. Main source is residential wood burning.<br>
40
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BBM
Berbamine
NP
<b>Berbamine</b> is a bisbenzylisoquinoline alkaloid, meaning it is composed of two benzylisoquinoline moieties. Its unique structure distinguishes it from many other natural alkaloids Berbamine is most often isolated from the plant Berberis, commonly known as barberry. Various species within this genus have been used in traditional Chinese medicine and other herbal traditions. plants in genera like Stephania have also been reported to contain bisbenzylisoquinoline alkaloids like berbamine. These plants are used in various parts of Asia both for their stimulant effects and other medicinal purposes.<br> <br> Oxidative Stress:<br> Berbamine can increase the production of reactive oxygen species within cancer cells. Elevated ROS levels may push cancer cells beyond their threshold of tolerance, leading to oxidative stress–induced cell death. This property also ties in with its ability to modulate apoptosis and autophagy.<br> <br> Berbamine is a promising natural compound with multifaceted anticancer properties. Its ability to induce apoptosis, cause cell cycle arrest, modulate key signal transduction pathways (such as JAK/STAT, NF-κB, and PI3K/Akt/mTOR), and affect autophagy, makes it a candidate for further investigation in various cancer models.<br> <br> A calcium channel blocker.<br>
41
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BBR
Berberine
NP
<b>Berberine</b> is a chemical found in some plants like European barberry, goldenseal, goldthread, Oregon grape, phellodendron, and tree turmeric. Berberine is a bitter-tasting and yellow-colored chemical.<br> Coptis (commonly referring to Coptidis Rhizoma, a traditional Chinese medicinal herb) contains bioactive alkaloids (most notably berberine and coptisine) that have been studied for their pharmacological effects—including their influence on reactive oxygen species (ROS) and related pathways.<br> <br> – Berberine is known for its relatively low oral bioavailability, often cited at less than 1%. This low bioavailability is mainly due to poor intestinal absorption and active efflux by transport proteins such as P-glycoprotein.<br> – Despite the low bioavailability, berberine is still pharmacologically active, and its metabolites may also contribute to its overall effects.<br> <br> • Effective Dosage in Studies<br> – Many clinical trials or preclinical studies use dosages in the range of 500 to 1500 mg per day, typically administered in divided doses.<br> – Therefore, to obtain a bioactive dose of berberine, supplementation in a standardized extract form is necessary.<br> <br> -IC50 in cancer cell lines: Approximately 10–100 µM (commonly around 20–50 µM in many models)<br> -IC50 in normal cell lines: Generally higher (often above 100 µM), although this can vary with cell type<br> - In vivo studies: Dosing regimens in animal models generally range from about 50 to 200 mg/kg<br> <br> <br> -Note <a href="tbResList.php?qv=41&tsv=1109&wNotes=on&exSp=open">half-life</a> reports vary 2.5-90hrs?.<br> -low solubility of apigenin in water : <a href="tbResList.php?qv=41&tsv=792&wNotes=on&exSp=open">BioAv</a> <br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - induce <a href="tbResList.php?qv=41&tsv=275&wNotes=on">ROS</a> production<br> - ROS↑ related: <a href="tbResList.php?&qv=41&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?&qv=41&tsv=103&wNotes=on">ER Stress↑</a>, <a href="tbResList.php?&qv=41&tsv=38&wNotes=on">Ca+2↑</a>, <a href="tbResList.php?&qv=41&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?&qv=41&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?&qv=41&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?&qv=41&tsv=459&wNotes=on">UPR↑</a>, <a href="tbResList.php?&qv=41&tsv=239&wNotes=on">cl-PARP↑</a>, <a href="tbResList.php?&qv=41&wNotes=on&word=HSP">HSP↓</a> <br> <!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, --> - Lowers AntiOxidant defense in Cancer Cells: <a href="tbResList.php?&qv=41&tsv=226&wNotes=on&word=NRF2↓">NRF2↓</a>, <a href="tbResList.php?&qv=41&tsv=137&wNotes=on&word=GSH↓">GSH↓</a> <br> - Raises <a href="tbResList.php?&qv=41&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?&qv=41&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?&qv=41&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?&qv=41&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?&qv=41&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?&qv=41&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?&qv=41&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?&qv=41&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, <a href="tbResList.php?&qv=41&tsv=235&wNotes=on&word=p38↓">p38↓</a>, Pro-Inflammatory Cytokines : <a href="tbResList.php?&qv=41&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, <a href="tbResList.php?&qv=41&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?&qv=41&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <a href="tbResList.php?&qv=41&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a> <br> - PI3K/AKT(Inhibition), JAK/STATs, Wnt/β-catenin, AMPK, MAPK/ERK, and JNK.<br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓--> - inhibit Growth/Metastases : <a href="tbResList.php?&qv=41&tsv=96&wNotes=on"EMT↓</a>, <a href="tbResList.php?&qv=41&tsv=204&wNotes=on">MMPs↓</a>, <a href="tbResList.php?&qv=41&tsv=201&wNotes=on">MMP2↓</a>, <a href="tbResList.php?&qv=41&tsv=203&wNotes=on">MMP9↓</a>, <a href="tbResList.php?&qv=41&tsv=415&wNotes=on">IGF-1↓</a>, <a href="tbResList.php?&qv=41&tsv=428&wNotes=on">uPA↓</a>, <a href="tbResList.php?&qv=41&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?&qv=41&tsv=1284&wNotes=on">ROCK1↓</a>, <a href="tbResList.php?&qv=41&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?&qv=41&tsv=273&wNotes=on">RhoA↓</a>, <a href="tbResList.php?&qv=41&tsv=214&wNotes=on">NF-κB↓</a>, <a href="tbResList.php?&qv=41&tsv=79&wNotes=on">CXCR4↓</a>, <a href="tbResList.php?&qv=41&tsv=304&wNotes=on">TGF-β↓</a>, <a href="tbResList.php?&qv=41&tsv=719&wNotes=on">α-SMA↓</a>, <a href="tbResList.php?&qv=41&tsv=105&wNotes=on">ERK↓</a> <br> <!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, --> - reactivate genes thereby inhibiting cancer cell growth : <a href="tbResList.php?qv=41&tsv=140&wNotes=on">HDAC↓</a>, <a href="tbResList.php?qv=41&tsv=85&wNotes=on">DNMT1↓</a>, <a href="tbResList.php?qv=41&tsv=108&wNotes=on">EZH2↓</a>, <a href="tbResList.php?qv=41&tsv=236&wNotes=on">P53↑</a>, <a href="tbResList.php?&qv=41&wNotes=on&word=HSP">HSP↓</a> <br> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?&qv=41&tsv=322&wNotes=on">TumCCA↑</a>, <a href="tbResList.php?&qv=41&tsv=73&wNotes=on">cyclin D1↓</a>, <a href="tbResList.php?&qv=41&tsv=378&wNotes=on">cyclin E↓</a>, <a href="tbResList.php?&qv=41&tsv=467&wNotes=on">CDK2↓</a>, <a href="tbResList.php?&qv=41&tsv=894&wNotes=on">CDK4↓</a>, <a href="tbResList.php?&qv=41&tsv=895&wNotes=on">CDK6↓</a>, <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?&qv=41&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?&qv=41&tsv=324&wNotes=on">TumCI↓</a>, <a href="tbResList.php?&qv=41&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?&qv=41&tsv=105&wNotes=on">ERK↓</a>, <br> <!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS --> - inhibits <a href="tbResList.php?qv=41&tsv=129&wNotes=on">glycolysis</a> /<a href="tbResList.php?qv=41&tsv=947&wNotes=on">Warburg Effect</a> and <a href="tbResList.php?qv=41&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> : <a href="tbResList.php?&qv=41&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?&qv=41&tsv=772&wNotes=on">PKM2↓</a>, <a href="tbResList.php?&qv=41&tsv=35&wNotes=on">cMyc↓</a>, <a href="tbResList.php?&qv=41&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>, <a href="tbResList.php?&qv=41&tsv=906&wNotes=on">LDH↓</a>, <a href="tbResList.php?&qv=41&tsv=175&wNotes=on&word=LDH">LDHA↓</a>, <a href="tbResList.php?&qv=41&tsv=773&wNotes=on">HK2↓</a>, <a href="tbResList.php?&qv=41&wNotes=on&word=PFK">PFKs↓</a>, <a href="tbResList.php?&qv=41&wNotes=on&word=PDK">PDKs↓</a>, <a href="tbResList.php?&qv=41&tsv=1278&wNotes=on">Glucose↓</a>, <a href="tbResList.php?&qv=41&tsv=623&wNotes=on">GlucoseCon↓</a> <br> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - inhibits <a href="tbResList.php?qv=41&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=41&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?&qv=41&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?&qv=41&wNotes=on&word=NOTCH">Notch↓</a>, <a href="tbResList.php?&qv=41&wNotes=on&word=FGF">FGF↓</a>, <a href="tbResList.php?&qv=41&tsv=361&wNotes=on">PDGF↓</a>, <a href="tbResList.php?&qv=41&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, <a href="tbResList.php?&qv=41&&wNotes=on&word=ITG">Integrins↓</a>, <br> <!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, --> - inhibits Cancer Stem Cells : <a href="tbResList.php?qv=41&tsv=795&wNotes=on">CSC↓</a>, <a href="tbResList.php?qv=41&tsv=141&wNotes=on">Hh↓</a>, <a href="tbResList.php?qv=41&tsv=124&wNotes=on">GLi1↓</a>, <a href="tbResList.php?qv=41&tsv=677&wNotes=on">CD133↓</a>, <a href="tbResList.php?qv=41&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=41&tsv=357&wNotes=on">n-myc↓</a>, <a href="tbResList.php?qv=41&tsv=656&wNotes=on">sox2↓</a>, <a href="tbResList.php?qv=41&tsv=222&wNotes=on">notch2↓</a>, <a href="tbResList.php?qv=41&tsv=1024&wNotes=on">nestin↓</a>, <a href="tbResList.php?qv=41&tsv=508&wNotes=on">OCT4↓</a>, <br> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=41&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=41&tsv=4&wNotes=on">AKT↓</a>, <a href="tbResList.php?qv=41&wNotes=on&word=JAK">JAK↓</a>, <a href="tbResList.php?qv=41&wNotes=on&word=STAT">STAT↓</a>, <a href="tbResList.php?qv=41&tsv=377&wNotes=on">Wnt↓</a>, <a href="tbResList.php?qv=41&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=41&tsv=9&wNotes=on">AMPK↓</a>, <a href="tbResList.php?qv=41&tsv=475&wNotes=on">α↓</a>, <a href="tbResList.php?qv=41&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=41&tsv=168&wNotes=on">JNK</a>, <br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=41&tsv=1106&wNotes=on">chemo-sensitization</a>, <a href="tbResList.php?qv=41&tsv=1171&wNotes=on">chemoProtective</a>, <a href="tbResList.php?qv=41&tsv=1107&wNotes=on">RadioSensitizer</a>, <a href="tbResList.php?qv=41&tsv=1185&wNotes=on">RadioProtective</a>, <a href="tbResList.php?qv=41&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <a href="tbResList.php?qv=41&tsv=1105&wNotes=on">Neuroprotective</a>, <a href="tbResList.php?qv=41&tsv=557&wNotes=on">Cognitive</a>, <a href="tbResList.php?qv=41&tsv=1175&wNotes=on">Renoprotection</a>, <a href="tbResList.php?qv=41&tsv=1179&wNotes=on">Hepatoprotective</a>, <a href="tbResList.php?&qv=41&tsv=1188&wNotes=on">CardioProtective</a>, <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=41&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br> <br>
194
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betaCar
beta-carotene
NP
<b>Beta carotene</b> is a red-orange pigment found in plants and fruits, especially carrots and colorful vegetables. The body converts beta carotene into vitamin A.<br> Beta carotene is a carotenoid and an antioxidant.<br> beta-carotene is known to have pro-oxidant activity in vitro<br> Beta carotene, a precursor of vitamin A and a well-known antioxidant, has been investigated for its potential roles in cancer prevention and therapy.<br> <br> -By mitigating oxidative stress, beta carotene may indirectly reduce NF-κB activation.<br> -As a lipid-soluble molecule, beta carotene is integrated into cellular membranes, where it helps maintain membrane integrity and fluidity.<br> -at high concentrations or in the presence of high oxygen tension), beta carotene can exhibit pro-oxidant behavior, which may contribute to cellular damage.<br>
245
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B-Gluc
beta-glucans
NP
<b>Beta-glucans</b> are polysaccharides found in the cell walls of certain fungi, bacteria, and plants.<br> • Enhanced anti-tumor activity: Beta-glucans have been shown to stimulate the immune system, increasing the production of cytokines and activating natural killer cells, which can help to destroy cancer cells.<br> • Improved survival rates: <br> • Increased expression of tumor suppressor genes: <br> • Inhibition of cancer cell proliferation: <br> • Enhanced chemotherapy efficacy: <br> • Reduced cancer recurrence:<br>
42
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BetA
Betulinic acid
NP
<b>Betulinic acid</b> "buh-TOO-li-nik acid" is a natural compound with antiretroviral, anti malarial, anti-inflammatory and anticancer properties. It is found in the bark of several plants, such as white birch, ber tree and rosemary, and has a complex mode of action against tumor cells.<br> -Betulinic acid is a naturally occurring pentacyclic triterpenoid<br> -vitro concentrations range from 1–100 µM, in vivo studies in rodents have generally used doses from 10–100 mg/kg<br> -<a href="tbResList.php?qv=42&tsv=1109&wNotes=on&exSp=open">half-life</a> reports vary 3-5 hrs?.<br> <a href="tbResList.php?qv=42&tsv=792&wNotes=on&exSp=open">BioAv</a> -hydrophobic molecule with relatively poor water solubility. <br> <br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - induce <a href="tbResList.php?qv=42&tsv=275&wNotes=on">ROS</a> production<br> - ROS↑ related: <a href="tbResList.php?&qv=42&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?&qv=42&tsv=103&wNotes=on">ER Stress↑</a>, <a href="tbResList.php?&qv=42&tsv=459&wNotes=on">UPR↑</a>, <a href="tbResList.php?&qv=42&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?&qv=42&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>, <a href="tbResList.php?&qv=42&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?&qv=42&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?&qv=42&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?&qv=42&tsv=239&wNotes=on">cl-PARP↑</a>, <a href="tbResList.php?&qv=42&wNotes=on&word=HSP">HSP↓</a> <br> <!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, --> - Lowers AntiOxidant defense in Cancer Cells: <a href="tbResList.php?&qv=42&tsv=226&wNotes=on&word=NRF2↓">NRF2↓</a>, <a href="tbResList.php?&qv=42&tsv=298&wNotes=on&word=SOD↓">SOD↓</a>, <a href="tbResList.php?&qv=42&tsv=137&wNotes=on&word=GSH↓">GSH↓</a> <br> - Raises <a href="tbResList.php?&qv=42&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?&qv=42&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?&qv=42&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?&qv=42&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?&qv=42&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?&qv=42&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?&qv=42&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?&qv=42&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, <a href="tbResList.php?&qv=42&tsv=235&wNotes=on&word=p38↓">p38↓</a>, Pro-Inflammatory Cytokines : <a href="tbResList.php?&qv=42&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, <a href="tbResList.php?&qv=42&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?&qv=42&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <a href="tbResList.php?&qv=42&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a> <br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓ inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.--> - inhibit Growth/Metastases : <a href="tbResList.php?&qv=42&tsv=96&wNotes=on"EMT↓</a>, <a href="tbResList.php?&qv=42&tsv=204&wNotes=on">MMPs↓</a>, <a href="tbResList.php?&qv=42&tsv=201&wNotes=on">MMP2↓</a>, <a href="tbResList.php?&qv=42&tsv=203&wNotes=on">MMP9↓</a>, <a href="tbResList.php?&qv=42&tsv=308&wNotes=on">TIMP2</a>, <a href="tbResList.php?&qv=42&tsv=415&wNotes=on">IGF-1↓</a>, <a href="tbResList.php?&qv=42&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?&qv=42&tsv=1284&wNotes=on">ROCK1↓</a>, <a href="tbResList.php?&qv=42&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?&qv=42&tsv=214&wNotes=on">NF-κB↓</a>, <a href="tbResList.php?&qv=42&tsv=304&wNotes=on">TGF-β↓</a>, <a href="tbResList.php?&qv=42&tsv=719&wNotes=on">α-SMA↓</a>, <a href="tbResList.php?&qv=42&tsv=105&wNotes=on">ERK↓</a> <br> <!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, --> - reactivate genes thereby inhibiting cancer cell growth : <a href="tbResList.php?qv=42&tsv=236&wNotes=on">P53↑</a>, <a href="tbResList.php?&qv=42&wNotes=on&word=HSP">HSP↓</a>, <a href="tbResList.php?&qv=42&tsv=506&wNotes=on">Sp proteins↓</a>, <br> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?&qv=42&tsv=322&wNotes=on">TumCCA↑</a>, <a href="tbResList.php?&qv=42&tsv=73&wNotes=on">cyclin D1↓</a>, <a href="tbResList.php?&qv=42&tsv=467&wNotes=on">CDK2↓</a>, <a href="tbResList.php?&qv=42&tsv=894&wNotes=on">CDK4↓</a>, <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?&qv=42&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?&qv=42&tsv=324&wNotes=on">TumCI↓</a>, <a href="tbResList.php?&qv=42&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?&qv=42&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?&qv=42&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?&qv=42&tsv=1117&wNotes=on">TOP1↓</a>, <br> <!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS --> - inhibits <a href="tbResList.php?qv=42&tsv=129&wNotes=on">glycolysis</a> <a href="tbResList.php?qv=42&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> : <a href="tbResList.php?&qv=42&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?&qv=42&tsv=772&wNotes=on">PKM2↓</a>, <a href="tbResList.php?&qv=42&tsv=35&wNotes=on">cMyc↓</a>, <a href="tbResList.php?&qv=42&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>, <a href="tbResList.php?&qv=42&tsv=906&wNotes=on">LDH↓</a>, <a href="tbResList.php?&qv=42&tsv=175&wNotes=on&word=LDH">LDHA↓</a>, <a href="tbResList.php?&qv=42&tsv=773&wNotes=on">HK2↓</a>, <a href="tbResList.php?&qv=42&wNotes=on&word=PFK">PFKs↓</a>, <a href="tbResList.php?&qv=42&wNotes=on&word=PDK">PDKs↓</a>, <a href="tbResList.php?&qv=42&tsv=773&wNotes=on">HK2↓</a>, <a href="tbResList.php?&qv=42&tsv=847&wNotes=on">ECAR↓</a>, <a href="tbResList.php?&qv=42&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?&qv=42&tsv=623&wNotes=on">GlucoseCon↓</a> <br> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - inhibits <a href="tbResList.php?qv=42&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=42&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?&qv=42&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?&qv=42&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, <br> <!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, --> - inhibits Cancer Stem Cells : <a href="tbResList.php?qv=42&tsv=795&wNotes=on">CSC↓</a>, <a href="tbResList.php?qv=42&tsv=124&wNotes=on">GLi1↓</a>, <a href="tbResList.php?qv=42&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=42&tsv=508&wNotes=on">OCT4↓</a>, <br> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=42&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=42&tsv=4&wNotes=on">AKT↓</a>, <a href="tbResList.php?qv=42&wNotes=on&word=JAK">JAK↓</a>, <a href="tbResList.php?qv=42&wNotes=on&word=STAT">STAT↓</a>, <a href="tbResList.php?qv=42&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=42&tsv=9&wNotes=on">AMPK↓</a>, <a href="tbResList.php?qv=42&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=42&tsv=168&wNotes=on">JNK</a>, <br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=42&tsv=1106&wNotes=on">chemo-sensitization</a>, <a href="tbResList.php?qv=42&tsv=1171&wNotes=on">chemoProtective</a>, <a href="tbResList.php?qv=42&tsv=1107&wNotes=on">RadioSensitizer</a>, <a href="tbResList.php?qv=42&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <a href="tbResList.php?qv=42&tsv=1105&wNotes=on">Neuroprotective</a>, <a href="tbResList.php?qv=42&tsv=557&wNotes=on">Cognitive</a>, <a href="tbResList.php?qv=42&tsv=1175&wNotes=on">Renoprotection</a>, <a href="tbResList.php?qv=42&tsv=1179&wNotes=on">Hepatoprotective</a>, <a href="tbResList.php?&qv=42&tsv=1188&wNotes=on">CardioProtective</a>, <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=42&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br>
3
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BEV
Bevacizumab (brand Avastin)
D
<b>Bevacizumab</b> monoclonal antibody medication used to treat a number of types of cancers and a specific eye disease. Cancer, IV used for colon cancer, lung cancer, ovarian cancer, glioblastoma, hepatocellular carcinoma, and renal-cell carcinoma.<br> Serious side effects, such as treatment-related mortality <br>
186
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Bical
Bicalutamide
D
<b>Bicalutamide</b> brand name Casodex. An antiandrogen medication that is primarily used to treat prostate cancer.<br>
43
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HCO3
Bicarbonate
NP
<b>Bicarbonate</b> one central carbon atom surrounded by three oxygen atoms in a triogonal planer arrangement with a hydrogen atom attached to one of the oxygens. <br> -Bicarbonate’s primary role is in pH buffering. Its administration has been studied as an adjuvant strategy to modify the tumor microenvironment.<br> <br> -Many solid tumors exhibit an acidic microenvironment due to high rates of glycolysis (the “Warburg effect”) and poor perfusion. Bicarbonate supplementation can buffer this acidity, raising the extracellular pH.<br> <br> -By modulating pH, bicarbonate may influence pathways tied to glycolysis and oxidative phosphorylation<br>
44
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Bif
Bifidobacterium
NP
Bacteria
<b>Bifidobacterium</b> has been associated with improved responses to immune checkpoint inhibitors such as anti–PD-L1 antibodies. The suggested mechanisms include:<br> -Enhancing dendritic cell function.<br> -Promoting the activation and proliferation of T cells.<br> -Modulating cytokine profiles in a way that favors anti-tumor immunity.<br> <br> Bifidobacterium is a genus of gram-positive, nonmotile, often branched anaerobic bacteria. They are ubiquitous inhabitants of the gastrointestinal tract.<br> <br> Bifidobacterium longum: Gram-positive, catalase-negative, rod-shaped bacterium.<br> <br> Here are several notable species:<br> Bifidobacterium longum<br> Often found in the human gastrointestinal tract, B. longum has been extensively studied for its role in modulating the immune system and improving gut barrier function. Bifidobacterium breve<br> Known for its anti-inflammatory properties, B. breve is used in many probiotic formulations and has been researched for its potential to alleviate gastrointestinal disorders, which may indirectly support cancer patients.<br> Bifidobacterium bifidum<br> This species is a common member of the gut microbiota and plays a role in maintaining mucosal integrity and immune modulation.<br> Bifidobacterium infantis<br> Commonly found in the intestines of breast-fed infants, B. infantis is studied for its beneficial effects on gut health and its potential to modulate immune responses.<br> Bifidobacterium animalis (including subspecies such as B. animalis subsp. lactis).<br> <br> Widely incorporated into commercial probiotic products, this species has been researched for its role in digestive health, and emerging studies suggest potential benefits in the context of systemic health, including immune regulation.<br>
45
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BCA
Biochanin A
NP
<b>Biochanin A</b> is a O-methylated isoflavone. <br> Found in soy, alfalfa sprouts, peanuts, chickpeas and other legumes.<br> Inhibits fatty acid amide hydrolase.<br>
281
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BP
Black phosphorus
D
<b>Black phosphorus (BP)</b> has attracted considerable attention in cancer research—not only as a material for bioimaging and phototherapy but also for its ability to modulate various cellular signaling pathways.<br> <br> Black phosphorus (BP), a two-dimensional nanomaterial, exhibits excellent light-absorption performance, high photothermal conversion efficiency, biodegradability, and large specific surface area. BP can be gradually degraded into phosphate ions under physiological conditions without biological toxicity. BP has shown great potential in the biomedical field for PTT, PDT, and SDT applications.<br>
301
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born
borneol
NP
<b>Borneol</b> is a bicyclic organic compound and a type of monoterpenoid that occurs naturally in various essential oils.<br> -Recent studies have been exploring borneol’s ability to enhance drug delivery—especially across the blood-brain barrier.<br> -Borneol is particularly known for its ability to act as a penetration enhancer. This quality can improve the absorption of various drugs, potentially increasing their efficacy when used in combination with other therapeutic agents.<br> -Borneol is thought to temporarily open tight junctions between endothelial cells, enhancing drug penetration. It may also downregulate efflux transporters such as P-glycoprotein (P-gp), allowing higher intracellular concentrations of co-administered drugs.<br> <br> Sources:<br> -Cinnamomum camphora (camphor tree), its essential oil contains borneol along with camphor.<br> -Dryobalanops aromatica,Often referred to as the camphor tree in Southeast Asia, its oleoresin is a well-known source of natural borneol. <br> -Blumea balsamifera<br>
46
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Bor
Boron
NP
micronutrient
<b>Boron</b> is a trace mineral.<br> Used in treating yeast infections, improving athletic performance, or preventing osteoporosis.<br> <br> Current research suggests that boric acid can modulate intercellular calcium levels—with potential implications for cancer therapy—by:<br> -Altering calcium channel activity and calcium influx,<br> -Modifying downstream calcium-dependent signaling, and<br> -Inducing apoptotic pathways preferentially in cancer cells due to their altered calcium handling dynamics.<br> Abnormal increases in [Ca²⁺]ᵢ can trigger mitochondrial dysfunction and activate calcium-dependent apoptotic pathways. Boric acid has been observed in some cell culture studies to induce apoptosis in cancer cells.<br> In normal cells, modest changes in [Ca²⁺]ᵢ induced by boric acid may not reach a threshold that triggers apoptosis or other stress responses. This could lead to a relative sparing of normal cells compared to cancer cells.<br> <br> Pathways:<br> 1.Calcium Signaling Pathway<br> In many cases, boron appears to normalize dysregulated calcium levels in cancer cells, often leading to an increase in calcium levels that can trigger calcium-dependent apoptotic pathways. 2.Apoptotic Pathways (Intrinsic and Extrinsic).<br> Direction of Modulation:<br> • Boron compounds may enhance the activation of apoptotic cascades.<br> • Typically, an increase in intracellular calcium (as noted above) can further lead to mitochondrial dysfunction, cytochrome c release, and subsequent caspase activation, thereby promoting apoptosis.<br> 3.PI3K/AKT/mTOR Pathway<br> • Some studies indicate that boron-containing compounds can inhibit this pathway.<br> • Inhibition of PI3K/AKT/mTOR signaling reduces survival signals and can decrease cellular proliferation and growth in tumor cell.<br> 4.MAPK/ERK Pathway <br> Boron may modulate the MAPK/ERK cascade by either dampening overactive mitogenic signals or altering the stress response.<br> • This modulation can lead to reduced proliferation signals and may promote cell cycle arrest in cancer cells.<br> 5.NF-κB Signaling Pathway<br> • Some reports indicate that boron compounds can suppress NF-κB activity.<br> • This suppression might be achieved indirectly through modulation of upstream signals (such as changes in calcium or the cellular redox status) leading to decreased transcription of pro-survival and pro-inflammatory genes.<br> 6.Wnt/β-Catenin Pathway<br> • Inhibition of Wnt/β-catenin signaling may interfere with proliferation and the maintenance of cancer stem cell populations.<br> <br> ROS:<br> -ROS induction may be dose related.<br> -Some studies report that when boron compounds are combined with other treatments (like chemotherapy or radiotherapy), there is a synergistic increase in ROS generation.<br> Boron’s effects in a cancer context generally lean toward:<br> • Normalizing dysregulated calcium signaling to push cells toward apoptotic death<br> • Inhibiting pro-survival pathways such as <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC4712861/">PI3K/AKT/mTOR and NF-κB</a><br> <br> (1) is essential for the growth and maintenance of bone;<br> (2) greatly improves wound healing;<br> (3) beneficially impacts the body's use of estrogen, testosterone, and vitamin D;<br> (4) boosts magnesium absorption;<br> (5) reduces levels of inflammatory biomarkers, such as high-sensitivity C-reactive protein (hs-CRP) and tumor necrosis factor α (TNF-α);<br> (6) raises levels of antioxidant enzymes, such as superoxide dismutase (SOD), catalase, and glutathione peroxidase;<br> (7) protects against pesticide-induced oxidative stress and heavy-metal toxicity;<br> (8) improves the brains electrical activity, cognitive performance, and short-term memory for elders;<br> (9) influences the formation and activity of key biomolecules, such as S-adenosyl methionine (SAM-e) and nicotinamide adenine dinucleotide (NAD(+));<br> (10) has demonstrated preventive and therapeutic effects in a number of cancers, such as prostate, cervical, and lung cancers, and multiple and non-Hodgkin's lymphoma; and<br> (11) may help ameliorate the adverse effects of traditional chemotherapeutic agents.<br> <br> -Note <a href="tbResList.php?qv=46&tsv=1109&wNotes=on&exSp=open">half-life</a> 21 hrs average<br> <a href="tbResList.php?qv=46&tsv=792&wNotes=on&exSp=open">BioAv</a> very high, 85-100% <br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - induce <a href="tbResList.php?qv=46&tsv=275&wNotes=on">ROS</a> productionin cancer cells, while reducing ROS in normal cells.<br> - ROS↑ related: <a href="tbResList.php?qv=46&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?qv=46&tsv=103&wNotes=on">ER Stress↑</a>, <a href="tbResList.php?qv=46&tsv=459&wNotes=on">UPR↑</a>, <a href="tbResList.php?qv=46&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=46&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>,(contrary) <a href="tbResList.php?qv=46&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?qv=46&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?qv=46&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?qv=46&tsv=239&wNotes=on">cl-PARP↑</a>,(contrary) <a href="tbResList.php?qv=46&wNotes=on&word=HSP">HSP↓</a>, <!-- <a href="tbResList.php?qv=46&wNotes=on&word=Prx">Prx</a>, --><!-- mitochondrial antioxidant enzyme--> <br> <!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, --> - Debateable if Lowers AntiOxidant defense in Cancer Cells: <a href="tbResList.php?qv=46&tsv=226&wNotes=on&word=NRF2">NRF2↓</a>(most contrary), <!-- <a href="tbResList.php?qv=46&word=Trx&wNotes=on">TrxR↓**</a>, --><!-- major antioxidant system --> <a href="tbResList.php?qv=46&tsv=298&wNotes=on&word=SOD">SOD↓</a>(some contrary), <a href="tbResList.php?qv=46&tsv=137&wNotes=on&word=GSH↓">GSH↓</a>, <a href="tbResList.php?qv=46&tsv=46&wNotes=on">Catalase↓</a>(some contrary), <a href="tbResList.php?qv=46&tsv=597&wNotes=on">HO1↓</a>(contrary), <a href="tbResList.php?qv=46&wNotes=on&word=GPx">GPx↓</a>(some contrary) <br> - Raises <a href="tbResList.php?qv=46&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?qv=46&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>, <a href="tbResList.php?qv=46&tsv=226&wNotes=on&word=NRF2">NRF2↑</a>, <a href="tbResList.php?qv=46&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?qv=46&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?qv=46&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <!-- genes involved in the oxidative stress-antioxidant defense system PRNP, NQO1, and GCLM --> <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?qv=46&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?qv=46&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?qv=46&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, <!-- <a href="tbResList.php?qv=46&tsv=235&wNotes=on&word=p38↓">p38↓</a>, --> Pro-Inflammatory Cytokines : <a href="tbResList.php?qv=46&tsv=908&wNotes=on&word=NLRP3↓">NLRP3↓</a>, <a href="tbResList.php?qv=46&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, <a href="tbResList.php?qv=46&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?qv=46&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <!-- <a href="tbResList.php?qv=46&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a> --> <br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓ inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.--> - inhibit Growth/Metastases : <a href="tbResList.php?qv=46&tsv=604&wNotes=on">TumMeta↓</a>, <a href="tbResList.php?qv=46&tsv=323&wNotes=on">TumCG↓</a>, <a href="tbResList.php?qv=46&tsv=96&wNotes=on">EMT↓</a>, <!-- <a href="tbResList.php?qv=46&tsv=204&wNotes=on">MMPs↓</a>, --> <!-- <a href="tbResList.php?qv=46&tsv=201&wNotes=on">MMP2↓</a>, --> <!-- <a href="tbResList.php?qv=46&tsv=203&wNotes=on">MMP9↓</a>, --> <!-- <a href="tbResList.php?qv=46&tsv=308&wNotes=on">TIMP2</a>, --> <a href="tbResList.php?qv=46&tsv=415&wNotes=on">IGF-1↓</a>, <!-- <a href="tbResList.php?qv=46&tsv=428&wNotes=on">uPA↓</a>, --> <a href="tbResList.php?qv=46&tsv=334&wNotes=on">VEGF↓</a>, <!-- <a href="tbResList.php?qv=46&tsv=1284&wNotes=on">ROCK1↓</a>, --> <!-- <a href="tbResList.php?qv=46&tsv=110&wNotes=on">FAK↓</a>, --> <a href="tbResList.php?qv=46&tsv=273&wNotes=on">RhoA↓</a>, <a href="tbResList.php?qv=46&tsv=214&wNotes=on">NF-κB↓</a>, <!-- <a href="tbResList.php?qv=46&tsv=79&wNotes=on">CXCR4↓</a>, --> <!-- <a href="tbResList.php?qv=46&tsv=1247&wNotes=on">SDF1↓</a>, --> <a href="tbResList.php?qv=46&tsv=304&wNotes=on">TGF-β↓</a>, <a href="tbResList.php?qv=46&tsv=719&wNotes=on">α-SMA↓</a>, <a href="tbResList.php?qv=46&tsv=105&wNotes=on">ERK↓</a> <!-- <a href="tbResList.php?qv=46&tsv=1178&wNotes=on">MARK4↓</a> --><!-- contributing to tumor growth, invasion, and metastasis--> <br> <!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, --> - reactivate genes thereby inhibiting cancer cell growth : <a href="tbResList.php?qv=46&tsv=140&wNotes=on">HDAC↓</a>, <!-- <a href="tbResList.php?qv=46&wNotes=on&word=DNMT">DNMTs↓</a>, --> <!-- <a href="tbResList.php?qv=46&tsv=108&wNotes=on">EZH2↓</a>, --> <a href="tbResList.php?qv=46&tsv=236&wNotes=on">P53↑</a>, <a href="tbResList.php?qv=46&wNotes=on&word=HSP">HSP↓</a>, <!-- <a href="tbResList.php?qv=46&tsv=506&wNotes=on">Sp proteins↓</a>, --> <!-- <a href="tbResList.php?qv=46&wNotes=on&word=TET">TET↑</a> --> <br> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - some indication of Cell cycle arrest : <a href="tbResList.php?qv=46&tsv=322&wNotes=on">TumCCA↑</a>, <a href="tbResList.php?qv=46&tsv=73&wNotes=on">cyclin D1↓</a>, <a href="tbResList.php?qv=46&tsv=378&wNotes=on">cyclin E↓</a>, <a href="tbResList.php?qv=46&tsv=467&wNotes=on">CDK2↓</a>, <a href="tbResList.php?qv=46&tsv=894&wNotes=on">CDK4↓</a>, <a href="tbResList.php?qv=46&tsv=895&wNotes=on">CDK6↓</a>, <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?qv=46&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?qv=46&tsv=324&wNotes=on">TumCI↓</a>, <a href="tbResList.php?qv=46&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <!-- encourages invasion, proliferation, EMT, and angiogenesis --> <!-- <a href="tbResList.php?qv=46&tsv=110&wNotes=on">FAK↓</a>, --> <a href="tbResList.php?qv=46&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=46&tsv=96&wNotes=on">EMT↓</a>, <!-- <a href="tbResList.php?qv=46&wNotes=on&word=TOP">TOP1↓</a>, --> <!-- <a href="tbResList.php?qv=46&tsv=657&wNotes=on">TET1</a>, --> <br> <!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS --> - small indication of inhibiting <a href="tbResList.php?qv=46&tsv=129&wNotes=on">glycolysis</a> <!-- /<a href="tbResList.php?qv=46&tsv=947&wNotes=on">Warburg Effect</a> and <a href="tbResList.php?qv=46&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> -->: <a href="tbResList.php?qv=46&tsv=143&wNotes=on">HIF-1α↓</a>, <!-- <a href="tbResList.php?qv=46&tsv=772&wNotes=on">PKM2↓</a>, --> <a href="tbResList.php?qv=46&tsv=35&wNotes=on">cMyc↓</a>, <!-- <a href="tbResList.php?qv=46&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>, --> <!-- <a href="tbResList.php?qv=46&tsv=906&wNotes=on">LDH↓</a>, --> <!-- <a href="tbResList.php?qv=46&tsv=175&wNotes=on&word=LDH">LDHA↓</a>, --> <!-- <a href="tbResList.php?qv=46&tsv=773&wNotes=on">HK2↓</a>, --> <!-- <a href="tbResList.php?qv=46&wNotes=on&word=PFK">PFKs↓</a>, --> <!-- <a href="tbResList.php?qv=46&wNotes=on&word=PDK">PDKs↓</a>, --> <!-- <a href="tbResList.php?qv=46&tsv=847&wNotes=on">ECAR↓</a>, --> <!-- <a href="tbResList.php?qv=46&tsv=230&wNotes=on">OXPHOS↓</a>, --> <a href="tbResList.php?qv=46&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=46&tsv=1278&wNotes=on">Glucose↓</a>, <!--<a href="tbResList.php?qv=46&tsv=623&wNotes=on">GlucoseCon↓</a> --> <br> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - small indication of inhibiting <a href="tbResList.php?qv=46&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=46&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=46&tsv=143&wNotes=on">HIF-1α↓</a>, <!-- <a href="tbResList.php?qv=46&wNotes=on&word=NOTCH">Notch↓</a>, --> <!-- <a href="tbResList.php?qv=46&wNotes=on&word=FGF">FGF↓</a>, --> <!-- <a href="tbResList.php?qv=46&wNotes=on&word=PDGF">PDGF↓</a>, --> <a href="tbResList.php?qv=46&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, <!--<a href="tbResList.php?qv=46&&wNotes=on&word=ITG">Integrins↓</a>, --> <br> <!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, --> <!-- - inhibits Cancer Stem Cells : <a href="tbResList.php?qv=46&tsv=795&wNotes=on">CSC↓</a>, <a href="tbResList.php?qv=46&tsv=524&wNotes=on">CK2↓</a>, <a href="tbResList.php?qv=46&tsv=141&wNotes=on">Hh↓</a>, <a href="tbResList.php?qv=46&tsv=434&wNotes=on">GLi↓</a>, <a href="tbResList.php?qv=46&tsv=124&wNotes=on">GLi1↓</a>, <a href="tbResList.php?qv=46&tsv=677&wNotes=on">CD133↓</a>, <a href="tbResList.php?qv=46&tsv=655&wNotes=on">CD24↓</a>, <a href="tbResList.php?qv=46&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=46&tsv=357&wNotes=on">n-myc↓</a>, <a href="tbResList.php?qv=46&tsv=656&wNotes=on">sox2↓</a>, <a href="tbResList.php?qv=46&wNotes=on&word=NOTCH">Notch2↓</a>, <a href="tbResList.php?qv=46&tsv=1024&wNotes=on">nestin↓</a>, <a href="tbResList.php?qv=46&tsv=508&wNotes=on">OCT4↓</a>, <br> --> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=46&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=46&tsv=4&wNotes=on">AKT↓</a>, <a href="tbResList.php?qv=46&wNotes=on&word=JAK">JAK↓</a>, <a href="tbResList.php?qv=46&wNotes=on&word=STAT">STAT↓</a>, <a href="tbResList.php?qv=46&tsv=377&wNotes=on">Wnt↓</a>, <a href="tbResList.php?qv=46&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=46&tsv=9&wNotes=on">AMPK</a>, <!-- <a href="tbResList.php?qv=46&tsv=475&wNotes=on">α↓</a>, --> <a href="tbResList.php?qv=46&tsv=105&wNotes=on">ERK↓</a>, <!-- <a href="tbResList.php?qv=46&tsv=1014&wNotes=on">5↓</a>, --> <!-- <a href="tbResList.php?qv=46&tsv=168&wNotes=on">JNK</a>, --> - <a href="tbResList.php?qv=46&wNotes=on&word=SREBP">SREBP</a> (related to cholesterol).<br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=46&tsv=1106&wNotes=on">chemo-sensitization</a>, <a href="tbResList.php?qv=46&tsv=1171&wNotes=on">chemoProtective</a>, <a href="tbResList.php?qv=46&tsv=1107&wNotes=on">RadioSensitizer</a>, <a href="tbResList.php?qv=46&tsv=1185&wNotes=on">RadioProtective</a>, <a href="tbResList.php?qv=46&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <a href="tbResList.php?qv=46&tsv=1105&wNotes=on">Neuroprotective</a>, <a href="tbResList.php?qv=46&tsv=557&wNotes=on">Cognitive</a>, <a href="tbResList.php?qv=46&tsv=1175&wNotes=on">Renoprotection</a>, <a href="tbResList.php?qv=46&tsv=1179&wNotes=on">Hepatoprotective</a>, <a href="tbResList.php?&qv=46&tsv=1188&wNotes=on">CardioProtective</a>, <br> <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=46&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br>
257
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BTZ
Bortezomib
D
<b>Bortezomib</b> (often abbreviated as BTZ) is a proteasome inhibitor that has been approved for the treatment of certain types of cancers, most notably multiple myeloma and mantle cell lymphoma.<br> Mechanism of Action<br> Proteasome Inhibition:<br> Bortezomib targets the 26S proteasome, a complex responsible for degrading ubiquitinated proteins. By inhibiting the proteasome’s activity, bortezomib causes an accumulation of unwanted or misfolded proteins within the cell.<br> <br> Induction of Apoptosis:<br> The buildup of these proteins leads to cellular stress and activation of the unfolded protein response (UPR). In cancer cells, which often have high levels of protein synthesis and turnover, this stress quickly tips the balance toward apoptosis (programmed cell death).<br> <br> Disruption of Cell Signaling Pathways:<br> Proteasome inhibition affects several signaling pathways, including the nuclear factor-kappa B (NF-κB) pathway. NF-κB is a key regulator of cell survival, proliferation, and inflammation. Its inhibition contributes to decreased survival signals for cancer cells, enhancing the cytotoxic effects of the treatment.<br>
47
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Bos
Boswellia (frankincense)
NP
<b>Boswellia</b> is an herbal extract from the Boswellia serrata tree that may help reduce inflammation.<br> May help with rheumatoid arthritis, inflammatory bowel disease, asthma, and cancer.<br> -Naturally occurring pentacyclic triterpenoids include ursolic acid (UA), oleanolic acid (OA), betulinic acid (BetA), bosewellic acid (BA), Asiatic acid (AA), α-amyrin, celastrol, glycyrrhizin, 18-β-glycyrrhetinic acid, lupeol, escin, madecassic acid, momordin I, platycodon D, pristimerin, saikosaponins, soyasapogenol B, and avicin<br> Boswellia refers to a group of resinous extracts obtained from Boswellia trees (e.g., Boswellia serrata). Traditionally used in Ayurvedic and traditional Chinese medicine, Boswellia is reputed for its anti-inflammatory, analgesic, and immunomodulatory properties. Its bioactive components—such as boswellic acids.<br> -Anti-inflammatory Activity (blocking the enzyme 5-lipoxygenase) <a href="tbResList.php?qv=47&tsv=1090&wNotes=on">5LOX↓</a>,.<br> -AKBA used to reduce <a href="tbResList.php?qv=47&tsv=1206&wNotes=on">Methionine </a>***** (help in Methionine reduced diet) <br> Boswellia extracts are often administered in doses ranging from 300 mg to 1,200 mg per day<br> <br> AKBA (Acetyl-11-keto-β-boswellic acid) is a bioactive compound derived from Boswellia serrata, a plant used traditionally for its anti-inflammatory properties. (upto 30% AKBA in <a href="https://www.mcsformulas.com/vitamins-supplements/boswellia-akba-liposomal/"> Boswellia MEGA AKBA</a>)<br> AKBA also available in Inflasanum @ 90% AKDA (MCSformulas)<br> <br> -Note <a href="tbResList.php?qv=47&tsv=1109&wNotes=on&exSp=open">half-life</a> reports vary 2.5-90hrs?.<br> <a href="tbResList.php?qv=47&tsv=792&wNotes=on&exSp=open">BioAv</a> <br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - induce or lower <a href="tbResList.php?qv=47&tsv=275&wNotes=on">ROS</a> production (not consistant increase for cancer cells)<br> - ROS↑ related: <a href="tbResList.php?qv=47&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?qv=47&tsv=103&wNotes=on">ER Stress↑</a>, <a href="tbResList.php?qv=47&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=47&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>, <a href="tbResList.php?qv=47&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?qv=47&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?qv=47&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?qv=47&tsv=239&wNotes=on">cl-PARP↑</a>, <br> - Raises <a href="tbResList.php?qv=47&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?qv=47&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>, <a href="tbResList.php?qv=47&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?qv=47&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?qv=47&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?qv=47&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?qv=47&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?qv=47&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?qv=47&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, <a href="tbResList.php?qv=47&tsv=235&wNotes=on&word=p38↓">p38↓</a>, Pro-Inflammatory Cytokines : <a href="tbResList.php?qv=47&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, <a href="tbResList.php?qv=47&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?qv=47&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓ inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.--> - inhibit Growth/Metastases : <a href="tbResList.php?qv=47&tsv=96&wNotes=on"EMT↓</a>, <a href="tbResList.php?qv=47&tsv=204&wNotes=on">MMPs↓</a>, <a href="tbResList.php?qv=47&tsv=201&wNotes=on">MMP2↓</a>, <a href="tbResList.php?qv=47&tsv=203&wNotes=on">MMP9↓</a>, <a href="tbResList.php?qv=47&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=47&tsv=214&wNotes=on">NF-κB↓</a>, <a href="tbResList.php?qv=47&tsv=79&wNotes=on">CXCR4↓</a>, <a href="tbResList.php?qv=47&tsv=105&wNotes=on">ERK↓</a> <br> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?qv=47&tsv=322&wNotes=on">TumCCA↑</a>, <a href="tbResList.php?qv=47&tsv=73&wNotes=on">cyclin D1↓</a>, <a href="tbResList.php?qv=47&tsv=378&wNotes=on">cyclin E↓</a>, <a href="tbResList.php?qv=47&tsv=467&wNotes=on">CDK2↓</a>, <a href="tbResList.php?qv=47&tsv=894&wNotes=on">CDK4↓</a>, <a href="tbResList.php?qv=47&tsv=895&wNotes=on">CDK6↓</a>, <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?qv=47&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?qv=47&tsv=324&wNotes=on">TumCI↓</a>, <a href="tbResList.php?qv=47&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=47&tsv=1117&wNotes=on">TOP1↓</a>, <br> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - inhibits <a href="tbResList.php?qv=47&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=47&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=47&wNotes=on&word=NOTCH">Notch↓</a>, <a href="tbResList.php?qv=47&tsv=361&wNotes=on">PDGF↓</a>, <br> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=47&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=47&tsv=4&wNotes=on">AKT↓</a>, <a href="tbResList.php?qv=47&wNotes=on&word=STAT">STAT↓</a>, <a href="tbResList.php?qv=47&tsv=377&wNotes=on">Wnt↓</a>, <a href="tbResList.php?qv=47&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=47&tsv=9&wNotes=on">AMPK↓</a>, <a href="tbResList.php?qv=47&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=47&tsv=168&wNotes=on">JNK</a>, <br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=47&tsv=1106&wNotes=on">chemo-sensitization</a>, <a href="tbResList.php?qv=47&tsv=1171&wNotes=on">chemoProtective</a>, <a href="tbResList.php?qv=47&tsv=1185&wNotes=on">RadioProtective</a>, <a href="tbResList.php?qv=47&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <a href="tbResList.php?qv=47&tsv=1105&wNotes=on">Neuroprotective</a>, <a href="tbResList.php?qv=47&tsv=557&wNotes=on">Cognitive</a>, <a href="tbResList.php?qv=47&tsv=1179&wNotes=on">Hepatoprotective</a>, <br> <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=47&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br>
216
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BML
Bromelain
NP
<b>Bromelain</b> is a mixture of enzymes found in pineapples, particularly in the stem and fruit. key points regarding bromelain and cancer:<br> -Anti-Inflammatory Properties: <br> -Immune System Support: <br> -Direct Anticancer Effects: <br> -Synergistic Effects with Chemotherapy:<br> <br> Biological activity, bromelain has been reported to exhibit a range of effects, including:<br> Anti-inflammatory activity: 10-50 μM<br> Antioxidant activity: 10-100 μM<br> Anti-cancer activity: 50-100 μM<br> Cardiovascular health: 20-50 μM<br> Digestive health: 10-50 μM<br> <br> Approximate μM concentrations of bromelain, the active compound in pineapples, that can be achieved with different amounts of pineapple:<br> 1 cup of fresh pineapple chunks (165g): approximately 10-50 μM of bromelain<br> 1 cup of pineapple juice (240ml): approximately 5-20 μM of bromelain<br> 1 tablespoon of pineapple extract (15g): approximately 20-100 μM of bromelain<br> 1 teaspoon of bromelain powder (5g): approximately 50-200 μM of bromelain<br> <br> Cooking can affect the concentration of bromelain in pineapple. Heat can denature the enzymes, making them less active. The extent of the loss of activity depends on the temperature, cooking time, and method of cooking. For example:<br> -Boiling or steaming pineapple for 10-15 minutes can reduce the bromelain activity by 50-70%<br> -Baking or roasting pineapple at 350°F (30-40min) reduce the bromelain activity by 70-90%<br>
48
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BJ
Brucea javanica
NP
<b>Brucea javanica</b> is a plant in the family Simaroubaceae.<br> <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC8971814/"> "Brucea javanica (Ya-dan-zi in Chinese)</a> is a well-known Chinese herbal medicine, which is traditionally used in Chinese medicine for the treatment of intestinal inflammation, diarrhea, malaria, and cancer. The formulation of the oil (Brucea javanica oil) has been widely used to treat various types of cancer." <br> Pathways:<br> -Induce mitochondrial dysfunction leading to cytochrome c release and subsequent activation of caspases.<br> -Inhibit Akt phosphorylation/activity<br> -Inhibit NF-κB activation<br> -Inhibition of STAT3 phosphorylation <br> -Cell cycle at specific checkpoints (e.g., G0/G1 or G2/M)<br> -Elevating intracellular ROS<br>
270
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Brut
Bruteridin
NP
<b>Bruteridin</b> is a lesser-known phytochemical that has been isolated from certain plant sources. Like other natural compounds with polyphenolic characteristics, bruteridin is of interest because of its potential antioxidant and anti-inflammatory activities. However, due to the limited body of research, its specific role as an anticancer agent remains largely underexplored.<br> Typically associated with natural cardenolide mixtures from specific cardenolide-producing plants (e.g., species in the Digitalis or Adonis genera) and possibly from amphibian secretions.<br> <br> -Antioxidant Activity<br> -Anti-inflammatory Effects<br> -Changes in histone acetylation status and chromatin remodeling can lead to altered gene expression profiles that favor tumor suppression.<br> -Na+/K+-ATPase Inhibition<br> -interfere with the PI3K/Akt/mTOR signaling cascade<br> -linked to the generation of ROS within cells<br> -Cell Cycle Arrest<br> -Inhibition of NF-κB Signaling<br> -alter the MAPK/ERK signaling cascade<br>
49
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BF
Bufalin
NP
<b>Bufalin</b> is a component from Chinese toad venom. Bufalin is classified as a cardiac glycoside, specifically a type of bufadienolide.<br> <br> Pathways:<br> -release of cytochrome c and subsequent activation of caspases<br> -enhance the expression of death receptors<br> -inhibit the PI3K/Akt/mTOR<br> -modulate the MAPK/ERK pathway<br> -inhibit NF-κB signaling<br> -induce cell cycle arrest at different checkpoints (commonly G0/G1 or G2/M)<br> -elevate intracellular ROS levels<br> -interfere with the Wnt/β-catenin signaling pathway<br> -modulate autophagy, a process that can either promote cell survival or lead to cell death <br> -Stabilization or activation of p53 <br>
50
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BA
Butyrate
NP
<b>Butyrate</b> is a four-carbon, short-chain fatty acid (SCFA) produced during dietary fiber fermentation by microbes in the lower digestive tract.<br> Butyrate, a short‐chain fatty acid primarily produced by the gut microbiota through the fermentation of dietary fibers.<br> <br> Pathways:<br> -Histone Deacetylase (HDAC) Inhibition<br> -Modulation of Wnt/β-Catenin Signaling<br> -induce cell cycle arrest.<br> -G-Protein-Coupled Receptors (GPCRs) Activation<br> -inhibition of NF-κB<br> -activate AMPK<br> -promoting regulatory T-cell (Treg) differentiation<br>
51
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CA
Caffeic acid
NP
<b>Caffeic acid</b> is a polyphenol antioxidant found in coffee, fruits, vegetables, and herbs. It may have anti-inflammatory, anticancer, anti-aging, and other health benefits.<br> <br> -Caffeic acid phenethyl ester, the main representative component of propolis<br> -Black chokeberry 141.14 mg/100 g F<br> -Sunflower seed, meal 8.17 mg/100 g FW<br> -Common sage, dried 26.40 mg/100 g FW<br> -Ceylan cinnamon 24.20 mg/100 g FW<br> -Nutmeg 16.30 mg/100 g FW<br> <br> -Dual capacity of CA to act as an antioxidant during carcinogenesis and as a pro-oxidant against cancer cells, promoting their apoptosis or sensitizing them to chemotherapeutic drugs.<br> <br> Pathways:<br> -Caffeic acid is a potent antioxidant<br> -Caffeic acid may also exhibit pro-oxidant behavior. At higher concentrations( 50–100 µM ?) or/and in the presence of transition metal ions (such as copper or iron), caffeic acid cab participate in Fenton-like reactions, potentially leading to increased ROS generation.<br> -Shown to inhibit NF-κB activation<br> -Inhibitory effects on MAPK/ERK Pathway<br> -PI3K/Akt Signaling Pathway<br> -Activation of the Nrf2/ARE pathway <br> -Cell cycle arrest at various checkpoints<br> -Angiogenesis Inhibition<br> <br> Caffeic acid typically shows low oral bioavailability (sometimes only a few percent of the ingested dose is systemically available) and a short plasma half-life (around 1–2 hours in animal models).<br>
52
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Caff
Caffeine
NP
<b>Caffeine</b> is a natural chemical with stimulant effects. It is found in coffee, tea, cola, cocoa, guarana, yerba mate, and over 60 other products.<br> Natural stimulant<br> <br> -Caffeine appears to interact with several pathways relevant to cancer biology—including adenosine receptor signaling, DNA damage response, cell cycle regulation, apoptosis, PI3K/Akt/mTOR, and NF-κB <br> —Its overall impact likely depends on the cancer type, stage, microenvironment, and the dosage administered<br>
244
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Calc
Calcium
NP
<b>Calcium</b>
284
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CRMs
Calorie Restriction Mimetics
NP
<b>Caloric restriction mimetics (CRMs)</b><br> <br> Examples of the most studied CRM and their anti-cancer effects include metformin, rapamycin, aspirin, and resveratrol and its by-products.<br>
204
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CPT
Camptothecin
NP
<b>Camptothecin (CPT)</b> and its derivatives function as inhibitors of topoisomerase and as potent anticancer agents against a variety of cancers. <br> Camptothecin is a cytotoxic quinoline alkaloid that is isolated from the bark and fruit of the Camptotheca acuminata tree, native to China. It is a topoisomerase I inhibitor, which means it blocks the enzyme topoisomerase I, an essential enzyme in DNA replication.<br> Camptothecin derivatives, such as irinotecan and topotecan, have been approved for the treatment of various types of cancer, including colorectal, ovarian, and small cell lung cancer. These derivatives have improved solubility and stability compared to camptothecin, making them more suitable for clinical use.<br>
53
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CBC
Cannabichromene
NP
<b>Cannabichromene (CBC)</b> is a phytocannabinoid found in the Cannabis plant. It has anti-inflammatory, antitumor and anticonvulsant properties, and may affect THC psychoactivity.<br>
54
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CBD
Cannabidiol
NP
<b>Cannabidiol (CBD)</b> is a cannabinoid compound found in cannabis plants.<br> Cannabidiol (CBD) is a non-psychoactive phytocannabinoid derived from Cannabis sativa that has drawn interest for its potential anticancer properties. <br> Pathways:<br> -Mitochondrial dysfunction, with loss of membrane potential leading to the release of cytochrome c and activation of caspase cascades<br> -Receptor-Mediated Signaling (CB Receptors and Beyond)<br> -Can increase reactive oxygen species (ROS)<br> -Can induce ER stress, which activates the unfolded protein response.<br> -Suppress key survival and proliferation signaling cascades such as the PI3K/Akt/mTOR pathway.<br> -Impair angiogenesis<br>
258
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CBDA
cannabidiolic acid
NP
<b>Cannabidiolic acid (CBDA)</b> is the acidic precursor of cannabidiol (CBD) found in Cannabis sativa.<br> - Note that although CBDA shares some pharmacological properties with CBD, its profile can differ due to its carboxylic acid group, which may affect its bioavailability, receptor binding, and overall cellular uptake. <br> <br> Cannabidiolic acid (CBDA) shows promise in modulating several pathways that are relevant to cancer biology—including COX-2 inhibition, PPARγ activation, apoptosis induction, and anti-inflammatory effects. In parallel, CBDA may offer additional benefits such as anti-emetic, anxiolytic, and potential neuroprotective effects. However, the current body of research is largely preclinical. CBDA is often found in raw cannabis plants and does not undergo decarboxylation like its more well-known counterpart cannabidiol (CBD).<br> Unlike the tetrahydrocannabinol (THC) found in cannabis, CBDA is non-psychoactive. This means it does not cause the "high" or altered state of mind commonly associated with cannabis use.<br> CBDA does not directly bind to the primary cannabinoid receptors (CB1 and CB2) in the brain that are responsible for psychoactive effects.<br> <br> Pathways:<br> -CBDA may modulate receptors beyond the classical CB1 and CB2, such as transient receptor potential (TRP) channels (e.g., TRPV1) and possibly the orphan receptor GPR55, thereby influencing cell signaling, calcium homeostasis, and related pathways.<br> -Inhibition of cyclooxygenase enzymes (COX)<br> -Mitochondrial dysfunction and the activation of caspases<br> -Modulation of the PI3K/Akt Pathway<br> -Affect the MAPK family of pathways, including ERK, JNK, and p38 kinases<br> -Modulating matrix metalloproteinases (MMPs)<br> -As an antioxidant (or under some conditions a pro-oxidant)<br>
328
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capec
capecitabine
D
<b>Capecitabine</b> is an oral chemotherapy medication used primarily in the treatment of various cancers.<br> Capecitabine is an antimetabolite chemotherapeutic agent. It's classified as a prodrug, meaning it is metabolized in the body to its active form, 5-fluorouracil (5-FU).<br> <br> Once ingested, capecitabine is absorbed and converted through a series of enzymatic reactions into 5-FU. 5-FU then interferes with DNA synthesis and RNA processing by inhibiting enzymes like thymidylate synthase. This disruption of nucleotide production hinders rapid cell division, making it effective against cancer cells that multiply quickly.<br> <br> One of the advantages of capecitabine is that it is taken by mouth in tablet form, as opposed to intravenous administration, which can be more convenient for patients<br>
55
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CAP
Capsaicin
NP
<b>Capsaicin </b>is a chemical compound that gives chili peppers their spicy flavor and heat.<br> <br> Biological activity, capsaicin has been reported to exhibit a range of effects, including:<br> Pain relief: 10-50 μM<br> Anti-inflammatory activity: 20-50 μM<br> Antioxidant activity: 10-100 μM<br> Anti-cancer activity: 50-100 μM<br> Cardiovascular health: 20-50 μM<br> <br> Approximate μM concentrations of capsaicin, the active compound in chili peppers, that can be achieved with different amounts of chili peppers:<br> 1 teaspoon of dried chili pepper flakes (5g):~10-50 μM of capsaicin<br> 1 tablespoon of dried chili pepper flakes (15g): ~30-150 μM of capsaicin<br> 1 cup of fresh chili peppers (100g): ~100-500 μM of capsaicin<br> 1 teaspoon of chili pepper extract (5g): ~100-500 μM of capsaicin<br> 1 tablespoon of chili pepper extract (15g): ~300-1500 μM of capsaicin<br> <br> Approximate μM concentrations of capsaicin in various foods that contain capsaicin:<br> Jalapeño peppers: 1 pepper (20g): ~20-100 μM of capsaicin 2–8 mg/100g of fresh Jalapeño <br> Serrano peppers: 1 pepper (10g): ~10-50 μM of capsaicin 5–15 mg/100g<br> Cayenne peppers: 1 pepper (10g): ~50-200 μM of capsaicin<br> Habanero peppers: 1 pepper (20g): ~100-500 μM of capsaicin 15–30 mg/100g<br> Ghost peppers: 1 pepper (20g): ~200-1000 μM of capsaicin<br> Hot sauce: 1 teaspoon (5g): ~10-50 μM of capsaicin<br> Chili flakes: 1 teaspoon (5g): ~10-50 μM of capsaicin<br> Spicy sauces and marinades: 1 tablespoon (15g): ~10-50 μM of capsaicin<br> <br> Cayenne Pepper Powder – Approximate capsaicin content: roughly 5–20 mg/g (15-30g human for 100uM?) <br> <br> -IC50 in Cancer Cell Lines: Approximately 50–300 µM (consume 150mg of capsaican not possible?)<br> -IC50 in Normal Cell Lines: Generally higher—often 2–3 times greater <br> <br> Pathways:<br> -disrupting mitochondrial membrane potential, leading to cytochrome c release and subsequent activation of caspases<br> -Activation of TRPV1: resulting in increased intracellular calcium levels<br> -capsaicin can lead to increased production of ROS within cancer cells<br> -Inhibition of NF-κB<br> -Inhibit PI3K/AKT/mTOR signaling<br> -STAT3 Inhibition<br> -Cell Cycle Arrest<br> -reduce the expression of vascular endothelial growth factor (VEGF)<br> -COX-2<br>
265
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carbop
carboplatin
D
<b>Carboplatin</b> is a platinum-based chemotherapy drug, structurally related to cisplatin.<br> Advantages Over Cisplatin:<br> • Compared to cisplatin, carboplatin is associated with a more favorable side-effect profile, particularly with regard to reduced nephrotoxicity (renal toxicity).<br> • However, it may still cause bone marrow suppression, so careful monitoring of blood counts is essential.<br> <br> Carboplatin is a key platinum-based chemotherapy agent that interferes with cancer cell DNA, leading to cell death. Its relatively favorable toxicity profile, compared to cisplatin, makes it a popular choice for treating a variety of solid tumors such as ovarian, lung, head and neck, bladder, and certain cases of testicular cancers. Due to its side-effect profile, particularly bone marrow suppression, patients receiving carboplatin require careful monitoring and dosage adjustments based on their renal function and other clinical factors.<br>
56
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CA
Carnosic acid
NP
<b>Carnosic acid (CA)</b> natural antioxidant diterpene found in rosemary and sage. <br> <br> Pathways:<br> -Inhibit the PI3K/Akt pathway, which is typically overactivated in many cancers.<br> -inhibits ERK activation, reducing cell proliferation.<br> -JNK and p38 MAPK: Activation of these kinases by carnosic acid may contribute to stress responses leading to cell cycle arrest or apoptosis.<br> -Block the activation of NF-κB,<br> -Induce apoptosis by disturbing mitochondrial membrane potential, leading to the release of cytochrome c and activation of caspases.<br> -Dual role: as an antioxidant under normal conditions and, in the context of cancer cells, it can induce ROS production beyond a critical threshold.<br> -Interfere with STAT3 activation, <br> -AMPK Activation<br> -Inhibition of Angiogenesis and Metastasis<br> -Induction of endoplasmic reticulum (ER) stress<br> <br> -At lower concentrations, carnosic acid might exhibit antioxidant activity, protecting cells by scavenging free radicals. However, cancer cells often have altered redox balances which can make them more vulnerable to further ROS increases.<br> -While carnosic acid has antioxidant properties in some contexts, it is typically observed to have a prooxidant effect in cancer cells under specific conditions, particularly at concentrations that favor ROS accumulation and the subsequent induction of apoptotic cell death<br> <br> -10-100uM, or 10–100 mg/kg for achieving anticancer effects.<br> -Typically available in standardized rosemary extracts.<br>
57
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CAR
Carvacrol
NP
<b>Carvacrol</b> monoterpenoid phenol with odor of oregano. Found in essential oils and plants, has antimicorbial and antioxidant properties.<br>
221
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Cats
Cat’s Claw
NP
<b>Cat’s Claw (Uncaria tomentosa)</b> – Known for its immune-boosting properties.<br> Dose: Tea 1-2g, 1-3x/d. Extract 250-500mg/d <br>
228
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Catechins
Catechins
NP
<b>Catechins</b> belong to the category of flavanols, which have two isomeric forms, a positive (+) form and a negative (−) form (epicatechin). The (+)-catechins have antioxidative properties, whereas the (−)-epicatechins act as pro-oxidants inducing oxidative effects.<br> (−)-epicatechins Examples: EGCG, EGC, GCG GC ECTG, EC (all found in green tea, and maybe dark chocolate)<br>
317
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Cela
Celastrol
NP
<b>Celastrol</b>—a bioactive compound extracted from traditional Chinese medicinal plants such as Tripterygium wilfordii (Thunder God Vine).<br> <br> Pathways:<br> -inhibit NF-κB activation<br> -disrupt the function of chaperone proteins like HSP90 and HSP70, which are often overexpressed in cancer cells<br> -attenuate Akt phosphorylation and downstream mTOR signaling<br> -modulate components of the MAPK pathway, including ERK, JNK, and p38.<br> -increase intracellular ROS levels in cancer cells<br> -inhibiting STAT3<br>
4
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CEL
Celecoxib
D
NSAID
<b>Celecoxib</b> inhibits the formation of prostaglandins: used primarily to treat pain and other symptoms of osteoarthritis, rheumatoid arthritis, joint and musculoskeletal conditions.<br>
5
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CET
cetuximab
D
antineoplastic drug
<b>Cetuximab</b> a genetically engineered monoclonal antibody (IV): inhibit tumor growth for colorectal cancer, head and neck cancer. <br> Cardiopulmonary arrest side effect. <br>
280
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CDT
chemodynamic therapy
T
<b>Chemodynamic therapy (CDT)</b> is an emerging cancer treatment strategy that leverages the unique tumor microenvironment to generate toxic reactive oxygen species (ROS) in situ. Unlike conventional chemotherapy, which often has systemic toxicity, CDT aims to induce localized cell death through chemical reactions that occur preferentially within tumors.<br> <br> How Chemodynamic Therapy Works<br> 1.Tumor Microenvironment Exploitation:<br> Tumors often exhibit a higher concentration of hydrogen peroxide (H₂O₂), an acidic environment, and elevated levels of certain metal ions (e.g., Fe²⁺). CDT exploits these characteristics to trigger chemical reactions selectively within the tumor.<br> <br> 2.Fenton and Fenton-like Reactions:<br> At the heart of CDT is the Fenton reaction, where transition metal ions (typically iron) catalyze the decomposition of H₂O₂ to generate hydroxyl radicals (•OH). These radicals are highly reactive and induce oxidative damage to cellular components like lipids, proteins, and DNA. The basic Fenton reaction:<br> Fe²⁺ + H₂O₂ → Fe³⁺ + •OH + OH⁻<br> <br> 3.Minimizing Systemic Toxicity:<br> Because the reaction heavily depends on the tumor’s specific conditions (e.g., acidic pH and high H₂O₂ levels), CDT can achieve a localized therapeutic effect with reduced harm to healthy tissues.<br> <br> 4.Nanomaterials as Catalysts:<br> Often, CDT is facilitated by nanoparticle catalysts (e.g., iron oxide, copper-based, or other metal-based nanoparticles) that can be engineered to accumulate in tumor tissues. These nanomaterials not only provide a catalytic surface but can also be modified for improved tumor targeting and controlled release.<br> <br> Chemodynamic therapy provides a promising approach for cancer treatment by using the tumor’s inherent properties—like high H₂O₂ and acidic pH—to catalyze ROS generation via Fenton reactions. By targeting pathways related to oxidative stress, iron metabolism, redox balance, and cell survival signaling, CDT aims to selectively induce cancer cell death while reducing collateral damage to normal tissues.<br> <br> Target Pathways in Chemodynamic Therapy<br> Oxidative Stress Pathways:ROS Generation, Mitochondrial Dysfunction, MMP, DNA Damage<br> Iron Homeostasis and Metabolism: Fenton Reaction Catalysis: The availability of Fe²⁺ is crucial for the Fenton reaction, making the iron uptake pathways a critical target.<br> MAPK/ERK Pathway, PI3K/Akt Pathway: increased ROS can inhibit pro-survival pathways like PI3K/Akt, tipping the balance towards cell death.<br> Glutathione (GSH) Depletion: <br> Nrf2 Pathway Inhibition: Inhibiting Nrf2 can make cancer cells more susceptible to ROS.<br> Acidic Tumor Microenvironment: Many nanomaterials used in CDT are designed to be activated in acidic conditions, ensuring that the Fenton reaction proceeds efficiently within the tumor milieu.<br> Autophagic: Increased ROS levels can also affect autophagy—a cellular “self-eating” process<br>
233
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Chemo
Chemotherapy
D
treatment category
<b>Chemotherapy</b> is a treatment approach that uses drugs to target and kill rapidly dividing cells, primarily cancer cells. However, because many normal cells also divide quickly (such as those in the bone marrow, digestive tract, and hair follicles), chemotherapy can also affect these cells, leading to a range of side effects. <br> <br> Main Classes of Chemotherapy Agents and Examples<br> Alkylating Agents:<br> -work by adding alkyl groups to DNA, which interferes with the DNA’s structure and prevents replication.<br> Examples: Cyclophosphamide, Ifosfamide, Melphalan, Chlorambucil, Busulfan.<br> <br> Anti-metabolites:<br> -interfere with DNA and RNA synthesis by substituting for the normal building blocks of nucleic acids.<br> Examples: Methotrexate, 5-Fluorouracil (5-FU), Cytarabine, Gemcitabine, 6-Mercaptopurine.<br> <br> Anti-microtubule Agents:<br> -interfere with the structures that separate chromosomes during cell division (mitosis). Examples: Paclitaxel, Docetaxel, Vincristine, Vinblastine.<br> <br> Topoisomerase Inhibitors:<br> -target the enzymes topoisomerase I and II, which control the changes in DNA structure required for replication.<br> Examples: Etoposide (topoisomerase II inhibitor), Irinotecan (topoisomerase I inhibitor), Topotecan. <br> <br> Cytotoxic Antibiotics:<br> -intercalate into DNA, inhibiting the replication of cancer cells.<br> Examples: Doxorubicin, Daunorubicin, Bleomycin, Mitoxantrone.<br> <br> Platinum-Based Agents:<br> -contain platinum and cause cross-linking of DNA, which interferes with DNA repair and replication. Examples: Cisplatin, Carboplatin, Oxaliplatin.<br> <br> Many chemotherapy agents exert their effects, at least in part, by inducing oxidative stress in cancer cells. They can increase ROS levels through several mechanisms:<br> -Direct generation of free radicals.<br> -Disruption of mitochondrial function, leading to increased production of ROS.<br> -Interference with the cell’s antioxidant systems.<br> <br> -May want to avoid antioxidants 7 days bef<br>ore and 7 days after chemo.<br> Examples: NAC, Glutathione, Alpha Lipoic Acid, Vitamin E<br> -anti-oxidants known to have pro-oxidant effects (like Quercetin, Curcumin, etc.) should not be taken 2-3 days before and after chemo<br> -pro-oxidants known to bring good benefit to chemo can be continued during chemo. Examples are: Omega 3, Aremisia Annua, Silver NanoParticles.<br>
210
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Chit
chitosan
NP
<b>Chitosan</b> is a naturally occurring polysaccharide derived from the exoskeletons of crustaceans, such as crabs and shrimp.<br> Chitosan has been shown to inhibit the growth of various types of cancer cells, including breast, lung, and colon cancer cells.<br> Chitosan has been shown to inhibit angiogenesis, stimulate the immune system, and anti-inflammatory.<br>
59
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CGA
Chlorogenic acid
NP
<b>Chlorogenic acid (CGA)</b> is a polyphenol compound found in various plant-based foods, such as green coffee beans, apples, and pears.<br> May lower blood pressure, blood sugar, and weight. May improve mood and cognitive function. Chlorogenic acid (CGA), one of the most abundant polyphenols in the human diet, has been reported to inhibit cancer cell growth.<br> • Inhibiting the growth of cancer cells: CGA has been shown to inhibit the growth of cancer cells in vitro and in vivo, including breast, colon, and prostate cancer cells.<br> • Inducing apoptosis: CGA has been found to induce apoptosis (cell death) in cancer cells, which can help prevent the spread of cancer.<br> • Reducing inflammation: CGA has anti-inflammatory properties, which can help reduce the risk of cancer by reducing chronic inflammation.<br> • Antioxidant activity: CGA has antioxidant properties, which can help protect cells from damage caused by free radicals.<br>
218
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CHL
Chlorophyllin
NP
<b>Chlorophyllin</b> is a semi-synthetic derivative of chlorophyll, the green pigment found in plants that is essential for photosynthesis.<br> -Antioxidant Activity<br> -Detoxification<br> -Inhibition of Tumor Growth(unknown pathway?)<br> -Modulation of Gene Expression<br> -Anti-inflammatory Effects<br> Dose: 100-300mg/d split 1-3x/d<br>
60
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CHOC
Chocolate
NP
<b>Chocolate</b> made from roasted and ground cocoa beans.
61
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CHr
Chrysin
NP
<b>Chrysin</b> is found in passion flower and honey. It is a flavonoid.<br> -To reach plasma levels that might more closely match the concentrations used in in vitro studies (typically micromolar), considerably high doses or advanced delivery mechanisms would be necessary.<br> <br> -Note <a href="tbResList.php?qv=61&tsv=1109&wNotes=on&exSp=open">half-life</a> 2 hrs, <a href="tbResList.php?qv=61&tsv=792&wNotes=on&exSp=open">BioAv</a> very poor <br> Pathways:<br> <a href="https://cancerci.biomedcentral.com/articles/10.1186/s12935-021-01906-y/figures/3">Graphical Pathways</a><br> <br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - induce <a href="tbResList.php?qv=61&tsv=275&wNotes=on">ROS</a> production<br> - ROS↑ related: <a href="tbResList.php?qv=61&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?qv=61&tsv=103&wNotes=on">ER Stress↑</a>, <a href="tbResList.php?qv=61&tsv=459&wNotes=on">UPR↑</a>, <a href="tbResList.php?qv=61&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=61&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>, <a href="tbResList.php?qv=61&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?qv=61&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?qv=61&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?qv=61&tsv=239&wNotes=on">cl-PARP↑</a>, <a href="tbResList.php?qv=61&wNotes=on&word=HSP">HSP↓</a> <br> <!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, --> - Lowers AntiOxidant defense in Cancer Cells: <a href="tbResList.php?qv=61&tsv=226&wNotes=on&word=NRF2↓">NRF2↓</a>, <a href="tbResList.php?qv=61&tsv=137&wNotes=on&word=GSH↓">GSH↓</a> <a href="tbResList.php?qv=61&tsv=597&wNotes=on">HO1↓</a> <br> - Raises <a href="tbResList.php?qv=61&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?qv=61&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>, <a href="tbResList.php?qv=61&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?qv=61&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?qv=61&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?qv=61&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?qv=61&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?qv=61&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?qv=61&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, Pro-Inflammatory Cytokines : <a href="tbResList.php?qv=61&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, <a href="tbResList.php?qv=61&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?qv=61&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓ inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.--> - inhibit Growth/Metastases : <a href="tbResList.php?qv=61&tsv=604&wNotes=on">TumMeta↓</a>, <a href="tbResList.php?qv=61&tsv=323&wNotes=on">TumCG↓</a>, <a href="tbResList.php?qv=61&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=61&tsv=201&wNotes=on">MMP2↓</a>, <a href="tbResList.php?qv=61&tsv=203&wNotes=on">MMP9↓</a>, <a href="tbResList.php?qv=61&tsv=308&wNotes=on">TIMP2</a>, <a href="tbResList.php?qv=61&tsv=428&wNotes=on">uPA↓</a>, <a href="tbResList.php?qv=61&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=61&tsv=1284&wNotes=on">ROCK1↓</a>, <a href="tbResList.php?qv=61&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?qv=61&tsv=273&wNotes=on">RhoA↓</a>, <a href="tbResList.php?qv=61&tsv=214&wNotes=on">NF-κB↓</a>, <a href="tbResList.php?qv=61&tsv=105&wNotes=on">ERK↓</a> <br> <!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, --> - reactivate genes thereby inhibiting cancer cell growth : <a href="tbResList.php?qv=61&tsv=140&wNotes=on">HDAC↓</a>, <a href="tbResList.php?qv=61&tsv=236&wNotes=on">P53↑</a>, <a href="tbResList.php?qv=61&wNotes=on&word=HSP">HSP↓</a>, <br> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?qv=61&tsv=322&wNotes=on">TumCCA↑</a>, <a href="tbResList.php?qv=61&tsv=73&wNotes=on">cyclin D1↓</a>, <a href="tbResList.php?qv=61&tsv=467&wNotes=on">CDK2↓</a>, <a href="tbResList.php?qv=61&tsv=894&wNotes=on">CDK4↓</a>, <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?qv=61&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?qv=61&tsv=324&wNotes=on">TumCI↓</a>, <a href="tbResList.php?qv=61&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?qv=61&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=61&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=61&tsv=1117&wNotes=on">TOP1↓</a>, <a href="tbResList.php?qv=61&tsv=657&wNotes=on">TET1↓</a>, <br> <!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS --> - inhibits <a href="tbResList.php?qv=61&tsv=129&wNotes=on">glycolysis</a> and <a href="tbResList.php?qv=61&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> : <a href="tbResList.php?qv=61&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=61&tsv=35&wNotes=on">cMyc↓</a>, <a href="tbResList.php?qv=61&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>, <a href="tbResList.php?qv=61&tsv=906&wNotes=on">LDH↓</a>, <a href="tbResList.php?qv=61&tsv=773&wNotes=on">HK2↓</a>, <a href="tbResList.php?qv=61&wNotes=on&word=PDK">PDKs↓</a>, <a href="tbResList.php?qv=61&tsv=773&wNotes=on">HK2↓</a>, <a href="tbResList.php?qv=61&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=61&tsv=623&wNotes=on">GlucoseCon↓</a> <br> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - inhibits <a href="tbResList.php?qv=61&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=61&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=61&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=61&wNotes=on&word=NOTCH">Notch↓</a>, <a href="tbResList.php?qv=61&tsv=361&wNotes=on">PDGF↓</a>, <a href="tbResList.php?qv=61&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, <br> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=61&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=61&tsv=4&wNotes=on">AKT↓</a>, <a href="tbResList.php?qv=61&wNotes=on&word=STAT">STAT↓</a>, <a href="tbResList.php?qv=61&tsv=377&wNotes=on">Wnt↓</a>, <a href="tbResList.php?qv=61&tsv=9&wNotes=on">AMPK↓</a>, <a href="tbResList.php?qv=61&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=61&tsv=168&wNotes=on">JNK</a>, <a href="tbResList.php?qv=61&tsv=825&wNotes=on">TrxR</a>, <br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=61&tsv=1106&wNotes=on">chemo-sensitization</a>, <a href="tbResList.php?qv=61&tsv=1171&wNotes=on">chemoProtective</a>, <a href="tbResList.php?qv=61&tsv=1107&wNotes=on">RadioSensitizer</a>, <a href="tbResList.php?qv=61&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <a href="tbResList.php?qv=61&tsv=1105&wNotes=on">Neuroprotective</a>, <a href="tbResList.php?qv=61&tsv=557&wNotes=on">Cognitive</a>, <a href="tbResList.php?qv=61&tsv=1175&wNotes=on">Renoprotection</a>, <a href="tbResList.php?qv=61&tsv=1179&wNotes=on">Hepatoprotective</a>, <a href="tbResList.php?&qv=61&tsv=1188&wNotes=on">CardioProtective</a>, <br> <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=61&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br>
62
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Cin
Cinnamon
NP
<b>Cinnamon</b> is a spice from inner bark from several tree species.<br> <br> Biological activity, cinnamaldehyde from Ceylon cinnamon:<br> Antimicrobial activity: 10-50 μM<br> Antioxidant activity: 10-100 μM<br> Anti-inflammatory activity: 20-50 μM<br> Anticancer activity: 50-100 μM<br> Cardiovascular health: 20-50 μM<br> <br> 5 g of Ceylon cinnamon might contain roughly between 30 mg and 150 mg of cinnamaldehyde, with an approximate mid-range estimate of about 70 mg.<br> Assuming a moderate supplemental intake 50–200 mg of cinnamaldehyde, peak plasma levels might be anticipated in the vicinity of 1–10 μM.<br>
197
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Cisplatin
Cisplatin
D
<b>Cisplatin</b> is a chemotherapy medication used to treat various types of cancer. It is a platinum-based drug that works by interfering with the DNA of cancer cells, preventing them from reproducing and ultimately leading to cell death.<br>
211
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Citrate
Citric Acid
NP
<b>Citric acid</b> is the acid form, and citrate is the salt or conjugate base form. The two terms are often used interchangeably in casual conversation, but chemically they refer to different states depending on the pH of the environment.<br> Citrate is a naturally occurring compound found in various forms in nature. It is a conjugate base of citric acid, a weak organic acid that is commonly found in citrus fruits, such as lemons and oranges.<br> Citrate plays a crucial role in the production of energy in cells. It is a key intermediate in the citric acid cycle (also known as the Krebs cycle or tricarboxylic acid cycle), which is a series of chemical reactions that occur in the mitochondria of cells.<br> Naturally found in citrus fruits and many other plants.<br> Citric acid is a key metabolic intermediate in the tricarboxylic acid (TCA) cycle. <br> • Citric acid is central to cellular energy metabolism as part of the TCA cycle. Changes in its concentration can affect the flux through the cycle and the overall cellular redox state.<br> • Enhanced TCA activity may lead to increased production of reducing equivalents (NADH, FADH₂) and subsequent electron transport chain (ETC) activity. If the ETC becomes overloaded or dysfunctional, it can lead to electron leakage and increased ROS production.<br> • Although citric acid itself is not a classical antioxidant, it can act as a chelating agent for certain metal ions. By binding transition metals (such as iron and copper), citrate can potentially reduce metal-catalyzed ROS formation.<br> • This chelating property can indirectly protect cells from oxidative damage, especially under conditions where free metal ions might otherwise catalyze ROS-generating reactions.<br> -Crucial role of citrate to supply the acetyl-CoA pool for fatty acid synthesis and histone acetylation in tumors<br> <br> -Citrate is a major product of mitochondria, the engine of the cell.<br> -The more Citrate builds up in the cell, the more the cell will think it has enough of what it needs and will reduce or even shut down the glycolisis process.<br> Citrate is produced inside the mitochondria within the Krebs cycle. When the cell has excess energy, citrate is transported out of the mitochondrial matrix across the inner membrane via the mitochondrial citrate transport protein (CTP). In the cytoplasm, is then broken down by the ACLY (ACL) enzyme into<br> acetyl-CoA: for fatty acid synthesis and cholesterol production<br> oxaloacetate: to be converted back to pyruvate and enter mitochondria again<br> (might be desirable to inhibit ACYL with HCA) and maybe Statins.<br> -May also synergize with Metformin?<br> <br> Sodium citrate is the sodium salt of citric acid, used as a buffer and food additive, while citric acid is a weak organic acid, naturally found in citrus fruits.<br> Summary:<br> -Citrate is considered to play a crucial role in cancer metabolism by virtue of its production in the reverse Krebs cycle from glutamine<br> -Chelation of Ca2+ by sodium citrate resulted in inactivation of CAMKK2 and AMPK (inhibited the Ca2+/CAMKK2/AKT/mTOR signaling)<br> -”promoter of cell proliferation (at lower concentrations) and as an anticancer agent (at higher concentrations)”<br> -”ACLY, which has been found to be overexpressed in many cancers, converts citrate into acetyl-CoA and OAA.“<br> -”administration of citrate at high level mimics a strong inhibition of ACLY” (HCA is a known natural ACLY inhibitor)<br> -Citrate is a well-known physiological inhibitor of PFK1.<br> -Some reduction in Mcl-1 expression<br> -May low ROS by decreasing oxygen consumption (ie not compatible with proxidant treatment?)<br> -Deactivation of the NF-κB signaling ?<br> <br> -Lemons: 5–8% citric acid by weight<br> -Limes: 4–7% citric acid.<br> -Grapefruits: 2–5% in the juice<br> -Oranges (and Tangerines/Mandarins): 1–2% in the juice<br> Many commercially prepared beverages (like some soft drinks, citrus-based jams, and preserves) and sour candies have citric acid added as a flavoring agent or preservative. In these products, the citric acid concentration can sometimes be higher than that in the unprocessed fruit juice.<br> <br> Acid Reflux & Dental Health: Increasing citric acid, especially from highly concentrated sources (like pure citric acid or very sour juices), may exacerbate symptoms in individuals with acid reflux or cause enamel erosion on teeth. Drinking water after consuming citrus products or using a straw (when drinking acidic beverages) can help reduce the direct contact of acid with your teeth.<br> <br> • Low/Moderate Doses: In some models, low to moderate citrate supplementation can actually help cells maintain redox balance.<br> • High Doses: At higher concentrations, citrate can overload certain metabolic pathways. An excess supply of citrate may drive the TCA cycle at a rate that overwhelms the electron transport chain, potentially increasing the leakage of electrons and therefore raising ROS production. <br> • Cancer vs. Non-Cancer Cells: Cancer cells frequently have reprogrammed metabolism. In some cases, citrate supplementation in cancer cells can have different effects compared to healthy cells. For instance, due to the metabolic alterations in cancer cells, a high dose of citrate might exacerbate mitochondrial dysfunction, leading to higher ROS levels. Conversely, in a non-cancer context or cells with robust metabolic flexibility, the same dose might be better tolerated or even beneficial for redox balance.<br> <br> ROS:<br> Antioxidant Role:<br> • In some contexts, citrate can act as an antioxidant. It has the capacity to chelate metal ions (like iron and copper), which can catalyze ROS formation via reactions such as the Fenton reaction.<br> • Moreover, as a key intermediate in the tricarboxylic acid (TCA) cycle, citrate contributes to cellular energy metabolism, which, when properly balanced, may help maintain homeostasis and limit excessive ROS production.<br> Potential Pro-Oxidant Effects:<br> • At high doses or under certain conditions, an overload of citrate might alter normal cellular metabolic pathways. For example, excess citrate can affect mitochondrial function and the TCA cycle’s balance, potentially leading to metabolic disturbances that contribute to increased ROS formation in some in vitro models or under pathological conditions.<br> • In certain experimental settings, drastic changes in cellular intermediate concentrations can trigger compensatory mechanisms that might inadvertently lead to oxidative stress.<br> Context Matters:<br> • The net effect of high-dose citrate on ROS largely depends on the experimental model and the presence of additional factors (such as the concentration of available metal ions, the oxidative state of the cell, and the cell’s overall metabolic status).<br> • In a well-regulated physiological environment, moderate levels of citrate may support antioxidant defenses, whereas in stress or disease states, high doses might tip the balance toward increased ROS production.<br> -High doses of citric acid/citrate in cancer cells are generally associated with an increase in ROS due to metabolic and mitochondrial stress. However, because the effect is highly context-specific, the overall outcome may depend on multiple factors related to the cancer cell type and its existing metabolic state. (Note this statement might not be supported by research papers-but rather chat ai)<br> <br> <br> DoseCitric acid: 4g-30g/day. 4g-8g/day most common? split 3-4 times/day? with meals<br>
64
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Cu
Copper and Cu NanoParticlex
NP
<b>Copper</b><br> Metal<br> Copper levels are considerably elevated in various malignancies.<br> Copper [Cu(II)] is a transition and trace element in living organisms. It increases reactive oxygen species (ROS) and free-radical generation that might damage biomolecules like DNA, proteins, and lipids.<br> <br> - Copper acts as a critical cofactor for numerous enzymes involved in redox reactions, energy production, and connective tissue formation.<br> - Increased copper levels in the tumor microenvironment can enhance angiogenic signaling and thus supply the tumor with necessary oxygen and nutrients, facilitating tumor growth and metastasis.<br> - Copper can participate in redox cycling reactions, similar to the Fenton reaction, leading to the production of reactive oxygen species (ROS).<br> - Cancer cells often exhibit altered copper homeostasis, with some studies showing elevated copper levels in tumor tissues relative to normal tissues.<br> <br> Two main approaches are:<br> - Copper Chelation: Drugs that bind copper (chelators) can reduce the bioavailability of copper, potentially inhibiting angiogenesis and other copper-dependent tumor processes.<br> - Copper Ionophores: These agents facilitate the transport of copper into cancer cells to induce cytotoxicity by elevating intracellular copper levels beyond a tolerable threshold, leading to cell death.<br> <br> - Depletion of glutathione and stimulation of lipid peroxidation, catalase and superoxide dismutase.<br> - Studies have shown that the level of copper in tumour cells and blood serum from cancer patients is elevated, and the conclusion is that cancer cells need more copper than healthy cells. (but also sometimes depleted).<br> - Copper is a double-edged sword, maintaining normal cell development and promoting tumor development.<br> - Tumor tissue has a higher demand for copper and is more susceptible to copper homeostasis, copper may modulate cancer cell survival through reactive oxygen species (ROS) excessive accumulation, proteasome inhibition and anti-angiogenesis.<br>
249
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Croc
Crocetin
NP
<b>Crocetin</b> is a carotenoid pigment found in saffron (Crocus sativus) and has been studied for its potential anti-cancer properties. Research has shown that crocetin may have anti-tumor and anti-proliferative effects, inhibiting the growth of various types of cancer cells.<br> The mechanisms by which crocetin exerts its anti-cancer effects are not fully understood, but it is thought to involve:<br> <br> • Inhibition of cell proliferation and induction of apoptosis (cell death)<br> • Modulation of signaling pathways involved in cell growth and survival<br> • Antioxidant and anti-inflammatory effects<br> • Inhibition of angiogenesis (the formation of new blood vessels that feed cancer cells)<br> <br> Crocetin is a LDH inhibitor.<br>
195
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Cuc
Cucurbitacin
NP
<b>Cucurbitacin</b>, produced by some plants, especially Cucurbitaceae, as a defense against herbivores. Toxic compound that can form in plants in the gourd family (Zucchini, Squash).<br> Cucurbitacins have been shown to inhibit the growth of various cancer cell lines by interfering with cell cycle progression. Cucurbitacins can affect various signaling pathways involved in cancer progression, such as the NF-κB and STAT3 pathways, which are often dysregulated in cancer.<br>
65
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CUR
Curcumin
NP
<b>Curcumin</b> is the main active ingredient in Tumeric. Member of the ginger family.Curcumin is a polyphenol extracted from turmeric with anti-inflammatory and antioxidant properties.<br> - Has <a href="tbResList.php?qv=65&tsv=835&wNotes=on">iron-chelating</a>, iron-chelating properties. <a href="tbResList.php?qv=65&tsv=573&wNotes=on">Ferritin</a>. But still known to increase <a href="tbResList.php?qv=65&tsv=160&wNotes=on">Iron</a> in Cancer cells. <br> - <a href="tbResList.php?qv=65&tsv=137&wNotes=on&word=GSH↓">GSH</a> depletion in cancer cells, exhaustion of the antioxidant defense system. But still raises <a href="tbResList.php?qv=65&tsv=137&wNotes=on&word=GSH↑">GSH↑</a> in normal cells.<br> - Higher concentrations (5-10 μM) of curcumin induce autophagy and ROS production<br> - Inhibition of <a href="tbResList.php?qv=65&wNotes=on&word=Trx">TrxR</a>, shifting the enzyme from an antioxidant to a prooxidant<br> - Strong inhibitor of <a href="tbResList.php?qv=65&tsv=125&wNotes=on">Glo-I</a>, , causes depletion of cellular ATP and GSH<br> - Curcumin has been found to act as an activator of <a href="tbResList.php?qv=65&tsv=226&wNotes=on&word=NRF2↑">Nrf2</a>, (maybe bad in cancer cells?), hence could be combined with Nrf2 knockdown<br> <br> Clinical studies testing curcumin in cancer patients have used a range of dosages, often between 500 mg and 8 g per day; however, many studies note that doses on the lower end may not achieve sufficient plasma concentrations for a therapeutic anticancer effect in humans.<br> • Formulations designed to improve curcumin absorption (like curcumin combined with piperine, nanoparticle formulations, or liposomal curcumin) are often employed in clinical trials to enhance its bioavailability.<br> <br> -Note <a href="tbResList.php?qv=65&tsv=1109&wNotes=on&exSp=open">half-life</a> 6 hrs.<br> <a href="tbResList.php?qv=65&tsv=792&wNotes=on&exSp=open">BioAv</a> is poor, use piperine or other <a href="https://nestronics.ca/dbx/tbResList.php?qv=65&qv2=&tsv=1310&ssv=%25&esv=2&wNotes=on&exSp=open"> enhancers</a> <br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - induce <a href="tbResList.php?qv=65&tsv=275&wNotes=on">ROS</a> production at high concentration. Lowers ROS at lower concentrations<br> - ROS↑ related: <a href="tbResList.php?qv=65&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?qv=65&tsv=103&wNotes=on">ER Stress↑</a>, <a href="tbResList.php?qv=65&tsv=459&wNotes=on">UPR↑</a>, <a href="tbResList.php?qv=65&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=65&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?qv=65&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?qv=65&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?qv=65&tsv=239&wNotes=on">cl-PARP↑</a>, <a href="tbResList.php?qv=65&wNotes=on&word=HSP">HSP↓</a> <br> <!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, --> - Lowers AntiOxidant defense in Cancer Cells: <a href="tbResList.php?qv=65&tsv=137&wNotes=on&word=GSH↓">GSH↓</a> <a href="tbResList.php?qv=65&tsv=46&wNotes=on">Catalase↓</a> <a href="tbResList.php?qv=65&tsv=597&wNotes=on">HO1↓</a> <a href="tbResList.php?qv=65&wNotes=on&word=GPx">GPx↓</a> <br> but conversely is known as a <a href="tbResList.php?qv=65&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a> activator in cancer <br> - Raises <a href="tbResList.php?qv=65&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?qv=65&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>, <a href="tbResList.php?qv=65&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?qv=65&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?qv=65&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?qv=65&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?qv=65&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?qv=65&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?qv=65&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, <a href="tbResList.php?qv=65&tsv=235&wNotes=on&word=p38↓">p38↓</a>, Pro-Inflammatory Cytokines : <a href="tbResList.php?qv=65&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?qv=65&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <a href="tbResList.php?qv=65&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a> <br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓ inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.--> - inhibit Growth/Metastases : <a href="tbResList.php?qv=65&tsv=604&wNotes=on">TumMeta↓</a>, <a href="tbResList.php?qv=65&tsv=323&wNotes=on">TumCG↓</a>, <a href="tbResList.php?qv=65&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=65&tsv=204&wNotes=on">MMPs↓</a>, <a href="tbResList.php?qv=65&tsv=201&wNotes=on">MMP2↓</a>, <a href="tbResList.php?qv=65&tsv=203&wNotes=on">MMP9↓</a>, <a href="tbResList.php?qv=65&tsv=428&wNotes=on">uPA↓</a>, <a href="tbResList.php?qv=65&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=65&tsv=214&wNotes=on">NF-κB↓</a>, <a href="tbResList.php?qv=65&tsv=79&wNotes=on">CXCR4↓</a>, <a href="tbResList.php?qv=65&tsv=1247&wNotes=on">SDF1↓</a>, <a href="tbResList.php?qv=65&tsv=304&wNotes=on">TGF-β↓</a>, <a href="tbResList.php?qv=65&tsv=719&wNotes=on">α-SMA↓</a>, <a href="tbResList.php?qv=65&tsv=105&wNotes=on">ERK↓</a> <br> <!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, --> - reactivate genes thereby inhibiting cancer cell growth : <a href="tbResList.php?qv=65&tsv=140&wNotes=on">HDAC↓</a>, <a href="tbResList.php?qv=65&tsv=85&wNotes=on">DNMT1↓</a>, <a href="tbResList.php?qv=65&tsv=86&wNotes=on">DNMT3A↓</a>, <a href="tbResList.php?qv=65&tsv=108&wNotes=on">EZH2↓</a>, <a href="tbResList.php?qv=65&tsv=236&wNotes=on">P53↑</a>, <a href="tbResList.php?qv=65&wNotes=on&word=HSP">HSP↓</a>, <a href="tbResList.php?qv=65&tsv=506&wNotes=on">Sp proteins↓</a>, <br> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?qv=65&tsv=322&wNotes=on">TumCCA↑</a>, <a href="tbResList.php?qv=65&tsv=73&wNotes=on">cyclin D1↓</a>, <a href="tbResList.php?qv=65&tsv=467&wNotes=on">CDK2↓</a>, <a href="tbResList.php?qv=65&tsv=894&wNotes=on">CDK4↓</a>, <a href="tbResList.php?qv=65&tsv=895&wNotes=on">CDK6↓</a>, <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?qv=65&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?qv=65&tsv=324&wNotes=on">TumCI↓</a>, <a href="tbResList.php?qv=65&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=65&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=65&tsv=1117&wNotes=on">TOP1↓</a>, <a href="tbResList.php?qv=65&tsv=657&wNotes=on">TET1↓</a>, <br> <!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS --> - inhibits <a href="tbResList.php?qv=65&tsv=129&wNotes=on">glycolysis</a> /<a href="tbResList.php?qv=65&tsv=947&wNotes=on">Warburg Effect</a> and <a href="tbResList.php?qv=65&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> : <a href="tbResList.php?qv=65&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=65&tsv=772&wNotes=on">PKM2↓</a>, <a href="tbResList.php?qv=65&tsv=35&wNotes=on">cMyc↓</a>, <a href="tbResList.php?qv=65&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>, <a href="tbResList.php?qv=65&tsv=175&wNotes=on&word=LDH">LDHA↓</a>, <a href="tbResList.php?qv=65&tsv=773&wNotes=on">HK2↓</a>, <a href="tbResList.php?qv=65&wNotes=on&word=PFK">PFKs↓</a>, <a href="tbResList.php?qv=65&wNotes=on&word=PDK">PDKs↓</a>, <a href="tbResList.php?qv=65&tsv=773&wNotes=on">HK2↓</a>, <a href="tbResList.php?qv=65&tsv=847&wNotes=on">ECAR↓</a>, <a href="tbResList.php?qv=65&tsv=230&wNotes=on">OXPHOS↓</a>, <a href="tbResList.php?qv=65&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=65&tsv=623&wNotes=on">GlucoseCon↓</a> <br> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - inhibits <a href="tbResList.php?qv=65&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=65&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=65&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=65&wNotes=on&word=NOTCH">Notch↓</a>, <a href="tbResList.php?qv=65&wNotes=on&word=FGF">FGF↓</a>, <a href="tbResList.php?qv=65&tsv=361&wNotes=on">PDGF↓</a>, <a href="tbResList.php?qv=65&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, <a href="tbResList.php?qv=65&&wNotes=on&word=ITG">Integrins↓</a>, <br> <!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, --> - inhibits Cancer Stem Cells : <a href="tbResList.php?qv=65&tsv=795&wNotes=on">CSC↓</a>, <a href="tbResList.php?qv=65&tsv=524&wNotes=on">CK2↓</a>, <a href="tbResList.php?qv=65&tsv=141&wNotes=on">Hh↓</a>, <a href="tbResList.php?qv=65&tsv=124&wNotes=on">GLi1↓</a>, <a href="tbResList.php?qv=65&tsv=677&wNotes=on">CD133↓</a>, <a href="tbResList.php?qv=65&tsv=655&wNotes=on">CD24↓</a>, <a href="tbResList.php?qv=65&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=65&tsv=357&wNotes=on">n-myc↓</a>, <a href="tbResList.php?qv=65&tsv=656&wNotes=on">sox2↓</a>, <a href="tbResList.php?qv=65&tsv=508&wNotes=on">OCT4↓</a>, <br> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=65&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=65&tsv=4&wNotes=on">AKT↓</a>, <a href="tbResList.php?qv=65&wNotes=on&word=JAK">JAK↓</a>, <a href="tbResList.php?qv=65&wNotes=on&word=STAT">STAT↓</a>, <a href="tbResList.php?qv=65&tsv=377&wNotes=on">Wnt↓</a>, <a href="tbResList.php?qv=65&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=65&tsv=9&wNotes=on">AMPK↓</a>, <a href="tbResList.php?qv=65&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=65&tsv=168&wNotes=on">JNK</a>, <a href="tbResList.php?qv=65&tsv=825&wNotes=on">TrxR**</a>, <br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=65&tsv=1106&wNotes=on">chemo-sensitization</a>, <a href="tbResList.php?qv=65&tsv=1171&wNotes=on">chemoProtective</a>, <a href="tbResList.php?qv=65&tsv=1107&wNotes=on">RadioSensitizer</a>, <a href="tbResList.php?qv=65&tsv=1185&wNotes=on">RadioProtective</a>, <a href="tbResList.php?qv=65&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <a href="tbResList.php?qv=65&tsv=1105&wNotes=on">Neuroprotective</a>, <a href="tbResList.php?qv=65&tsv=557&wNotes=on">Cognitive</a>, <a href="tbResList.php?qv=65&tsv=1175&wNotes=on">Renoprotection</a>, <a href="tbResList.php?qv=65&tsv=1179&wNotes=on">Hepatoprotective</a>, <a href="tbResList.php?&qv=65&tsv=1188&wNotes=on">CardioProtective</a>, <br> <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=65&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br>
296
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CUSP9
CUSP9
PC
<b>CUSP9 </b>coordinated undermining of survival paths with nine repurposed drugs<br> -includes aprepitant, artesunate, auranofin, captopril, celecoxib, disulfiram, itraconazole, sertraline, ritonavir<br>
66
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CP
Cyclopamine
NP
<b>Cyclopamine</b> is a natural steroidal alkaloid derived from the corn lily, Veratrum californicum, which specifically disrupts the Hh signaling pathway.<br>
67
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CBC/D
Cynanbungeigenin C (CBC) and D (CBD)
NP
<b>Cynanbungeigenin C (CBC) and D (CBD)</b> from the plant Cynanchum bungei Decne <br>
68
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DL
D-limonene
NP
<b>Limonene</b>, an oil extracted from the peels of citrus fruits.<br>
222
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Dand
Dandelion Root
NP
<b>Dandelion root</b> (Taraxacum officinale) <br> -Various phytochemicals, including flavonoids and phenolic compounds, which have antioxidant properties.<br> -Root extract can induce apoptosis<br> -Anti-inflammatory properties<br> -Immune System Support<br> Dosage: dried root 2-8g/d. Extract 250-500mg/d Tea 1-2g, 1-3x/d<br>
6
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DAS
Dasatinib
D
<b>Dasatinib</b>, (brand name Sprycel) is a targeted therapy medication used to treat certain cases of chronic myelogenous leukemia and acute lymphoblastic leukemia.<br>
69
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Deg
Deguelin
NP
Insect poisoning, anti-cancer
<b>Deguelin</b> is a natural compound of the flavonoid family of products isolated from several plant species, including Derris trifoliata Lour and Mundulea sericea (Leguminosae) (4)<br> <br> Deguelin’s ability to modulate multiple signaling pathways—including PI3K/Akt, mTOR, NF-κB, HIF-1α, and MAPK<br> While preclinical studies have utilized dosages in the approximate range of 4–8 mg/kg in animal models, these figures are specific to the experimental conditions and species used in those studies.<br>
193
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Anamu
dibenzyl trisulphide(DTS) from Anamu
NP
<b>Anamu</b> (Guinea Hen Weed) Anamu (Petiveria alliacea)<br> A herb that is indigenous to the Amazon rainforest and the tropical areas of the Caribbean, Central and South America and Africa. <br> Anamu has been used for a wide variety of conditions, including arthritis, digestive disorders, infections, diabetes, cancer, for pain relief, and to induce abortion.<br>
288
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DCA
Dichloroacetate
RD
<b>Dichloroacetate (DCA)</b> is a metabolic modulator that targets the altered metabolic state of cancer cells by inhibiting PDKs. This action impacts several key pathways:<br> <br> • Reversal of the Warburg effect<br> • Restoration of mitochondrial function and promotion of apoptosis<br> • suppresses glycolysis and promotes oxidative phosphorylation, thereby increasing mitochondrial ROS-mediated apoptosis in tumor cells • Increase in ROS production leading to oxidative stress<br> • Inhibition of cell cycle progression<br> • Modulation of HIF-1α signaling: DCA might decrease HIF-1α stabilization, thereby reducing the expression of genes that support glycolysis, angiogenesis, and survival under low-oxygen conditions.<br> <br> -DCA has been primarily used in treating congenital lactic acidosis—a rare genetic disorder characterized by the buildup of lactic acid in the body.<br> -DCA is an anti-diabetic and lipid-lowering drug, as well as treating myocardial and cerebrovascular ischemia.<br> <br> -Do not add DCA to hot or warm beverages. DCA is unstable at higher temperatures<br> -Caffeinated increases effectiveness<br> -Vitamin B1 reduces neuropathy (500mg-2500mg/day)<br> -Possibly 20 grams of citric acid 20 minutes before taking DCA<br> -Procaine, Diclofenac or Sulindac to increase SMCT1 <br> -Omeprazole 80mg/day to increase DCA effectiveness<br> -Scorpion venom to increase DCA effectiveness <br> -Metformin 1000mg to 1500mg/day<br> -Propranolol (Ref.)<br> -Fenbendazole shows strong synergy when combined to DCA, So it may make very much sense to combine the two.<br> <a href="https://www.cancertreatmentsresearch.com/dichloroacetate-dca-treatment-strategy/"> "Note: DCA is not tumor cell specific,> and therefore the same shift in glucose metabolism that occurs in cancer cells will also take place in immune cells, leading to induction of Tregs (Ref.). In order to avoid this possibility, while using DCA I would also use Treg inhibitors such as Cimetidine (Ref.) or low dose Cyclophosphamide (Ref.)." </a><br> <br> Dose: 10mg/kg/day and increase slowly to about 25mg/kg/day:(1/2morn,1/2evening) take 5 days on, 2 off? OR 2wks on/ 1wk off: https://www.thedcasite.com/dca_dosage.html<br> Done by mixing it in water and drinking, suggested that DCA not be taken on an empty stomach.<br> <br> **** <br> DCA-induced apoptosis in cancer cells requires sodium-coupled monocarboxylates transporter SLC5A8 (SMCT1)<br> -Inhibitors of DNA methylation induce reactivation of SLC5A8<br> -Procaine is a DNA-demethylating agent with growth-inhibitory effects in human cancer cells.<br> -SMCT1 was found to be stimulated by some other NSAIDs (diclofenac, meclofenamate and sulindac), by activin A143 and by the probiotic Lactobacillus plantarum. <br> <br> <a href="https://www.sciencedirect.com/science/article/pii/S2444866416300034"> SMCT1 has been found to be inhibited by some NSAIDs (ibuprofen, ketoprofen, fenoprofen, naproxen135 and indomethacin94), phytochemicals (resveratrol and quercetin) </a> **** Hence these should be avoided with DCA. (also AVOID Bromide, iodide and sulfite )<br> <br> ****<br> GSTZ1 an/or chloride anion transport inhibitors also reduce resistance to DCA (if the tumor expresses GSTZ1 and contains a high chloride anions level, the GSTZ1 will be stable, maintaining the resistance to DCA).<br> <br> -<a href="https://www.cancertreatmentsresearch.com/">Dichloroacetate-dca-treatment-strategy </a>GSTZ1 an/or chloride anion transport inhibitors. .<br> -<a href="http://www.ncbi.nlm.nih.gov/pubmed/1839837">Etacrynic acid is a Cl(-)-ATPase inhibitor </a> <br> <a href="http://www.ncbi.nlm.nih.gov/pubmed/10711360">-Lansoprazole and Omeprazole inhibit chloride channels. </a><br> -<a href="https://en.wikipedia.org/wiki/Chlorotoxin">Chlorotoxin found in scorpion venom (see my post on scorpion venom) can also inhibit chlorine channels </a> <br> <br> Sources:<br> <a href="https://northernhealthproducts.com/shop/" >https://northernhealthproducts.com/shop/</a> <br> <a href="https://www.dcalab.com/">https://www.dcalab.com/ </a> <br>
289
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DAP
Dichloroacetophenone(2,2-)
D
<b>2,2-Dichloroacetophenone (DAP)</b> is an acetophenone derivative characterized by the presence of two chlorine atoms on the aromatic ring, typically at the 2‑position relative to the carbonyl group. Its structure and properties differ significantly from compounds like dichloroacetate (DCA). <br> -DAP may trigger the production of reactive oxygen species (ROS) in cells.<br> -Increased ROS can lead to cellular damage, which may trigger apoptosis (programmed cell death) in cancer cells that are already under metabolic and oxidative stress.<br> -Cytotoxic effects via DNA damage.<br> <br> *** Importantly, 2,2-dichloroacetophenone (DAP) is a much more potent inhibitor of PDK1(Than DCA). It is effective at concentrations in the micromolar (μM) range.<br>
200
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Dicl
Diclofenac
RD
<b>Diclofenac</b> is a nonsteroidal anti-inflammatory drug (NSAID) commonly used to treat pain, inflammation, and fever.<br>
309
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dietF
diet Fermented Foods
NP
<b>Fermented Food.</b> Some studies suggest that certain fermented foods (such as yogurt, kefir, sauerkraut, kimchi, and miso) can have health-promoting properties. These benefits may be due to probiotics (beneficial bacteria), bioactive compounds, and fermentation-derived metabolites.<br> <br> • Probiotics have been investigated for their potential to improve gut health and modulate the immune system. A robust gut microbiome may play a role in reducing systemic inflammation, which has been linked to a lower risk of several chronic diseases, including some types of cancer.<br> <br> • Fermented foods are often just one component of a diverse diet rich in fruits, vegetables, whole grains, and lean proteins, which collectively can contribute to a reduced risk of chronic diseases.<br> <br> <a href="https://haelan951.com/">https://haelan951.com/ </a> <br> <a href="https://avemar.com/">https://avemar.com/ </a> <br>
79
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dietFMD
diet FMD Fasting Mimicking Diet
NP
<b>5-day diet to mimic fasting without fasting.</b><br> FMDs are caloric-restricted plant–based diets containing low proteins, low sugar and high fats which represent a more feasible and safer option to water-only fasting.<br>
283
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dietKeto
diet Ketogenic
NP
<b>The ketogenic diet</b> is a high-fat, moderate-protein, and very low-carbohydrate diet. The drastic reduction in carbohydrate intake aims to shift the body’s metabolism from relying primarily on glucose (sugar) for energy to using ketone bodies produced from fat metabolism.<br> Many cancer cells predominantly rely on glucose for energy—a phenomenon known as the Warburg effect. By reducing carbohydrate intake, the KD lowers blood glucose levels, which theoretically could "starve" cancer cells of their preferred energy source.<br> -Lowering carbohydrate intake reduces insulin levels, which may indirectly decrease insulin-like growth factor (IGF) signaling—a pathway that can promote tumor growth in some cancers.<br> - MCT oil is rapidly metabolized in the liver to produce ketone bodies, making it a common component of ketogenic diets.<br>
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dietMet
diet Methionine-Restricted Diet
T
<b>Methionine (MET) restriction (MR)</b> has been shown to arrest cancer growth and sensitizes tumors to chemotherapy. <br> -Many cancer cells rely heavily on exogenous methionine to sustain rapid growth and proliferation because they often have impaired methionine salvage pathways.<br> -Methionine contributes to the synthesis of glutathione, a key antioxidant. (Methionine is a precursor of glutathione, a tripeptide that reduces reactive oxygen species.)<br> -MR diets might influence the redox state of cancer cells, increasing oxidative stress and thereby leading to cell death in metabolically compromised tumor cells.<br> -Proliferation and growth of several types of cancer cells are inhibited by MR, while normal cells are unaffected by limiting methionine as long as homocysteine is present.<br> -Methionine restriction is effective when the non-essential amino acid, cysteine, is absent from the diet or media. methionine is the precursor for cysteine which is essential for the formation of GSH.<br> -Malignant cells lack the enzyme required to recycle homocysteine therefore giving methionine restriction the capacity to alter cancer cells while maintaining normal, healthy cells. <br> <br> While vegan diets are typically low in methionine, some nuts and legumes (such as Brazil nuts and kidney beans) are rich in methionine.<br> <br> Foods to avoid for MR diet:<br> Animal Proteins: <br> -Red Meat (Beef, Pork, Lamb):<br> -Poultry (Chicken, Turkey): <br> -Fish and Seafood: <br> -Eggs: Both the egg whites and yolks are protein rich.<br> -Dairy Products: Milk, cheese, and yogurt <br> Certain Plant Proteins:<br> -Soy Products:<br> -Legumes: <br> Protein Supplements:<br> <br> Foods Lower in Methionine (Often Favorable on an MR Diet)<br> Fruits & Vegetables: leafy greens, berries, apples, and citrus fruits.<br> Grains & Cereals: rice, oats, and barley <br> Nuts and Seeds: can vary in methionine content. <br> Alternative Protein Sources: emphasize protein sources with a lower methionine-to-cysteine ratio.<br>
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dietP
diet Plant based
NP
<b>A diet high in whole grains, vegetables, and fruits</b> and low in red/processed meats, and low alcohol. <br> <br> -Some studies indicate high fruit consumption (but not orange juice) may be associated with poorer survival.<br> -Vegetable consumption, particularly green leafy and cruciferous vegetables, was associated with better overall survival.<br> <br> -If juice has higher sugar level (from fruits) they can affect blood glucose levels.<br> -If juice have high oxalate content they can be hard on kidneys.<br> -If juices have high vitamin K content they can affect blood thinners.<br>
71
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DHCA
Dihydrocaffeic Acid
NP
<b>Phenolic acid</b> found in plants, fungi and some foods. (grapes) Dihydrocaffeic acid is a phenolic acid. Chemically, it is the reduced (hydrogenated) form of caffeic acid.<br> <br> -DHCA is known for its antioxidant properties. It can scavenge reactive oxygen species (ROS).<br> -DHCA has shown potential anti-inflammatory properties which might help reduce tumor-promoting inflammation in some contexts.<br>
72
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DSMO
Dimethyl Sulfoxide
NP
<b>Chemical</b> that dissolves many substances that can affect the body.<br> It is used for bladder inflammation, limb pain, and IV leakage, but it can also cause side effects and interact with other drugs.<br>
293
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Dipy
Dipyridamole
D
<b>Dipyridamole</b> is a medication primarily used for its antiplatelet and vasodilatory effects. Dipyridamole is primarily known as a phosphodiesterase inhibitor and anti‐platelet agent.<br> <br> Mechanism: Dipyridamole inhibits phosphodiesterases (PDEs), enzymes that break down cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP).<br> Cancer Relevance: Increased cyclic nucleotide levels can affect cell proliferation, apoptosis, and differentiation. Elevated cAMP, for example, may contribute to growth arrest or modify signaling cascades in certain cancer cells.<br> <br> • Dipyridamole has been observed in some studies to exert antioxidant effects.<br> • There is evidence—albeit less definitive in some cases—that dipyridamole might influence mitochondrial function, potentially altering the balance between ROS production and detoxification.<br> <br> • By stabilizing mitochondrial membranes or affecting mitochondrial signaling pathways, dipyridamole could reduce the likelihood of excessive ROS generation.<br> <br> Current literature does not provide strong evidence that dipyridamole directly inhibits the mevalonate pathway??<br>
178
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docx
Docetaxel
D
<b>Docetaxel</b>, (brand name Taxotere) is a chemotherapy medication used to treat breast cancer, head and neck cancer, stomach cancer, prostate cancer and non-small-cell lung cancer.<br>
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DHA
Docosahexaenoic Acid
NP
<b>Omega-3 fatty acid</b> found in cold-water fish and some supplements.<br> – DHA is a major structural component of cell membranes in the brain, retina, and other tissues and plays a critical role in neural function and development.<br> <br> Role in Cancer<br> <br> Anti-Inflammatory Effects: – A reduction in chronic inflammation<br> Modulation of Cell Proliferation and Apoptosis<br> –Omega-3 fatty acids appear to influence cell cycle regulation and apoptosis (programmed cell death). By enhancing apoptosis and inhibiting proliferation, these agents may limit the growth of cancer cells.<br> Alteration of Membrane Composition and Signaling<br> –May affect processes such as angiogenesis (formation of new blood vessels), cell adhesion, and metastasis in cancer cells.<br> Impact on Oxidative Stress<br> –Although omega-3 fatty acids are prone to oxidation, their metabolites can have antioxidant properties. Balancing oxidation and antioxidant defenses is important in preventing oxidative stress—a known contributor to DNA damage and cancer development.<br> Anti-Angiogenic Effects<br> – Some studies have shown that EPA and DHA can inhibit angiogenesis.<br>
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doxoR
doxorubicin
D
<b>Doxorubicin</b>, (brand name Adriamycin) is a chemotherapy medication used to treat breast cancer, bladder cancer, Kaposi's sarcoma, lymphoma, and acute lymphocytic leukemia. Often used together with other chemotherapy agents. Given by injection into a vein.<br>
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Ech
Echinacea
NP
Immune system
<b>Echinacea</b> may have immune-modulating properties, which could theoretically help the body fight cancer.<br>
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EGCG
EGCG (Epigallocatechin Gallate)
NP
<a href="https://www.medicinenet.com/egcg_epigallocatechin_gallate_benefits_dosage/article.htm"> <b>EGCG (Epigallocatechin Gallate)</b> is found in green tea. 100 times more effective than Vitamin C and 25 times more effective than Vitamin E at protecting cells from damage associated with oxidative stress. </a> <br> EGCG Epigallocatechin Gallate (Green Tea) -Catechin<br> Summary:<br> 1. Concentration is a factor that could determine whether green tea polyphenols act as antioxidants or pro-oxidants.<br> 2. Poor bioavailability: taking EGCG capsules without food was better.<br> 3. Cancer dosage 4g/day (2g twice per day)? with curcumin may help (another ref says 700–2100 mg/d) <br> 4. EGCG is susceptible to oxidative degradation.<br> 5. “As for the pH level, the acidic environments enhance the stability of EGCG”.<br> 6. “EGCG may enhance nanoparticle uptake by tumor cells”<br> 7. Might be iron chelator (removing iron from cancer cells)<br> 8. Claimed as synergistic effect with chemotherapy ( cisplatin, bleomycin, gemcitabine.<br> 9. May suppress glucose metabolism, interfere with VEGF, downregulate NF-κB and MMP-9, down-regulation of androgen-regulated miRNA-21.<br> 10. Take with red pepper powder, Capsicum ratio 25:1 (based on half life, they did every 4 hr) (chili pepper vanilloid capsaicin).<br> 11. EGCG mediated ROS formation can upregulate CTR1 expression via the ERK1/2/NEAT1 pathway, which can increase the intake of chemotherapeutic drugs such as cisplatin in NSCLC cells and act as a chemosensitizer [58]<br> 12. Matcha green tea has highest EGCG (2-3X) because consuming leaf.<br> 13. EGCG is an ENOX2 inhibitor.<br> 14. Nrf2 activator in both cancer and normal cells. This <a href="https://nestronics.ca/dbx/tbResEdit.php?rid=3212"> example</a> of lung cancer show both directions in different cell lines, but both toward optimim level. <br> Biological activity, EGCG has been reported to exhibit a range of effects, including:<br> Antioxidant activity: 10-50 μM<br> Anti-inflammatory activity: 20-50 μM<br> Anticancer activity: 50-100 μM<br> Cardiovascular health: 20-50 μM<br> Neuroprotective activity: 10-50 μM<br> <br> Drinking a cup (or two cups) of green tea (in which one might ingest roughly 50–100 mg of EGCG from brewed tea) generally results in peak plasma EGCG concentrations in the range of approximately 0.1 to 0.6 μM.<br> <br> With higher, supplement-type doses (e.g., oral doses in the 500 mg–800 mg range that are sometimes studied for clinical benefits), peak plasma concentrations in humans can reach the low micromolar range, often reported around ~1–2 μM and in some cases up to 5 μM.<br> <br> Reported values can range from about 25–50 mg of EGCG per gram of matcha powder.<br> In cases where the matcha is exceptionally catechin-rich, the content could reach 200–250 mg or more in 5 g.<br> <br> -Peak plasma concentration roughly 1 to 2 hours after oral ingestion.<br> -Elimination half-life of EGCG in plasma is commonly reported to be in the range of about 3 to 5 hours.<br> <br> Supplemental EGCG <br> Dose (mg) ≈ Peak Plasma EGCG (µM)<br> ~50 mg ≈ 0.1–0.3 µM<br> ~100 mg ≈ 0.2–0.6 µM<br> ~250 mg ≈ 0.5–1.0 µM<br> ~500 mg ≈ 1–2 µM<br> ~800 mg or higher ≈ 1–5 µM<br> <br> 50mg of EGCG in 1g of matcha tea(1/2 teaspoon) <br> <br> Studies on green tea extracts have employed doses roughly equivalent to 300–800 mg/day of EGCG. Excessive doses can cause liver toxicity in some cases.<br> <br> Methods to improve bioavailability<br> -Lipid-based carriers or nanoemulsions<br> -Polymer-based nanoparticles or encapsulation<br> -Co-administration with ascorbic acid (vitamin C)<br> -Co-administration of adjuvants like piperine (perhaps sunflower lecithin and chitosan) -Using multiple smaller doses rather than one large single dose.<br> -Taking EGCG on an empty stomach or under fasting conditions, or aligning dosing with optimal pH conditions in the GI tract, may improve its absorption.(acidic environment is generally more favorable for its stability and absorption).<br> – EGCG is more stable under acidic conditions. In the stomach, where the pH is typically around 1.5 to 3.5, EGCG is less prone to degradation compared to the more neutral or basic environments of the small intestine.<br> - At neutral (around pH 7) or alkaline pH, EGCG undergoes auto-oxidation, reducing the effective concentration available for absorption.<br> – Although the stomach’s acidic pH helps maintain EGCG’s stability, most absorption occurs in the small intestine, where the pH is closer to neutral.<br> – To counterbalance the inherent instability in the intestine, strategies such as co-administration of pH-modifying agents (like vitamin C) are sometimes used. These agents help to maintain a slightly acidic environment in the gut microenvironment, potentially improving EGCG stability during its transit and absorption.<br> – The use of acidifiers or buffering agents in supplements may help preserve EGCG until it reaches the absorption sites.<br> <br> -Note <a href="tbResList.php?qv=73&tsv=1109&wNotes=on&exSp=open">half-life</a> 3–5 hours.<br> - low <a href="tbResList.php?qv=73&tsv=792&wNotes=on&exSp=open">BioAv</a> 1%? despite its limited absorption, it is rapidly disseminated throughout the body <br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - induce <a href="tbResList.php?qv=73&tsv=275&wNotes=on">ROS</a> production<br> - ROS↑ related: <a href="tbResList.php?qv=73&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?qv=73&tsv=103&wNotes=on">ER Stress↑</a>, <a href="tbResList.php?qv=73&tsv=459&wNotes=on">UPR↑</a>, <a href="tbResList.php?qv=73&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=73&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>, <a href="tbResList.php?qv=73&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?qv=73&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?qv=73&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?qv=73&tsv=239&wNotes=on">cl-PARP↑</a>, <a href="tbResList.php?qv=73&wNotes=on&word=HSP">HSP↓</a>, <a href="tbResList.php?qv=73&wNotes=on&word=Prx">Prx</a>,<!-- mitochondrial antioxidant enzyme--> <br> <!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, --> - Does NOT Lower AntiOxidant defense in Cancer Cells: <a href="tbResList.php?qv=73&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?qv=73&word=Trx&wNotes=on">TrxR↓**</a>,<!-- major antioxidant system --> <a href="tbResList.php?qv=73&tsv=298&wNotes=on&word=SOD">SOD</a>, <a href="tbResList.php?qv=73&tsv=137&wNotes=on&word=GSH">GSH</a> <a href="tbResList.php?qv=73&tsv=46&wNotes=on">Catalase</a> <a href="tbResList.php?qv=73&tsv=597&wNotes=on">HO1</a> <a href="tbResList.php?qv=73&wNotes=on&word=GPx">GPx</a> <br> - Raises <a href="tbResList.php?qv=73&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?qv=73&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>, <a href="tbResList.php?qv=73&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?qv=73&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?qv=73&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?qv=73&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?qv=73&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?qv=73&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?qv=73&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, <a href="tbResList.php?qv=73&tsv=235&wNotes=on&word=p38↓">p38↓</a>, Pro-Inflammatory Cytokines : <a href="tbResList.php?qv=73&tsv=908&wNotes=on&word=NLRP3↓">NLRP3↓</a>, <a href="tbResList.php?qv=73&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, <a href="tbResList.php?qv=73&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?qv=73&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <a href="tbResList.php?qv=73&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a> <br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓ inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.--> - inhibit Growth/Metastases : <a href="tbResList.php?qv=73&tsv=604&wNotes=on">TumMeta↓</a>, <a href="tbResList.php?qv=73&tsv=323&wNotes=on">TumCG↓</a>, <a href="tbResList.php?qv=73&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=73&tsv=204&wNotes=on">MMPs↓</a>, <a href="tbResList.php?qv=73&tsv=201&wNotes=on">MMP2↓</a>, <a href="tbResList.php?qv=73&tsv=203&wNotes=on">MMP9↓</a>, <!-- <a href="tbResList.php?qv=73&tsv=308&wNotes=on">TIMP2</a>, --> <a href="tbResList.php?qv=73&tsv=415&wNotes=on">IGF-1↓</a>, <a href="tbResList.php?qv=73&tsv=428&wNotes=on">uPA↓</a>, <a href="tbResList.php?qv=73&tsv=334&wNotes=on">VEGF↓</a>, <!-- <a href="tbResList.php?qv=73&tsv=1284&wNotes=on">ROCK1↓</a>, --> <a href="tbResList.php?qv=73&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?qv=73&tsv=273&wNotes=on">RhoA↓</a>, <a href="tbResList.php?qv=73&tsv=214&wNotes=on">NF-κB↓</a>, <!-- <a href="tbResList.php?qv=73&tsv=79&wNotes=on">CXCR4↓</a>, --> <!-- <a href="tbResList.php?qv=73&tsv=1247&wNotes=on">SDF1↓</a>, --> <a href="tbResList.php?qv=73&tsv=304&wNotes=on">TGF-β↓</a>, <a href="tbResList.php?qv=73&tsv=719&wNotes=on">α-SMA↓</a>, <a href="tbResList.php?qv=73&tsv=105&wNotes=on">ERK↓</a> <!-- <a href="tbResList.php?qv=73&tsv=1178&wNotes=on">MARK4↓</a> --><!-- contributing to tumor growth, invasion, and metastasis--> <br> <!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, --> - reactivate genes thereby inhibiting cancer cell growth : <a href="tbResList.php?qv=73&tsv=140&wNotes=on">HDAC↓</a>, <a href="tbResList.php?qv=73&wNotes=on&word=DNMT">DNMTs↓</a>, <a href="tbResList.php?qv=73&tsv=108&wNotes=on">EZH2↓</a>, <a href="tbResList.php?qv=73&tsv=236&wNotes=on">P53↑</a>, <a href="tbResList.php?qv=73&wNotes=on&word=HSP">HSP↓</a>, <a href="tbResList.php?qv=73&tsv=506&wNotes=on">Sp proteins↓</a>, <!-- <a href="tbResList.php?qv=73&wNotes=on&word=TET">TET↑</a> --> <br> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?qv=73&tsv=322&wNotes=on">TumCCA↑</a>, <a href="tbResList.php?qv=73&tsv=73&wNotes=on">cyclin D1↓</a>, <a href="tbResList.php?qv=73&tsv=378&wNotes=on">cyclin E↓</a>, <a href="tbResList.php?qv=73&tsv=467&wNotes=on">CDK2↓</a>, <a href="tbResList.php?qv=73&tsv=894&wNotes=on">CDK4↓</a>, <a href="tbResList.php?qv=73&tsv=895&wNotes=on">CDK6↓</a>, <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?qv=73&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?qv=73&tsv=324&wNotes=on">TumCI↓</a>, <a href="tbResList.php?qv=73&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <!-- encourages invasion, proliferation, EMT, and angiogenesis --> <a href="tbResList.php?qv=73&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?qv=73&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=73&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=73&wNotes=on&word=TOP">TOP1↓</a>, <!-- <a href="tbResList.php?qv=73&tsv=657&wNotes=on">TET1↓</a>, --> <br> <!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS --> - inhibits <a href="tbResList.php?qv=73&tsv=129&wNotes=on">glycolysis</a> /<a href="tbResList.php?qv=73&tsv=947&wNotes=on">Warburg Effect</a> and <a href="tbResList.php?qv=73&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> : <a href="tbResList.php?qv=73&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=73&tsv=772&wNotes=on">PKM2↓</a>, <a href="tbResList.php?qv=73&tsv=35&wNotes=on">cMyc↓</a>, <a href="tbResList.php?qv=73&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>, <a href="tbResList.php?qv=73&tsv=906&wNotes=on">LDH↓</a>, <a href="tbResList.php?qv=73&tsv=175&wNotes=on&word=LDH">LDHA↓</a>, <a href="tbResList.php?qv=73&tsv=773&wNotes=on">HK2↓</a>, <a href="tbResList.php?qv=73&wNotes=on&word=PFK">PFKs↓</a>, <!-- <a href="tbResList.php?qv=73&wNotes=on&word=PDK">PDKs↓</a>, --> <a href="tbResList.php?qv=73&tsv=847&wNotes=on">ECAR↓</a>, <a href="tbResList.php?qv=73&tsv=230&wNotes=on">OXPHOS↓</a>, <a href="tbResList.php?qv=73&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=73&tsv=1278&wNotes=on">Glucose↓</a>, <a href="tbResList.php?qv=73&tsv=623&wNotes=on">GlucoseCon↓</a> <br> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - inhibits <a href="tbResList.php?qv=73&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=73&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=73&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=73&wNotes=on&word=NOTCH">Notch↓</a>, <a href="tbResList.php?qv=73&wNotes=on&word=FGF">FGF↓</a>, <a href="tbResList.php?qv=73&wNotes=on&word=PDGF">PDGF↓</a>, <a href="tbResList.php?qv=73&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, <a href="tbResList.php?qv=73&&wNotes=on&word=ITG">Integrins↓</a>, <br> <!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, --> - inhibits Cancer Stem Cells : <a href="tbResList.php?qv=73&tsv=795&wNotes=on">CSC↓</a>, <!-- <a href="tbResList.php?qv=73&tsv=524&wNotes=on">CK2↓</a>, --> <a href="tbResList.php?qv=73&tsv=141&wNotes=on">Hh↓</a>, <a href="tbResList.php?qv=73&tsv=434&wNotes=on">GLi↓</a>, <a href="tbResList.php?qv=73&tsv=124&wNotes=on">GLi1↓</a>, <a href="tbResList.php?qv=73&tsv=677&wNotes=on">CD133↓</a>, <a href="tbResList.php?qv=73&tsv=655&wNotes=on">CD24↓</a>, <a href="tbResList.php?qv=73&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=73&tsv=357&wNotes=on">n-myc↓</a>, <!-- <a href="tbResList.php?qv=73&tsv=656&wNotes=on">sox2↓</a>, --> <a href="tbResList.php?qv=73&wNotes=on&word=NOTCH">Notch↓</a>, <!-- <a href="tbResList.php?qv=73&tsv=1024&wNotes=on">nestin↓</a>, --> <a href="tbResList.php?qv=73&tsv=508&wNotes=on">OCT4↓</a>, <br> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=73&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=73&tsv=4&wNotes=on">AKT↓</a>, <a href="tbResList.php?qv=73&wNotes=on&word=JAK">JAK↓</a>, <a href="tbResList.php?qv=73&wNotes=on&word=STAT">STAT↓</a>, <a href="tbResList.php?qv=73&tsv=377&wNotes=on">Wnt↓</a>, <a href="tbResList.php?qv=73&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=73&tsv=9&wNotes=on">AMPK</a>, <!-- <a href="tbResList.php?qv=73&tsv=475&wNotes=on">α↓</a>, --> <a href="tbResList.php?qv=73&tsv=105&wNotes=on">ERK↓</a>, <!-- <a href="tbResList.php?qv=73&tsv=1014&wNotes=on">5↓</a>, --> <a href="tbResList.php?qv=73&tsv=168&wNotes=on">JNK</a>, - <a href="tbResList.php?qv=73&wNotes=on&word=SREBP">SREBP</a> (related to cholesterol).<br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=73&tsv=1106&wNotes=on">chemo-sensitization</a>, <a href="tbResList.php?qv=73&tsv=1171&wNotes=on">chemoProtective</a>, <a href="tbResList.php?qv=73&tsv=1107&wNotes=on">RadioSensitizer</a>, <a href="tbResList.php?qv=73&tsv=1185&wNotes=on">RadioProtective</a>, <a href="tbResList.php?qv=73&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <a href="tbResList.php?qv=73&tsv=1105&wNotes=on">Neuroprotective</a>, <a href="tbResList.php?qv=73&tsv=557&wNotes=on">Cognitive</a>, <a href="tbResList.php?qv=73&tsv=1175&wNotes=on">Renoprotection</a>, <a href="tbResList.php?qv=73&tsv=1179&wNotes=on">Hepatoprotective</a>(possible damage at high dose), <a href="tbResList.php?&qv=73&tsv=1188&wNotes=on">CardioProtective</a>, <br> <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=73&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br>
259
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EPA
eicosapentaenoic acid
NP
<b>Eicosapentaenoic Acid (EPA)</b><br> – An omega-3 polyunsaturated fatty acid (PUFA) primarily found in marine sources such as fatty fish and algae.<br> – EPA is involved in the synthesis of eicosanoids, which are signaling molecules that modulate inflammatory processes.<br>
248
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EP
Electrical Pulses
NP
<b>Electrical Pulses</b><br>
74
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EA
Ellagic acid
NP
<b>Polyphenol</b> found in fruits, vegetables, nuts and some mushrooms. Strawberries, raspberries, blackberries, cherries and walnuts, green tea and red wine.<br> <br> - Ellagitannins are high molecular weight polyphenols with a complex structure that includes one or more HHDP groups attached to a sugar.<br> - Ellagic Acid is the simpler, bioactive compound released when the HHDP groups in ellagitannins cyclize during hydrolysis.<br> <br> Pathways:<br> Apoptosis Regulation: (Bax, Bad) (Bcl-2, Bcl-xL) <br> Cell Cycle Arrest: G0/G1 or G2/M phases)<br> NF-κB (inhibit):<br> MAPK Pathways: (including ERK1/2, JNK, and p38 MAPK) <br> PI3K/Akt/mTOR: might downregulate this pathway<br> p53 Pathway: may influence the expression or activation of p53<br> Oxidative Stress and Nrf2 Pathway:exhibits antioxidant properties, <ROS, modulate the Nrf2 Angiogenesis Inhibition<br> <br> Summary:<br> - Anti-oxidant, with some evidence it can induce ROS in cancer (production of ROS)<br> - Works well with Curcumin<br> - Reduced the viability of cancer cells at a concentration of 10 µmol/L, while in healthy cells, this effect was observed only at a concentration of 200 µmol/L<br> - Pomegranate juice (PJ) (180 ml) containing EA (25 mg) and ETs (318 mg, as punicalagins, the major fruit ellagitannin). Plasma concentration (31.9 ng/ml) after 1 h post-ingestion but was rapidly eliminated by 4 h. (Hence might be difficult to consume enough EA!!!! to match vitro requirements)<br> - Likely need > 10mg/kg/day -> *180kg = 1800mg (might be possible)<br> - Increased the expression of p53 and p21 proteins as well as markers of apoptosis (Bax and caspase-3), and decreases Bcl-2, NF-кB, and iNOS<br> - EA has restricted bioavailability, primarily due to its hydrophobic nature and very low water solubility.<br> - Industrial processing of pomegranates for juice production increases the concentration of EA in juices, but freezing reduces concentration<br> <br> Punica granatum L. Pomegranate 700mg/kg (arils), 38700mg/kg(mesocarp)<br> Rubus idaeus L. Raspberry 2637–3309mg/kg <br> jaglandaceae Walnut 410mg/kg(freeEA) 8230mg/kg(totalEA)<br>
329
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RF
EMF
NP
<b>radiofrequency (RF) electromagnetic fields (EMF)</b><br> <br> -example 27.12 MHz https://www.therabionic.com/ TheraBionic P1<br>
75
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EMD
Emodin
NP
</b>Organic</b> compound isolated from rhubarb, buckthorn, knotweed. It has laxative, anticancer, antibacterial, antiinflammatory, and antiviral activities, and is used in traditional Chinese medicine.<br> Emodin, an anthraquinone derivative found in various plants (e.g., rhubarb, Polygonum cuspidatum).<br> <br> Pathways:<br> - Generation of Reactive Oxygen Species (ROS)<br> - Upregulation Bax downregulation of Bcl‑2, caspase activation and cyt_c release.<br> - Induce cell cycle arrest at various checkpoints (commonly G0/G1 or G2/M phases.<br> - Can inhibit NF‑κB activation<br> – MAPK Pathways<br> – PI3K/Akt Pathway<br> - Metalloproteinases (MMPs) <br> <br> -ic50 cancer cells 10-50uM, normal cells higher(supports a therapeutic window)<br>
206
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MS-275
entinostat
D
<b>Entinostat</b> is a small molecule that was specifically designed to inhibit the activity of histone deacetylases (HDACs), which are enzymes that play a crucial role in the regulation of gene expression.<br>
110
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EPI
epirubicin
D
<b>Epirubicin</b>, an anthracycline chemotherapeutic agent, has several mechanisms of action, one of which is the production of reactive oxygen species (ROS). Here are some key points regarding epirubicin and its relationship with ROS:<br> Mechanism of Action and ROS Generation<br> -Epirubicin exerts its anticancer effects primarily by intercalating into DNA and inhibiting topoisomerase II, leading to DNA strand breaks.<br>
241
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erastin
erastin
D
<b>Erastin</b> is often referred to as a "metabolic inhibitor" or a "ferroptosis inducer", rather than a traditional chemotherapy agent.<br> Erastin is primarily available as a research chemical—it's not an approved therapeutic for clinical use.<br> <br> Pathways:<br> -Erastin inhibits system xCT, thereby reducing cystine uptake. This leads to decreased intracellular cysteine, a precursor for GSH. As a consequence, the cell’s glutathione levels drop, compromising its ability to neutralize reactive oxygen species (ROS).<br> -Glutathione (GSH) Depletion and Increased Oxidative Stress<br> -Voltage-Dependent Anion Channels (VDACs): Altering VDAC function can affect mitochondrial metabolism, leading to changes in energy production and further enhancing oxidative stress.<br>
252
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Est
Estrogen
NP
<b>Estrogen</b> is a hormone that plays a crucial role in the development and progression of various types of cancer. (ER-positive cancers).<br> ER-positive cancers tend to have a better prognosis than ER-negative cancers, as they are more likely to respond to hormone therapy.<br> <br> Negative effects of estrogen supplements on cancer:<br> <b>Breast cancer:</b> Estrogen supplements can increase the risk of breast cancer, particularly in postmenopausal women. This is because estrogen can stimulate the growth of estrogen receptor-positive (ER+) breast cancer cells.<br> <b>Endometrial cancer:</b> Estrogen supplements can increase the risk of endometrial cancer, particularly in women who have not had a hysterectomy. This is because estrogen can stimulate the growth of endometrial cells, leading to an increased risk of cancer.<br> <b>Ovarian cancer:</b> Some studies suggest that estrogen supplements may increase the risk of ovarian cancer, although the evidence is not conclusive.<br> <br> Positive effects of estrogen supplements on cancer:<br> <b>Colorectal cancer:</b> Some studies suggest that estrogen supplements may reduce the risk of colorectal cancer, particularly in postmenopausal women.<br> <b>Prostate cancer:</b> Estrogen supplements may have a protective effect on prostate cancer, although the evidence is not conclusive.<br>
291
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EDTA
ethylene diamine tetraacetic acid
D
<b>EDTA (ethylene diamine tetraacetic acid)</b> is a synthetic compound and is not naturally occurring.<br> <br> -EDTA is a chelating agent, enables it to bind tightly to metal ions<br>
76
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EDM
Evodiamine
NP
<b>Evodiamine</b> is a bioactive alkaloid isolated primarily from the fruit of the traditional Chinese medicinal herb Evodia rutaecarpa. <b><a href="https://www.sciencedirect.com/science/article/abs/pii/S0378874120330464">Evodiamine</b> is a natural alkaloid from Evodia rutaecarpa, a traditional Chinese medicine. It has various pharmacological activities, such as anti-inflammatory, anti-cancer, anti-microbial and metabolic regulation, but also shows hepatotoxicity and cardiotoxicity.</a> <br>
171
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Ex
Exercise
NP
Therapy
<b>Regular physical activity</b> has been shown to influence cancer risk, progression, and survivorship. While exercise is not a cure for cancer, extensive research indicates that it can help reduce the risk of developing certain types of cancer and improve outcomes and quality of life for those diagnosed.<br> <br> -Lowering the levels of hormones levels.<br> -Preventing high blood levels of insulin.<br> -Regular physical activity leads to decreased levels of inflammatory markers (such as C-reactive protein and interleukin-6).<br> -Improving immune system function (enhancing the circulation of immune cells, including natural killer cells, T lymphocytes, and macrophages)<br> -Reducing the time it takes for food to travel through the digestive system.<br> -Helping to prevent obesity, which is a risk factor for many cancers.<br> -Exercise promotes the upregulation of antioxidant defenses.<br>
330
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Fenb
Fenbendazole
RD
<b>Fenbendazole</b> also known as methyl N-(6-phenylsulfanyl-1H-benzimidazole-2yl) is a benzimidazole anthelmintic drug primarily used to treat parasitic worm infections in animals, such as dogs, cats, and livestock. <br> <br> -Fenbendazole works by binding to tubulin, a protein that is important in cell division, which may theoretically affect rapidly dividing cells like cancer cells. However, this mechanism is not selective for cancer cells and could affect normal cells as well.<br> <br> -Albendazole and fenbendazole, two approved and commonly used benzimidazole anthelmintics<br> <br> -Panacure C :1g granules (or 222mg Fenbendazole, for small dogs)<br>
77
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FA
Ferulic acid
NP
<b>Ferulic acid</b> is an antioxidant found in some skin creams and serums.<br> Foods: popcorn, bamboo, whole-grain rye bread, whole-grain oat flakes, sweet corn (cooked)<br> <br> -Ferulic acid found in dietary strand fractions, especially its free form, has important functions for protecting the human health.<br> -Cooking results in an increase in free ferulic acid quantity and in a reduction in bound ferulic acid quantity.<br> <br> Bamboo shoots 243.6 mg/100g<br> Sugar-beet pulp 800 mg/100g<br> Popcorn 313 mg/100g<br> <br> <table Border="1" rules="rows"> <tr><th>Type of corn</th> <th>p-coumaric acid</th> <th>ferulic acid</th></tr> <tr><td> </td> <td> mg/kg, DW </td> <td>mg/kg, DW</td></tr> <tr><td>Yellow dent</td> <td>18.9 </td> <td>265</td></tr> <tr><td>American blue</td> <td>N.D. </td> <td>927</td></tr> <tr><td>Mexican blue</td> <td>1.3 </td> <td>202</td></tr> <tr><td>white</td> <td>6.6 </td> <td>2484</td></tr> </table>
285
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Fer
ferumoxytol
RD
<b>Ferumoxytol</b> is an intravenous iron replacement product composed of superparamagnetic iron oxide nanoparticles coated with a carbohydrate shell. It was primarily developed to treat iron deficiency anemia, particularly in patients with chronic kidney disease (CKD). The nanoparticle formulation offers both therapeutic iron supplementation and a potential role as a magnetic resonance imaging (MRI) contrast agent because of its unique magnetic properties.<br> <br> Because iron is essential for cell proliferation, there has been some concern about the theoretical risk of providing additional iron to environments where tumor cells might use it for growth. Nevertheless, the clinical significance of this in the context of ferumoxytol administration remains controversial and is not clearly established by current evidence.<br> <br> There has been some research combining Ferumoxytol with high dose Vitamin C. Some laboratory studies have examined whether the combination of ferumoxytol and vitamin C can enhance anticancer effects. For instance, exposure of cancer cell lines or tumor models to this combination has been evaluated to see if there is an increase in ROS-mediated cytotoxicity compared to using either agent alone.<br>
78
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FIS
Fisetin
NP
<b>Fisetin</b> is a plant based flavonoid. Found in strawberries(160ug/g), apples, persimmons, onions, cucumbers, grapes.<br> <br> -Note <a href="tbResList.php?qv=78&tsv=1109&wNotes=on&exSp=open">half-life</a> 3-4hrs<br> - Oral <a href="tbResList.php?qv=78&tsv=792&wNotes=on&exSp=open">BioAv</a> low (40-50%) <br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - induce <a href="tbResList.php?qv=78&tsv=275&wNotes=on">ROS</a> production in cancer cells, but also known to reduce it. <br> Also a claim <a href="https://nestronics.ca/dbx/tbResEdit.php?rid=2855">Fisetin-Induced Reactive Oxygen Species Production Has No Effect on Apoptosis</a> in RCC cells <br> Also one claim (NAC 10-20mM levels) that <a href="https://nestronics.ca/dbx/tbResEdit.php?rid=2856">NAC enhances ROS/apoptosis</a> <br> - ROS↑ related: <a href="tbResList.php?qv=78&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?qv=78&tsv=103&wNotes=on">ER Stress↑</a>, <a href="tbResList.php?qv=78&tsv=459&wNotes=on">UPR↑</a>, <a href="tbResList.php?qv=78&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=78&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>, <a href="tbResList.php?qv=78&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?qv=78&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?qv=78&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?qv=78&tsv=239&wNotes=on">cl-PARP↑</a>, <a href="tbResList.php?qv=78&wNotes=on&word=HSP">HSP↓</a> <br> <!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, --> - Does not appear to lower antioxidants in cancer cells <br> - Raises <a href="tbResList.php?qv=78&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?qv=78&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>, <a href="tbResList.php?qv=78&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?qv=78&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?qv=78&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?qv=78&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?qv=78&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?qv=78&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?qv=78&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, <a href="tbResList.php?qv=78&tsv=235&wNotes=on&word=p38↓">p38↓</a>, Pro-Inflammatory Cytokines : <a href="tbResList.php?qv=78&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, <a href="tbResList.php?qv=78&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?qv=78&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓ inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.--> - inhibit Growth/Metastases : <a href="tbResList.php?qv=78&tsv=604&wNotes=on">TumMeta↓</a>, <a href="tbResList.php?qv=78&tsv=323&wNotes=on">TumCG↓</a>, <a href="tbResList.php?qv=78&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=78&tsv=204&wNotes=on">MMPs↓</a>, <a href="tbResList.php?qv=78&tsv=201&wNotes=on">MMP2↓</a>, <a href="tbResList.php?qv=78&tsv=203&wNotes=on">MMP9↓</a>, <a href="tbResList.php?qv=78&tsv=415&wNotes=on">IGF-1↓</a>, <a href="tbResList.php?qv=78&tsv=428&wNotes=on">uPA↓</a>, <a href="tbResList.php?qv=78&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=78&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?qv=78&tsv=273&wNotes=on">RhoA↓</a>, <a href="tbResList.php?qv=78&tsv=214&wNotes=on">NF-κB↓</a>, <a href="tbResList.php?qv=78&tsv=304&wNotes=on">TGF-β↓</a>, <a href="tbResList.php?qv=78&tsv=105&wNotes=on">ERK↓</a> <br> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?qv=78&tsv=322&wNotes=on">TumCCA↑</a>, <a href="tbResList.php?qv=78&tsv=73&wNotes=on">cyclin D1↓</a>, <a href="tbResList.php?qv=78&tsv=378&wNotes=on">cyclin E↓</a>, <a href="tbResList.php?qv=78&tsv=467&wNotes=on">CDK2↓</a>, <a href="tbResList.php?qv=78&tsv=894&wNotes=on">CDK4↓</a>, <a href="tbResList.php?qv=78&tsv=895&wNotes=on">CDK6↓</a>, <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?qv=78&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?qv=78&tsv=324&wNotes=on">TumCI↓</a>, <a href="tbResList.php?qv=78&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?qv=78&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=78&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=78&tsv=1117&wNotes=on">TOP1↓</a>, <a href="tbResList.php?qv=78&tsv=657&wNotes=on">TET1↓</a>, <br> <!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS --> - inhibits <a href="tbResList.php?qv=78&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=78&tsv=35&wNotes=on">cMyc↓</a>, <a href="tbResList.php?qv=78&tsv=906&wNotes=on">LDH↓</a>, <a href="tbResList.php?qv=78&tsv=356&wNotes=on">GRP78↑</a>, <br> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - inhibits <a href="tbResList.php?qv=78&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=78&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=78&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=78&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, <br> <!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, --> - inhibits Cancer Stem Cells : <a href="tbResList.php?qv=78&tsv=677&wNotes=on">CD133↓</a>, <a href="tbResList.php?qv=78&tsv=342&wNotes=on">β-catenin↓</a>, <br> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=78&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=78&tsv=4&wNotes=on">AKT↓</a>, <a href="tbResList.php?qv=78&wNotes=on&word=JAK">JAK↓</a>, <a href="tbResList.php?qv=78&wNotes=on&word=STAT">STAT↓</a>, <a href="tbResList.php?qv=78&tsv=377&wNotes=on">Wnt↓</a>, <a href="tbResList.php?qv=78&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=78&tsv=9&wNotes=on">AMPK↓</a>, <a href="tbResList.php?qv=78&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=78&tsv=168&wNotes=on">JNK</a>, <br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=78&tsv=1106&wNotes=on">chemo-sensitization</a>, <a href="tbResList.php?qv=78&tsv=1171&wNotes=on">chemoProtective</a>, <a href="tbResList.php?qv=78&tsv=1107&wNotes=on">RadioSensitizer</a>, <a href="tbResList.php?qv=78&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <a href="tbResList.php?qv=78&tsv=1105&wNotes=on">Neuroprotective</a>, <a href="tbResList.php?qv=78&tsv=557&wNotes=on">Cognitive</a>, <a href="tbResList.php?qv=78&tsv=1175&wNotes=on">Renoprotection</a>, <a href="tbResList.php?qv=78&tsv=1179&wNotes=on">Hepatoprotective</a>, <a href="tbResList.php?&qv=78&tsv=1188&wNotes=on">CardioProtective</a>, <br> <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=78&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br>
227
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Flav
flavonoids
NP
<b>Flavonoids</b> compounds are found in a wide range of fruits, vegetables, and other plant-based foods, and have been shown to have a number of biological activities that may help to prevent or treat cancer.<br> Examples: Quercetin, Kaempferol, Isorhapontigenin, EGCG<br> <br> Flavonoids are classified into seven structural classes: <br> 1.flavanones<br> -Nargenin, Naringin, Hesperetin, Isosakuranetin, Eriodictyol, Taxifolin<br> 2.flavonols<br> -Quercetin, Myrcetin, Fisetin, Rutin Morin, Kaempferol <br> 3.chalcones<br> -Butein, Xanthohumol, Isoliquintigenin, Cardamonin, Bavachalone, Xanthohumol, Phloretin<br> 4.flavanols<br> -Catechin, Gallocatechin, Epicatechin, Epigallocatechin-3-galate<br> 5.anthocyanidins<br> -Cyanidin<br> 6.flavones<br> -Chrysin, Apigenin, Luteolin, Vitexin, Orientin, Bacalein, Wogonin, Oroxylin A, Saponarin<br> 7.isoflavonoids<br> -Daidzein, Genistein, Glycitein<br>
80
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FA
Folic Acid
NP
<b>B Vitamin supplement.</b> Helps form red blood cells.<br> Folic acid (vitamin B9) is converted into tetrahydrofolate (THF) and its derivatives. These folate coenzymes are essential for one‐carbon transfer reactions, which are critical for the synthesis of purines and thymidylate—key components of DNA.<br> <br> • Folate Deficiency and ROS: A deficiency in folic acid can exacerbate oxidative stress. Insufficient folate has been linked to increased ROS levels, which are capable of damaging cellular macromolecules, including DNA, proteins, and lipids. This oxidative DNA damage further increases mutation rates and contributes to carcinogenesis.<br> <br> The evidence suggests that while adequate dietary folate is important for cancer prevention (by maintaining genomic stability and proper methylation), excessive folate supplementation in individuals with undiagnosed or existing neoplasms might be problematic.<br>
274
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Form
Formononetin
NP
<b>Formononetin</b> is an O-methylated isoflavone.<br> Found in several plant sources, including:<br> <br> Red Clover (Trifolium pratense):<br> Astragalus membranaceus:<br> Other Leguminous Plants:<br> -Various plants in the legume family (Fabaceae) may also contain formononetin, although the levels and bioavailability can differ depending on the plant species and extraction methods.<br> <br> Pathways:<br> PI3K/Akt Pathway: formononetin may inhibit the phosphorylation of Akt<br> (MAPK) Pathway: may modulate components of the MAPK pathway<br> STAT3 Signaling Pathway: formononetin can downregulate STAT3 activity<br> NF-κB Pathway: modulating NF-κB activation<br> Apoptotic Pathways: via mitochondrial-dependent pathways, enhancing caspase activation <br> Induce cell cycle arrest at different checkpoints (e.g., G1 or G2/M phases)<br> <br> Formononetin, a naturally occurring isoflavone found in red clover, Astragalus membranaceus, and other leguminous plants, shows promise as an anticancer agent. Its ability to modulate key signaling pathways—including PI3K/Akt, MAPK, STAT3, NF-κB, and apoptotic and cell cycle regulatory mechanisms—suggests a multifaceted potential in cancer prevention and therapy.<br>
81
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F
Fucoidan
NP
<b>Fucoidan</b> is found in brown algae. Extracted from the seaweed species Fucus vesiculosus, Cladosiphon okamuranus, Laminaria japonica and Undaria pinnatifida.<br>
82
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GA
Gallic acid
NP
<b>Phenolic acid</b> found in gallnuts, sumac, witch hazel, tea leaves, oak bark. Has anitoxidant, antimicrobial and anti-obesity properties.<br> The GA derivatives include two types: ester and catechin derivatives. The most common ester derivatives of GA are alkyl esters, which are composed mainly of methyl gallate (MG), propyl gallate (PG), octyl gallate (OG), dodecyl gallate (DG), tetradecyl gallate (TG), and hexadecyl gallate (HG), and some of the main catechin derivatives are epicatechin (EC), epicatechin gallate (ECG), epigallocatechin (EGC), gallocatechin gallate (GCG), and epigallocatechin gallate (EGCG)<br> <br> Gallic acid is a naturally occurring polyphenol found in a variety of plant-based foods. Some of the best dietary sources include:<br> <br> Fruits:<br> Berries (strawberries, blackberries, blueberries)<br> Grapes, including red wine (grapes are rich in polyphenols)<br> Pomegranates and apples<br> Nuts and Seeds: Walnuts and almonds have been noted to contain GA in their skins<br> Herbs and Spices: Tea (especially green tea), Sumac and other spices<br> Other Plants: Gallnuts (from oak trees)<br> <br> Pathways:<br> -Apoptosis Induction: Activating caspase cascades, Shifting Bax versus Bcl-2, MMP, cyt-c release -Cell Cycle Arrest: typ @ G1 or G2/M checkpoints. <br> -Anti-inflammatory Effects: inhibiting NF-κB <br> -Angiogenesis Inhibition:<br> -Modulation of Signaling Pathways: MAPK Pathway, PI3K/Akt Pathway Inhibition, p53 Pathway<br> <br> Gallic acid exhibits a complex behavior with ROS in cancer cells, acting as both an antioxidant and a pro-oxidant depending on the context and its concentration:<br> <br> Antioxidant Effects at Low Doses:<br> -At lower concentrations, gallic acid is typically characterized by its ability to scavenge free radicals, thus reducing oxidative stress.<br> This antioxidant property may help protect normal cells from DNA damage, reducing the risk of mutations that could lead to cancer.<br> <br> Pro-oxidant Effects at High Doses: >50-100uM?<br> -At higher concentrations, GA can exert pro-oxidant effects, generating ROS within cancer cells. Elevated ROS levels can overwhelm the cellular antioxidant defenses of cancer cells, leading to oxidative stress, mitochondrial dysfunction, and ultimately cell death.<br>
177
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Gallo
Galloflavin
NP
<b>Galloflavin</b> is a flavonoid compound found in certain plants, such as the Galphimia gracilis. Studies have demonstrated that galloflavin can inhibit the growth of cancer cells and induce apoptosis (cell death) in various types of cancer, including breast, lung, and colon cancer. Galloflavin's anti-cancer effects are thought to be due to its ability to modulate various cellular signaling pathways, including the PI3K/Akt and NF-κB pathways, which are involved in cell survival and proliferation. Additionally, galloflavin has been shown to have antioxidant and anti-inflammatory properties, which may also contribute to its anti-cancer effects.<br> <br> Galloflavin has been reported to be a lactate dehydrogenase (LDH) inhibitor. LDH is an enzyme that plays a crucial role in the metabolism of cancer cells, particularly in the process of glycolysis, which is the breakdown of glucose to produce energy.<br> Galloflavin's LDH inhibitory activity has been demonstrated in various studies, which have shown that it can inhibit LDH activity in cancer cells, leading to a decrease in lactate production and an increase in the production of reactive oxygen species (ROS). The increase in ROS can lead to cell death, making galloflavin a potential therapeutic agent for the treatment of cancer.<br>
302
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GamB
Gambogic Acid
NP
<b>Gambogic acid</b> is a naturally occurring xanthonoid extracted from the resin of trees belonging to the Garcinia genus—most notably, Garcinia hanburyi. This tree is native to regions in Southeast Asia, particularly found in areas of China, India, and neighboring countries.<br> Gambogic acid (GA; C38H44O8, MW: 628.76), a polyprenylated xanthone and a widely used coloring agent, is the main active ingredient of gamboges secreted from the Garcinia hanburyi tree ([3, 4], which mainly grows in Southeast Asia. <br> GA has been approved by the Chinese FDA for the treatment of solid cancers in Phase II clinical trials.<br> <br> Pathways:<br> -evidence suggesting that it can inhibit thioredoxin reductase (TrxR).<br> -can indeed lead to an increase in reactive oxygen species (ROS) levels<br> -Gambogic acid can trigger mitochondrial dysfunction, leading to cytochrome c release<br> -influences death receptors<br> -Inhibition of NF-κB Signaling<br> -Inhibition of VEGF Pathway<br> -Cell Cycle Arrest:<br> -p53 Activation<br>
83
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GAR
Garcinol
NP
<b>Found</b> in dried fruit rind of Garcinia Indica with anti-inflammatory, antioxidant, anticancer, and antibacterial properties<br> Garcinia Cambogia Extract.<br> "We conclude that patients who are T-cadherin-positive could especially benefit from a therapy with garcinol."<br>
7
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GB
gefitinib, erlotinib
D
<b>selectively</b> targeting the mutant proteins in malignant cells. <br> epidermal growth factor receptor (EGFR) inhibitors (lung cancer)<br>
84
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GEM
Gemcitabine (Gemzar)
D
Chemo
<b>GEM</b> An IV antimetabolic antineoplastic used with cisplatin for inoperable non-small cell lung CA<br> Treats cancer of pancreas, lung, ovary and breast.<br>
85
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GEN
Genistein
NP
Estrogen-like activity
<b>Genistein</b> is a naturally occurring isoflavone predominantly found in soy products.<br> anticancer effects through several mechanisms:<br> -Modulation of Hormone Activity: can bind to estrogen receptors(hormone-dependent cancers like breast and prostate cancer).<br> -Inhibition of Cell Proliferation:- -inducing cell cycle arrest.<br> -Induction of Apoptosis:- by influencing pro- and anti-apoptotic regulators.<br> -Anti-inflammatory and Antioxidant Effects:-antioxidant properties help to neutralize ROS<br> -Anti-angiogenic Activity:may also inhibit tumor angiogenesis<br> <br> Key Cellular Signaling Pathways Involved<br> -Estrogen Receptor Signaling: interacting with estrogen receptors (ERα and ERβ)<br> -PI3K/Akt/mTOR Pathway:inhibits this pro-survival pathway, leading to reduced cell growth<br> -MAPK/ERK Pathway: can contribute to cell cycle arrest.<br> -NF-κB Pathway:may downregulate NF-κB, supporting a reduction in tumor-promoting inflammation.<br> -Wnt/β-catenin Pathway: involved in cell proliferation, differentiation, and oncogenic transformation.<br> <br> Dosages often ranging from approximately 40 mg to 100 mg per day for potential therapeutic effects. Genistein has limited bioavailability when ingested as part of the diet. Efforts to enhance its absorption include the use of specific formulations, such as those that combine genistein with other compounds or utilize novel delivery systems.<br>
86
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Ger
Germacranolide
NP
<b>A germacranolide sesquiterpene lactone (GSL)</b> was isolated from Siegesbeckia glabrescens<br>
87
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GE
Germanium
NP
<b>Essential microelement.</b> Common names include germanium-132 (Ge-132) and germanium sesquioxide. <br> Small amounts of germanium are found in certain minerals and plant products, including:<br> argyrodite<br> germanite<br> garlic<br> ginseng<br> aloe<br> comfrey<br> <br> On April 23, 2019 the Food and Drug Administration updated their ban on the import of all germanium-containing products that are promoted as drugs or dietary supplements for human consumption. The banned list includes but is not restricted to:<br> Germanium Sesquioxide<br> GE-132<br> GE-OXY-132<br> Vitamin “O””<br> Pro-Oxygen<br> Nutrigel 132<br> Immune Multiple<br> Germax<br>
88
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GI
Ginger/6-Shogaol/Gingerol
NP
<b>Flowering plant</b> uses ginger root for help with nausea, weight loss, arthritis, diabetes. Anti-inflammatory and antioxidant. <br> Gingerol is a phenolic phytochemical compound found in fresh ginger that activates heat receptors on the tongue. It is normally found as a pungent yellow oil in the ginger rhizome.<br>
89
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GB
Ginkgo biloba
NP
<b>Ginkgo biloba</b> from an ancient tree.<br>
219
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Gins
Ginseng
NP
<b>Ginseng (Panax ginseng)</b> – This herb has been studied for its ability to enhance the immune system.<br> -Antioxidant Properties: Ginseng contains ginsenosides, which have antioxidant properties.<br> -Immune System Support<br> -Inhibition of Tumor Growth<br> -Chemopreventive Effects<br> -Synergistic Effects with Cancer Treatments: ginseng may enhance the effectiveness of certain cancer treatments, such as chemotherapy, and may help reduce side effect<br> Dose: Standardized Extract:<br> Dosage: extract containing 4-7% ginsenosides 200-400mg/d<br> Dried Root:1-2g/d<br> Tea: 1-2g dried root, 1-3x/d<br>
90
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GlaB
Glabrescione B
NP
<b>Glabrescione B (GlaB)</b> was extracted and purified from seeds of Derris glabrescens (Leguminosae)<br>
335
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Gluc
Glucose
NP
<b>Glucose</b> is a fundamental energy source and its metabolism is essential for all cells, the reprogramming of glucose metabolism in cancer cells underlies many aspects of tumor growth and survival.<br> -Glucose generally aids cancer cells, but can be used as trojan horse.<br> -HIF-1 increases the expression of glycolytic enzymes<br> -Hexokinase II, which catalyzes the first step of glycolysis (often upregulated).<br>
225
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GlucDep
glucose deprivation
NP
<b>Tumor cells</b> use 200 times more glucose than healthy ones. Malignant tumor cells perform glycolysis at a ten times faster rate than their healthy tissue counterparts. While rapidly growing tumor cells do not have adequate vessels during their genesis, the limited capillary support often results in hypoxia within the tumor. In addition, some tumor cells overexpress specific glycolytic enzymes, resulting in higher glycolysis rates, referred to as the Warburg effect.<br>
180
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GoldNP
Gold NanoParticles
NP
<b>Gold NanoParticles</b> are often used as drug carrier. Has impressive optical properties.<br>
234
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Gos
Gossypol
NP
<b>Gossypol</b> is a natural compound found in cottonseed, a byproduct of the cotton industry. It has been studied for its potential anti-cancer properties. Research has shown that gossypol can inhibit the growth of various types of cancer cells, including breast, prostate, lung, and colon cancer.<br> <br> Gossypol's anti-cancer effects are thought to be due to its ability to:<br> <br> -Inhibit the activity of certain enzymes involved in cancer cell growth and survival<br> -Induce apoptosis (cell death) in cancer cells<br> -Inhibit the formation of new blood vessels that feed cancer cells (anti-angiogenesis)<br> -Modulate the immune system to attack cancer cells<br> <br> Some studies have also suggested that gossypol may have synergistic effects when combined with other anti-cancer agents, such as chemotherapy and radiation therapy.<br>
91
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Ge
Grapeseed extract
NP
<b>Made from seeds of grapes</b> and contains antioxidants Vitamin E, linolenic acid and OPCs.<br>
92
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Gra
Graviola
NP
<b>Soursop or Brazilian paw paw or guanabana.</b> People use fruit, roots, seeds and leaves. Graviola, also known as Annona muricata, is a tropical fruit-bearing tree native to the Americas.<br> GLUT1 inhibitor?<br> The major pathways involved in Graviola's anti-cancer effects include:<br> -Inhibition of glycolysis: Graviola extracts have been shown to inhibit the activity of lactate dehydrogenase (LDH), a key enzyme involved in glycolysis, the process by which cancer cells produce energy. By inhibiting LDH, Graviola reduces the production of lactate, a key metabolite that fuels cancer cell growth.<br> -Inhibition of glucose uptake: Graviola extracts have also been shown to inhibit the uptake of glucose by cancer cells, further reducing their energy production.<br> -Inhibition of the PI3K/AKT pathway: The PI3K/AKT pathway is a key signaling pathway involved in cell survival and proliferation. Graviola extracts have been shown to inhibit this pathway, leading to reduced cancer cell growth and survival.<br> -Induction of apoptosis: Graviola extracts have been shown to induce apoptosis in cancer cells by activating pro-apoptotic proteins and inhibiting anti-apoptotic proteins.<br> <br> The major compounds responsible for Graviola's anti-cancer effects are:<br> Annonaceous acetogenins: These are a group of compounds found in Graviola that have been shown to inhibit cancer cell growth and induce apoptosis.<br> Quercetin: A flavonoid found in Graviola that has been shown to inhibit cancer cell growth and induce apoptosis.<br>
93
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Hne
Helleborus niger extracts – Christmas Rose
NP
<b>Black hellebore</b> is a perennial herb with a shallow rhizome blossoming during winter.<br>
263
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HibSad
Hibiscus sabdariffa
NP
<b>Hibiscus sabdariffa</b> (commonly known as Roselle)<br> It is rich in bioactive components such as polyphenols, anthocyanins, flavonoids, organic acids, and other antioxidants.<br> Hibiscus sabdariffa is rich in antioxidants and bioactive compounds that show potential anti-cancer effects by reducing oxidative stress, inhibiting cell proliferation, inducing apoptosis, and modulating inflammatory pathways.<br>
334
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HOO
High-Ozonide Oil
NP
<b>High-ozonide oil</b>—which is oil that has been ozonated to form stable ozonide compounds.<br> • Ozone and its derivatives are highly reactive oxygen species (ROS). Some proposed theoretical mechanisms suggest that these reactive species may cause oxidative stress that could potentially lead to the death of cancer cells.<br> <br> • The same oxidative property, however, can also damage healthy cells and tissues if not arefully controlled, which creates concerns about therapeutic safety and side effects.<br> <br> <a href="https://www.thomashealthblog.com/?p=19903" >thomashealthblog.com </a><br>
94
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HNK
Honokiol
NP
<b>Honokiol</b> is a Lignan isolated from bark, seed cones and leaves of trees of Magnolia species. Honokiol was traditionally used for anxiety and stroke treatment, as well as the alleviation of flu symptoms.<br> -considered to have antioxidant properties<br> -low oral bioavailability and difficulty in intravenous administration<br> -the development of various formulations of honokiol, including microemulsion, liposomes, nanoparticles and micelle copolymers have successfully solved the problem of low water solubility.<br> <br> Pathways:<br> -Inhibit NF-κB activation<br> -Downregulate STAT3 signalin<br> -Inhibiting the PI3K/Akt pathway,<br> -Inhibition of mTOR<br> -Influences various MAPK cascades—including ERK, JNK, and p38<br> -Inhibition of EGFR<br> -Inhibiting Notch pathway (CSCs)<br> -GPx4 inhibit<br> -Can induce ER stress in cancer cells, which contributes to the activation of unfolded protein response (UPR) pathways<br> -Disrupt the mitochondrial membrane potential in cancer cells.<br> -Reported to increase ROS production in cancer cells<br> -Can exhibit antioxidant properties in normal cells. - has some inhibitor activity but Not classified as HDAC inhibitor as weaker and may work more indirectly.<br> - is well-known in the research community for its role in activating SIRT3<br> <br> -Note <a href="tbResList.php?qv=94&tsv=1109&wNotes=on&exSp=open">half-life</a> 40–60 minutes<br> <a href="tbResList.php?qv=94&tsv=792&wNotes=on&exSp=open">BioAv</a> <br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - induce <a href="tbResList.php?qv=94&tsv=275&wNotes=on">ROS</a> production in cancer cells, and typically lowers ROS in normal cells<br> - ROS↑ related: <a href="tbResList.php?qv=94&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?qv=94&tsv=103&wNotes=on">ER Stress↑</a>, <a href="tbResList.php?qv=94&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=94&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>, <a href="tbResList.php?qv=94&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?qv=94&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?qv=94&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?qv=94&tsv=239&wNotes=on">cl-PARP↑</a>, <a href="tbResList.php?qv=94&wNotes=on&word=HSP">HSP↓</a> <a href="tbResList.php?qv=94&wNotes=on&word=Prx">Prx</a><!-- mitochondrial antioxidant enzyme--> <br> - Raises <a href="tbResList.php?qv=94&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?qv=94&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>, <a href="tbResList.php?qv=94&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?qv=94&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?qv=94&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?qv=94&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?qv=94&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?qv=94&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?qv=94&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, Pro-Inflammatory Cytokines : <a href="tbResList.php?qv=94&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, <a href="tbResList.php?qv=94&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?qv=94&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓ inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.--> - inhibit Growth/Metastases : <a href="tbResList.php?qv=94&tsv=604&wNotes=on">TumMeta↓</a>, <a href="tbResList.php?qv=94&tsv=323&wNotes=on">TumCG↓</a>, <a href="tbResList.php?qv=94&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=94&tsv=204&wNotes=on">MMPs↓</a>, <a href="tbResList.php?qv=94&tsv=201&wNotes=on">MMP2↓</a>, <a href="tbResList.php?qv=94&tsv=203&wNotes=on">MMP9↓</a>, <a href="tbResList.php?qv=94&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=94&tsv=1284&wNotes=on">ROCK1↓</a>, <a href="tbResList.php?qv=94&tsv=273&wNotes=on">RhoA↓</a>, <a href="tbResList.php?qv=94&tsv=214&wNotes=on">NF-κB↓</a>, <a href="tbResList.php?qv=94&tsv=79&wNotes=on">CXCR4↓</a>, <a href="tbResList.php?qv=94&tsv=105&wNotes=on">ERK↓</a> <br> <!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, --> - reactivate genes thereby inhibiting cancer cell growth : <a href="tbResList.php?qv=94&tsv=140&wNotes=on">HDAC↓</a>, <a href="tbResList.php?qv=94&tsv=108&wNotes=on">EZH2↓</a>, <a href="tbResList.php?qv=94&tsv=236&wNotes=on">P53↑</a>, <a href="tbResList.php?qv=94&wNotes=on&word=HSP">HSP↓</a>, <br> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?qv=94&tsv=322&wNotes=on">TumCCA↑</a>, <a href="tbResList.php?qv=94&tsv=73&wNotes=on">cyclin D1↓</a>, <a href="tbResList.php?qv=94&tsv=378&wNotes=on">cyclin E↓</a>, <a href="tbResList.php?qv=94&tsv=467&wNotes=on">CDK2↓</a>, <a href="tbResList.php?qv=94&tsv=894&wNotes=on">CDK4↓</a>, <a href="tbResList.php?qv=94&tsv=895&wNotes=on">CDK6↓</a>, <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?qv=94&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?qv=94&tsv=324&wNotes=on">TumCI↓</a>, <a href="tbResList.php?qv=94&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=94&tsv=96&wNotes=on">EMT↓</a>, <br> <!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS --> - inhibits <a href="tbResList.php?qv=94&tsv=129&wNotes=on">glycolysis</a> and <a href="tbResList.php?qv=94&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> : <a href="tbResList.php?qv=94&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=94&tsv=35&wNotes=on">cMyc↓</a>, <a href="tbResList.php?qv=94&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>, <a href="tbResList.php?qv=94&tsv=906&wNotes=on">LDH↓</a>, <a href="tbResList.php?qv=94&tsv=175&wNotes=on&word=LDH">LDHA↓</a>, <a href="tbResList.php?qv=94&tsv=773&wNotes=on">HK2↓</a>, <a href="tbResList.php?qv=94&wNotes=on&word=PDK">PDKs↓</a>, <a href="tbResList.php?qv=94&tsv=847&wNotes=on">ECAR↓</a>, <a href="tbResList.php?qv=94&tsv=230&wNotes=on">OXPHOS↓</a>, <a href="tbResList.php?qv=94&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=94&tsv=623&wNotes=on">GlucoseCon↓</a> <br> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - inhibits <a href="tbResList.php?qv=94&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=94&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=94&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=94&wNotes=on&word=NOTCH">Notch↓</a>, <a href="tbResList.php?qv=94&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, <br> <!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, --> - inhibits Cancer Stem Cells : <a href="tbResList.php?qv=94&tsv=795&wNotes=on">CSC↓</a>, <a href="tbResList.php?qv=94&tsv=677&wNotes=on">CD133↓</a>, <a href="tbResList.php?qv=94&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=94&tsv=656&wNotes=on">sox2↓</a>, <a href="tbResList.php?qv=94&tsv=1024&wNotes=on">nestin↓</a>, <a href="tbResList.php?qv=94&tsv=508&wNotes=on">OCT4↓</a>, <br> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=94&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=94&tsv=4&wNotes=on">AKT↓</a>, <a href="tbResList.php?qv=94&wNotes=on&word=JAK">JAK↓</a>, <a href="tbResList.php?qv=94&wNotes=on&word=STAT">STAT↓</a>, <a href="tbResList.php?qv=94&tsv=377&wNotes=on">Wnt↓</a>, <a href="tbResList.php?qv=94&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=94&tsv=9&wNotes=on">AMPK</a>, <a href="tbResList.php?qv=94&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=94&tsv=168&wNotes=on">JNK</a>, <a href="tbResList.php?qv=94&wNotes=on&word=Trx">TrxR**</a>, - Shown to modulate the nuclear translocation of <a href="tbResList.php?qv=94&tsv=1132&wNotes=on&exSp=open&word=SREBP2">SREBP-2</a> (related to cholesterol).<br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=94&tsv=1106&wNotes=on">chemo-sensitization</a>, <a href="tbResList.php?qv=94&tsv=1171&wNotes=on">chemoProtective</a>, <a href="tbResList.php?qv=94&tsv=1107&wNotes=on">RadioSensitizer</a>, <a href="tbResList.php?qv=94&tsv=1185&wNotes=on">RadioProtective</a>, <a href="tbResList.php?qv=94&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <a href="tbResList.php?qv=94&tsv=1105&wNotes=on">Neuroprotective</a>, <a href="tbResList.php?qv=94&tsv=557&wNotes=on">Cognitive</a>, <a href="tbResList.php?qv=94&tsv=1175&wNotes=on">Renoprotection</a>, <a href="tbResList.php?qv=94&tsv=1179&wNotes=on">Hepatoprotective</a>, <a href="tbResList.php?&qv=94&tsv=1188&wNotes=on">CardioProtective</a>, <br> <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=94&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br>
220
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Hops
Hops (Humulus lupulus)
NP
<b>Hops (Humulus lupulus)</b> – Hops (known for beer brewing) contain compounds like xanthohumol that have demonstrated anticancer activity, particularly in breast and prostate cancer.<br> -Phytochemicals, including flavonoids and polyphenols, which have antioxidant properties.<br> -8-prenylnaringenin, may have estrogenic effects. (Hormone related cancers)<br> -Anti-inflammatory properties <br> Dose: Tea 1-3g/d, 1-3x/d. Extract 300-500mg/d<br>
243
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HRT
Hormone replacement therapy
D
<b>Hormone replacement therapy</b> <br>
295
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H2
Hydrogen Gas
NP
<b>Hydrogen Gas</b>, Powerful Antioxidant <br> <br> 1.Antioxidant and Nrf2/ARE Pathway: activate Nrf2, which induces antioxidant enzymes. <br> 2.NF-κB Pathway: reported to inhibit NF-κB activation, thereby reducing inflammatory cytokine production <br> 3.Mitochondrial Apoptosis Pathway <br> 4.MAPK (Mitogen-Activated Protein Kinases) Pathway <br> 5.PI3K/Akt/mTOR Pathway <br> 6.Inflammatory Cytokine Signaling: Reducing cytokines (such as IL-6, TNF-α) <br> 7.p53 Pathway <br> 8.Autophagy Pathways: might regulate autophagy, (dual roles in cancer) <br> <br> <a href="https://suiso-madoguchi.com/product/11/">Example unit sometimes used in studies</a><br> <a href="https://qlifecanada.ca/">Example Canadian Supplier</a><br> <br> Hydrogen gas can be generated in small amount by hydrogenase of certain members of the human gastrointestinal tract microbiota from unabsorbed carbohydrates in the intestine through degradation and metabolism, which then is partially diffused into blood flow and released and detected in exhaled breath, indicating its potential to serve as a biomarker.<br> <br> <a href="tbResList.php?qv=295&wNotes=on">Many studies</a> have shown that H2 therapy can reduce oxidative stress. This, however, contradicts radiation therapy and chemotherapy, in which ROS are required to induce apoptosis and combat cancer. Yet many studies show <a href="tbResList.php?qv=295&tsv=1171&wNotes=on">chemoprotective</a> and <a href="tbResList.php?qv=295&tsv=1185&wNotes=on">radioprotective</a> and some even show <a href="tbResList.php?qv=295&tsv=1106&wNotes=on">chemosentizing</a> <br> Nevertheless there are some papers claiming <a href="tbResList.php?qv=295&&tsv=275&esv=2&exSp=open&wNotes=on"> ROS ↑</a> for cancer cells<br> <br>
271
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HCQ
hydroxychloroquine
RD
<b>Chloroquine (and its analogue hydroxychloroquine)</b><br> Hydroxychloroquine (more commonly used because of its safety profile) <br> Chloroquine originates from synthetic modifications of quinoline derivatives (it has roots in natural alkaloids like quinine) and is now produced through chemical synthesis. Its repurposing in cancer therapy centers on its ability to disrupt autophagy and lysosomal function, modulate the immune response within the tumor microenvironment, and sensitize cancer cells to chemo- and radiotherapy. <br> Chloroquine is a synthetic derivative belonging to the 4-aminoquinoline class. It was initially developed in the 1930s from quinoline scaffolds, which themselves are derived from naturally occurring alkaloids like quinine (isolated from the bark of the cinchona tree). Unlike natural products that are directly extracted, chloroquine is produced by chemical synthesis in pharmaceutical laboratories.<br> <br> Pathways:<br> -Autophagy Inhibition: By raising intralysosomal pH, chloroquine impairs the fusion of autophagosomes with lysosomes, thereby blocking autophagic flux. This inhibition can sensitize tumor cells to chemotherapy and enhance cell death.<br> -Lysosomal Dysfunction: Chloroquine accumulates in lysosomes, altering their function. This can lead to lysosomal membrane permeabilization and subsequent activation of cell death pathways.<br> -Stress-Related Signaling: Chloroquine-induced disruption of autophagy can lead to the accumulation of damaged proteins and organelles, triggering stress responses such as the unfolded protein response (UPR) and reactive oxygen species (ROS) generation.<br> -TLR (Toll-Like Receptor) Signaling: There is evidence suggesting that chloroquine can inhibit TLR9 signaling<br> <br> Chemo- and Radiosensitization:<br> -One of the promising uses of chloroquine in oncology is as an adjuvant to standard therapies.<br> -By disrupting autophagy—a mechanism that many cancer cells use to survive after treatment—chloroquine can enhance the cytotoxic effects of chemotherapy and radiation. <br> <br> Hydroxychloroquine (more commonly used because of its safety profile) have used doses ranging from 400 mg per day up to 1200 mg per day in divided doses.<br> <br> Chloroquine effectiveness is pH sensitive: CQ concentrations in the whole-cell lysate were 7-fold lower at pH 6.8 as compared with pH 7.4<br>
95
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HCAs
Hydroxycinnamic-acid
NP
<b>Hydroxycinnamic acid</b> compounds (p-coumaric, caffeic acid (CA), ferulic acid) occur most frequently as simple esters with hydroxy carboxylic acids or glucose, while the hydroxybenzoic acid compounds (p-hydroxybenzoic, gallic acid, ellagic acid) are present mainly in the form of glucosides. https://www.sciencedirect.com/topics/chemistry/hydroxycinnamic-acid<br> <br> -Ferulic acid and p‐coumaric acid are naturally occurring hydroxycinnamic acids found in many plant-based foods (such as whole grains, fruits, and vegetables)<br> <br> CA showed pro-oxidant potential due to its ability to interact with metals like copper, inducing lipid peroxidation and causing DNA damage within tumor cells through either oxidation or covalent adduct formation.<br> <br> Summary:<br> -Such as caffeic acid, ferulic acid, and sinapic acid (SA)<br> -Increase sensitivity to chemotherapy<br> -Bioavailability is problem. Use liposome (phospholipid vesicles) or encapsulation<br> -Propolis has caffeic acid (Caffeic acid (0.639–4.172 mg/g propolis)<br> -SA at higher concentrations acts as a potent pro-oxidant agent<br> -SA acts in collaboration with other chemotherapeutic agents to improve treatment sensitivity. -Improve capacity of CA and CAPE in cancer suppression, it has been co-administered with other anti-tumor compounds such as gallic acid<br> -Combination of caffeic acid and endogenous copper ions can result in oxidative damage<br> -Ferulic Acid (popcorn): upregulate apoptotic protein and downregulate anti-apoptotic protein.upregulating (BAX), (p53), (CYCS) and downregulating (Bcl-2),<br>
96
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HCA
HydroxyCitric Acid
NP
<b>HCA</b> is a naturally occurring compound primarily known for its potential effects on appetite and lipid metabolism via inhibition of ATP citrate lyase.<br> Derivative of citric acid that is found in a variety of tropical plants including Garcinia cambogia and Hibiscus sabdariffa<br> <br> • Hydroxy-Citric Acid (HCA) is a compound extracted from Garcinia cambogia, primarily recognized for its potential effects on lipid metabolism and appetite suppression.<br> • It has been proposed to inhibit the enzyme ATP citrate lyase, which is involved in converting citrate into acetyl-CoA—a key step in fatty acid synthesis.<br> • By modulating lipid synthesis pathways, HCA has been studied in the context of obesity and metabolic disorders, with some exploratory research considering its implications in cancer metabolism.<br> <br> • Inhibition of ATP Citrate Lyase (ACLY)******<br> ACLY converts citrate into acetyl-CoA, a building block for fatty acid and cholesterol synthesis. Many cancer cells upregulate lipid synthesis to support membrane production and energy storage; hence, inhibiting ACLY presents a potential strategy to disrupt cancer cell metabolism.<br> <br> • Impact on Lipogenesis<br> Reduced acetyl-CoA production can impair de novo lipogenesis, potentially limiting the proliferation of rapidly dividing cells that have high lipid demands.<br> <br> • Interactions with Other Metabolic Pathways (modulation of citrate levels may affect the TCA cycle)<br> <br> -Dosages used in weight loss studies typically ranging from 500 mg to 1500 mg per day<br> Human cyclists: 3.1 mL/kg body wt of an HCA solution (19 g/L) --> 248mg<br> "Studies have shown that humans can safely ingest 13.5 g of hydroxycitrate per day with plasma levels of 82 mg/L (0.39 mM) achieved"<br> Typically, HCA used in dietary weight loss supplement is bound to calcium, which results in a poorly soluble (<50%) and less bioavailable form. Conversely, the structural characteristics of a novel Ca2+/K+ bound (-)-HCA salt (HCA-SX or Super CitriMax) make it completely water soluble as well as bioavailable.<br> <br> -HydroxyCitrate (HCA) typically used in a dose of about 1.5g/day or more for cancer (inhibition of the Melavonate Pathway?)<br>
229
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HTyr
Hydroxytyrosol
NP
<b>Hydroxytyrosol (HT)</b>, abundantly present in olives, has demonstrated anticancer properties. HT exhibited antiproliferative and pro-apoptotic effects in cancer cells through H2O2 generation. The mechanism of prooxidant activity of HT involves O2 and transition metals. First, the phenol moiety undergoes oxidation by Cu(II) or Fe(II), forming semiquinones, which then react with O2 generating O2•− and finally producing H2O2.<br>
97
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HP
Hyperoside
NP
<b>Hyperoside</b> is a chemical compound and a quercetin galactoside. It is found in various plants and has antibacterial, antifungal and UV blocking properties.<br> Hyperoside is an active ingredient in plants, such as Hypericum monogynum in Hypericaceae, Crataegus pinnatifida in Rosaceae and Polygonum aviculare in Polygonaceae.<br> Hyperoside is a natural flavonol glycoside in various plants, such as Crataegus pinnatifida Bge, Forsythia suspensa, and Cuscuta chinensis Lam.<br>
98
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HPT
Hyperthermia
T
<b>Mild Hyperthermia</b> (Approximately 39°C to 41°C<br> Pathways and Effects:<br> -Heat Shock Protein (HSP) Induction: Mild heat stress triggers the production of HSPs (e.g., HSP70, HSP90) that help cells cope with stress, which can sometimes provide a transient protective effect. However, these proteins can also act as immunomodulators.<br> -Modulation of the Immune System: Mild hyperthermia can enhance dendritic cell activation and improve antigen presentation, leading to the stimulation of anti-tumor immune responses.<br> -Vasodilation: Increased blood flow and improved oxygenation can sensitize tumors to radiation therapy and certain chemotherapeutics.<br> <br> Moderate Hyperthermia (Approximately 41°C to 43°C)<br> Pathways and Effects:<br> -Enhanced Cytotoxicity: At temperatures in this range, tumor cells become more vulnerable to radiation and some chemotherapeutic agents. This is partly due to the inhibition of DNA repair pathways.<br> -Increased Permeability: Moderate heat can increase the permeability of cellular membranes, aiding in drug delivery and the uptake of chemotherapeutic agents.<br> -Induction of Apoptosis: Elevated temperatures can trigger apoptotic signaling pathways in cancer cells, sometimes in conjunction with other therapies.<br> <br> High Hyperthermia / Thermal Ablation (Approximately 43°C to 50°C and above)<br> Pathways and Effects:<br> -Direct Cytotoxicity: High temperatures can lead to protein denaturation, membrane disruption, and direct cell death.<br> -Coagulative Necrosis: Sustained high temperatures cause irreversible cell injury leading to necrosis of tumor tissues.<br> -Vascular Damage: Hyperthermia in this range can damage tumor vasculature, reducing blood supply and indirectly causing tumor cell death.<br> -Enhanced Immune Response: Although high temperatures can cause immediate cell death, the release of tumor antigens and damage-associated molecular patterns (DAMPs) can stimulate an anti-tumor immune response<br>
9
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IMA
imatinib
D
<b>Inhibitor</b> of the tyrosine kinase enzyme BCR-ABL for chronic myelogenous leukemia<br>
207
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immuno
immunotherapy
T
<b>PD-1 blockade antibody therapy</b> is one of the cornerstone approaches in modern cancer immunotherapy.<br> Under normal physiological conditions, when PD-1 binds to its ligands (PD-L1 or PD-L2) on other cells, it functions as a "checkpoint" to reduce overly active T cell responses and prevent autoimmunity.<br> PD-1 blockade therapies involve monoclonal antibodies that target either PD-1 or its ligand PD-L1.<br> • By blocking the interaction between PD-1 and its ligands, these antibodies effectively release the "brakes" on T cells.<br> • The re-activated T cells can then recognize and destroy cancer cells more efficiently.<br>
99
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I3C
Indole-3-carbinol
NP
<b>Found</b> in broccoli, cabbage, cauliflower, brussel sprouts, collard greens and kale.<br>
100
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InA
Inoscavin A
NP
<b>Inoscavin A</b> was obtained from Sanghuangporus vaninii by the classic phytochemical separation technology.<br>
101
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Ins
Inositol
NP
<b>Inositol</b> is a form of sugar your body needs to grow.<br>
102
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IP
Inulin Prebiotic
NP
Prebiotic
<b>chicory root</b><br>
310
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iod
iodine
NP
<b>Iodine</b> deficiency can lead to thyroid enlargement (goiter) and hypothyroidism. In severe cases, longstanding iodine deficiency has been linked to an increased risk of developing certain thyroid disorders, including thyroid nodules and, less frequently, thyroid cancer.<br> <br> -Preliminary clinical research have suggested that molecular iodine may have antioxidant properties, modulate cell differentiation, and even exert antiproliferative effects in certain tissues.<br>
103
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IP6
IP6 (Inosital 1,2,3,4,5,6-hexakisphosphate)
NP
<b>Vitamin</b> like substance. Found in cereals, nuts and legumes.<br> Inositol hexaphosphate (IP6) is a dietary component that constitutes approximately 1 to 5% of the weight of most cereals, nuts, oil seeds, legumes, and grains [1, 2]. In particular, approximately 9.5 to 14.5% of the weight of rice bran is composed of IP6. <br> <br> • Antioxidant Activity<br> – IP6 can chelate metal ions and scavenge free radicals, thereby reducing oxidative stress and preventing DNA damage that could initiate or promote cancer.<br> <br> • Modulation of Signal Transduction Pathways<br> – IP6 influences key pathways such as PI3K/Akt and MAPK, which are involved in cell survival, growth, and proliferation. Its modulation can lead to reduced cell proliferation and enhanced apoptotic signaling.<br> <br> • Induction of Apoptosis<br> – By activating pro-apoptotic factors and suppressing anti-apoptotic proteins, IP6 promotes programmed cell death in cancer cells.<br> <br> • Cell Cycle Arrest<br> – IP6 has been shown to interfere with cell cycle progression, particularly by regulating cyclin-dependent kinases. This arrest can prevent the rapid and uncontrolled division of cancer cells.<br> <br> • Promotion of Cell Differentiation<br> – IP6 may encourage malignant cells to differentiate into more normal cell types, which typically have reduced proliferative abilities and lower tumorigenic potential.<br> <br> • Inhibition of Angiogenesis<br> – By disrupting the signals needed for new blood vessel formation, IP6 can limit the tumor’s blood supply, thereby restricting tumor growth and metastasis.<br> <br> • Immune Modulation<br> – Some studies suggest that IP6 may enhance the immune response against tumors, contributing to its overall anti-cancer activity.<br>
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lpi
ipilimumab
IM
Immunomodulatory antibodies
<b>Two</b> different inhibitory pathways that block antitumor T cell responses. <br>
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Fe
Iron
NP
<b>Metal</b><br> Iron is a vital trace element that plays essential roles in various physiological processes. Its importance stems from its involvement in oxygen transport, energy production, DNA synthesis, and numerous enzymatic reactions. <br> – Iron is a critical component of hemoglobin in red blood cells, enabling the binding and transport of oxygen from the lungs to tissues.<br> – Iron participates in redox reactions due to its ability to alternate between ferrous (Fe²⁺) and ferric (Fe³⁺) states.<br> <br> Tumor cells often require increased iron to support their rapid proliferation and metabolic demands. – Elevated iron availability can promote DNA synthesis, cell division, and tumor growth.<br> <br> • Promotion of Reactive Oxygen Species (ROS) Formation:<br> – Iron’s redox-active nature, while important for normal cell functions, can also lead to the generation of reactive oxygen species via reactions such as the Fenton reaction:<br> Fe²⁺ + H₂O₂ → Fe³⁺ + •OH + OH⁻<br> – The hydroxyl radicals (•OH) produced are highly reactive and can cause oxidative damage to cellular components (DNA, proteins, lipids).<br> – This oxidative damage may contribute to genomic instability, mutations, and the progression of cancer.<br> <br> Cancer cells often exhibit increased iron dependency, targeting iron metabolism is a strategy that is being explored for cancer therapy.<br> – Approaches include the use of iron chelators to sequester iron and limit its availability to tumor cells, thereby inhibiting their growth.<br> – Alternatively, therapies may aim to exploit iron’s capacity to generate toxic ROS beyond a threshold that cancer cells can manage, leading to selective cell death.<br>
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isoFl
isoflavones
NP
<b>Isoflavones</b> occur in many plant species, but are especially high in soybeans.<br> Major isoflavones in soybean are genistein and daidzein<br> Supplementation may help lower the risk of hormone-related cancers.<br>
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itraC
itraconazole
RD
<b>Itraconazole</b> is a medication used in the management and treatment of fungal infections.<br> <br> Cancer pathways:<br> -inhibit VEGF<br> -inhibit Hedghog Signaling Pathway<br> -P-glycoprotein Inhibition<br> -mTOR Pathway<br>
10
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IVM
Ivermectin
RD
<b>Medication</b> that treats some parasitic diseases<br>
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JG
Juglone
NP
<b>Found</b> in roots, leaves, nut-hulls, bark and wood of walnut trees.<br> Juglone (5-hydroxy-1,4-naphthoquinone) <br> Juglans nigra refers to the black walnut tree, which is one of the most well-known sources of juglone<br> -Research has focused on the hulls (the green outer covering of the walnut) because they have the highest concentrations.<br> -Fresh hulls can contain juglone levels in the range of approximately 1–5% of the dry weight<br> <br> -Juglone can redox cycle to generate reactive oxygen species (ROS). <br> -Increasing Bax, decreasing Bcl‑2, caspase activation, and MMP depolarization.<br> -Modulation of MAPK pathways (including ERK, JNK, and p38) <br> -May inhibit NF‑κB signaling<br> -Cause DNA damage or stress that, in turn, leads to p53 pathway activation— Pin1 Inhibition<br> –Pin1, a peptidyl-prolyl cis/trans isomerase, is frequently overexpressed in cancer.<br> <br> -ic50 maybe 5-10uM<br> -For matching 5uM, crude estimate is 5mg consumption of juglone required which might be 1.5 g of black walnut hull material<br>
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KaempF
Kaempferol
NP
<b>Kaempferol</b>—an abundant flavonoid found in various fruits, vegetables, and medicinal herbs—affects cancer cell behavior<br> <br> Pathways:<br> -Inhibit the PI3K/Akt signaling<br> -Modulation of the MAPK pathway (including ERK1/2) <br> -Inhibit NF-κB Signaling Pathway<br> -can upregulate or activate p53-dependent pathways<br> -Inhibitory action on STAT<br> -Activation of AMPK<br> -Reduce VEGF<br> -Can induce oxidative stress in cancer cells (ROS)<br>
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L-A
L-Alinine
NP
<b>Non-essential amino acid</b>. Helps build proteins in the body.<br>
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L-Orn
L-ornithine
NP
<b>Amino acid</b> that is made in the body and might help to increase arginine and hormones.<br>
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LA
Lactobacillus
NP
Bacteria
<b>Lactobacillus acidophilus</b>: Gram-positive, homofermentative, anaerobic microbe <br> Lactobacillus johnsonii: probiotic bacteria found in the human body and fermented foods. <br> Lactobacillus Plantarum: probiotic bacterium that may help with inflammation, blood sugar<br> <br> Lactobacillus crispatus<br> Lactobacillus rhamnosus<br>
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LF
Lactoferrin
NP
<b>Lactoferrin</b> is a protein in human and animal milk that helps regulate iron absorption and fight infections.Found in milk, saliva, tears and nasal secretions.<br>
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Lae
Laetrile B17 Amygdalin
NP
Sourced from apricot kernels
<b>Banned</b> in some states. May cause cyanide poisoning.<br> Laetrile B17 (Amygdalin )<br> Summary:<br> -Activation of the caspase-3 protease and downregulating Bcl-2, upregulates BAX<br> -Bax-to-Bcl-2 ratio and caspase-3 activity were increased<br> -Inhibits NF-kβ and NLRP3 signaling pathways<br> -Release of cyanide through the decomposition of amygdalin by the gut microfloral B-glucosidase enzyme. (bad)<br> -IV might be better to avoid the digestive tract which could convert to hydrogen cyanide.????<br> <br> Selective Toxicity (some challenges to this statement)<br> The amygdalin itself is not toxic, but the HCN released from it causes the amygdalin toxic effect [35]. Cancer cells are dominant in anaerobic glycolysis and β -glucosidase is at its highest activity in lactate-induced acidic conditions [36]. Therefore, cancer cells have a high level of the unlocking enzyme β -glucosidase activity that breaks down amygdalin, leading to the release of HCN On the other hand, normal cells are normo-oxygenated and contain low levels of the β -glucosidase enzyme as well as high levels of rhodanese enzyme which transforms hydrogen cyanide into harmless thiocyanate [46, 47]. Thiocyanate has positive effects on organisms such as lowering blood pressure and is also considered a precursor for vitamin B12.<br> <br> It is poisonous when combined with plant-rich beta-glucosidase.<br> Upon ingestion, amygdalin is hydrolyzed to cyanide by beta-glucuronidase in the small intestine [2]. Oral intake of 500 mg of amygdalin may contain as much as 30 mg of cyanide [3]. Oral amygdalin is estimated to be 40 times more potent than intravenous form due to its enzymatic conversion to hydrogen cyanide in the gastrointestinal tract [4]. <br>
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lamb
lambertianic acid
NP
<b>Lambertianic acid</b> is a naturally occurring diterpenoid, derived from Pinus koraiensis<br> <br> Pathways:<br> -inhibit the STAT3 signaling<br> -suppress NF-κB activation<br> -PI3K/Akt pathway<br> -inhibit PKM2<br> -increase ROS<br>
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LapC
Lapachol
NP
<b>Lapachol</b> is a natural naphthoquinone originally derived from the heartwood of the lapacho tree (Tabebuia species).<br> <br> Pathways:<br><br> Oxidative Stress and ROS Generation<br> –Like many quinones, lapachol can undergo redox cycling that generates reactive oxygen species (ROS).<br> -Oxidative damage to DNA, proteins, and lipids, thereby promoting cancer cell death.<br> -cell cycle at specific checkpoints (commonly at G0/G1 or G2/M phases)<br> -Inhibition of the NF‑κB signaling pathway<br> –MAPK Pathways<br> <br> -ic50 cancer cells 10-50uM, normal cells higher (existence of a therapeutic window)<br>
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Lap
Lapatinib
D
<b>Lapatinib</b> is a tyrosine kinase inhibitor primarily used in the treatment of HER2-positive breast cancer, among other cancer types. Its mechanism of action involves binding to the intracellular ATP-binding sites of the HER1 (also known as EGFR) and HER2 receptors, thereby inhibiting their autophosphorylation and subsequent activation of downstream signaling pathways. The major pathways involved include:<br> -PI3K/AKT/mTOR Pathway<br> Inhibition of this pathway leads to reduced cell survival and proliferation, as it normally promotes growth and survival signals through downstream effectors.<br> -RAS/RAF/MEK/ERK (MAPK) Pathway<br> Blocking the activation of this cascade affects cell cycle progression, proliferation, and differentiation. In many cancers, dysregulation of this pathway contributes to uncontrolled growth.<br> <br> By interfering with these signaling cascades, lapatinib can reduce tumor cell proliferation, induce apoptosis (programmed cell death), and potentially increase the sensitivity of tumor cells to additional therapeutic agents.<br> <br> The induction of oxidative stress is one of the ways by which lapatinib can exert cytotoxic effects on cancer cells. Elevated ROS levels can damage cellular components, such as lipids, proteins, and DNA, thereby contributing to cell death.<br>
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Las
Lasiodin
NP
<b>Lasiodin (Lasiokaurin)</b> is a diterpene compound from the plant Camellia sinensis
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LEC
Lecithin
NP
<b>Lecithin</b> a phospholipid-rich compound (often derived from soy or sunflower), can enhance the bioavailability of certain lipophilic (fat-soluble) and amphipathic compounds by improving their solubility, absorption, and cellular uptake.<br> <br> Supplements and Compounds with Improved Bioavailability via Lecithin<br> Curcumin Up to 20–30x better absorption in some formulations<br> Quercetin<br> Resveratrol<br> Silybin (from milk thistle)<br> Green tea catechins, EGCG Lecithin helps stabilize and protect catechins during digestion<br> Boswellic acids<br> Coenzyme Q10 (CoQ10)<br> Omega-3 fatty acids<br> Vitamin D, E, A, K (Fat-soluble vitamins)<br> Alpha-lipoic acid (ALA)<br> black seed oil (Nigella sativa) and its key active compound, thymoquinone.<br> <br> <br> <br>
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LE
Licorice
NP
<b>Glycyrrhizic acid (GA)</b> is a significant constituent of licorice root.<br> Glycyrrhizin, the main active component obtained from licorice roots, has many pharmacological and biological functions such as protecting liver cells, anti-inflammation, anti-virus, immunomodulation, has been widely applied in the treatment of clinically related hepatic diseases (Dastagir & Rizvi, 2016). Glycyrrhizin is a natural inhibitor of HMGB1<br>
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lign
lignans
NP
<b>Lignans</b> are a group of polyphenolic compounds found in various plant-based foods, particularly in seeds (especially flaxseeds), whole grains, fruits, and vegetables. They are known for their antioxidant properties and potential health benefits, including their role in cancer prevention.<br> Phytoestrogens: Lignans are classified as phytoestrogens, which means they can mimic estrogen in the body. This property is particularly relevant in the context of hormone-related cancers, such as breast and prostate cancer. <br> Antioxidant Activity: Lignans possess antioxidant properties, which can help protect cells from oxidative stress and damage. <br> Anti-Inflammatory Effects: Some research indicates that lignans may have anti-inflammatory effects, which could be beneficial since chronic inflammation is associated with the development and progression of cancer.<br>
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Lip
Lipoic acid
NP
<b>Fatty acid</b> helps convert blood sugar into energy. Also known as Alpha-lipoic acid.F<br>
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LDN
low dose naltrexone
RD
<b>Naltrexone</b> is a medication primarily used to treat opioid addiction and alcohol dependence. Some studies suggest that low-dose naltrexone (LDN) may have anti-cancer properties.<br> LDN has been shown to inhibit the growth of certain types of cancer cells, including breast, lung, and colon cancer cells, in laboratory studies.<br>
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LT
Luteolin
NP
<b>Luteolin</b> a Flavonoid found in celery, parsley, broccoli, onion leaves, carrots, peppers, cabbages, apple skins, and chrysanthemum flowers.<br> -MDR1 expression, MMP-9, IGF-1 and Epithelial to mesenchymal transition.<br> <br> *** ACTIVE WORK IN PROGRESS**<br> <br> -Note <a href="tbResList.php?qv=118&tsv=1109&wNotes=on&exSp=open">half-life</a> 2–3 hours<br> <a href="tbResList.php?qv=118&tsv=792&wNotes=on&exSp=open">BioAv </a> low, but could be improved with Res, or blend of castor oil, kolliphor and polyethylene glycol <br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - induce <a href="tbResList.php?qv=118&tsv=275&wNotes=on">ROS</a> production in cancer cell but a few reports of reduction. Always seems to reduce ROS in normal cells.<br> - ROS↑ related: <a href="tbResList.php?qv=118&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?qv=118&tsv=103&wNotes=on">ER Stress↑</a>, <a href="tbResList.php?qv=118&tsv=459&wNotes=on">UPR↑</a>, <a href="tbResList.php?qv=118&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=118&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>, <a href="tbResList.php?qv=118&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?qv=118&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?qv=118&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?qv=118&tsv=239&wNotes=on">cl-PARP↑</a>, <a href="tbResList.php?qv=118&wNotes=on&word=HSP">HSP↓</a> <br> <!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, --> - Lowers AntiOxidant defense in Cancer Cells: <a href="tbResList.php?qv=118&tsv=226&wNotes=on&word=NRF2↓">NRF2↓</a>, <a href="tbResList.php?qv=118&tsv=298&wNotes=on&word=SOD↓">SOD↓</a>, <a href="tbResList.php?qv=118&tsv=137&wNotes=on&word=GSH↓">GSH↓</a> <a href="tbResList.php?qv=118&tsv=46&wNotes=on">Catalase↓</a> <a href="tbResList.php?qv=118&tsv=597&wNotes=on">HO1↓</a> <a href="tbResList.php?qv=118&wNotes=on&word=GPx">GPx↓</a> <br> - Raises <a href="tbResList.php?qv=118&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?qv=118&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>, <a href="tbResList.php?qv=118&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?qv=118&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?qv=118&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?qv=118&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?qv=118&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?qv=118&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?qv=118&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, <a href="tbResList.php?qv=118&tsv=235&wNotes=on&word=p38↓">p38↓</a>, Pro-Inflammatory Cytokines : <a href="tbResList.php?qv=118&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, <a href="tbResList.php?qv=118&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?qv=118&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓ inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.--> - inhibit Growth/Metastases : <a href="tbResList.php?qv=118&tsv=604&wNotes=on">TumMeta↓</a>, <a href="tbResList.php?qv=118&tsv=323&wNotes=on">TumCG↓</a>, <a href="tbResList.php?qv=118&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=118&tsv=201&wNotes=on">MMP2↓</a>, <a href="tbResList.php?qv=118&tsv=203&wNotes=on">MMP9↓</a>, <a href="tbResList.php?qv=118&tsv=308&wNotes=on">TIMP2</a>, <a href="tbResList.php?qv=118&tsv=415&wNotes=on">IGF-1↓</a>, <a href="tbResList.php?qv=118&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=118&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?qv=118&tsv=273&wNotes=on">RhoA↓</a>, <a href="tbResList.php?qv=118&tsv=214&wNotes=on">NF-κB↓</a>, <a href="tbResList.php?qv=118&tsv=79&wNotes=on">CXCR4↓</a>, <a href="tbResList.php?qv=118&tsv=105&wNotes=on">ERK↓</a> <br> <!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, --> - reactivate genes thereby inhibiting cancer cell growth : <a href="tbResList.php?qv=118&tsv=140&wNotes=on">HDAC↓</a>, <a href="tbResList.php?qv=118&tsv=85&wNotes=on">DNMT1↓</a>, <a href="tbResList.php?qv=118&tsv=86&wNotes=on">DNMT3A↓</a>, <a href="tbResList.php?qv=118&tsv=108&wNotes=on">EZH2↓</a>, <a href="tbResList.php?qv=118&tsv=236&wNotes=on">P53↑</a>, <a href="tbResList.php?qv=118&wNotes=on&word=HSP">HSP↓</a>, <br> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?qv=118&tsv=322&wNotes=on">TumCCA↑</a>, <a href="tbResList.php?qv=118&tsv=73&wNotes=on">cyclin D1↓</a>, <a href="tbResList.php?qv=118&tsv=378&wNotes=on">cyclin E↓</a>, <a href="tbResList.php?qv=118&tsv=467&wNotes=on">CDK2↓</a>, <a href="tbResList.php?qv=118&tsv=894&wNotes=on">CDK4↓</a>, <a href="tbResList.php?qv=118&tsv=895&wNotes=on">CDK6↓</a>, <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?qv=118&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?qv=118&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?qv=118&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=118&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=118&tsv=1117&wNotes=on">TOP1↓</a>, <a href="tbResList.php?qv=118&tsv=657&wNotes=on">TET1↓</a>, <br> <!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS --> - inhibits <a href="tbResList.php?qv=118&tsv=129&wNotes=on">glycolysis</a> and <a href="tbResList.php?qv=118&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> : <a href="tbResList.php?qv=118&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=118&tsv=772&wNotes=on">PKM2↓</a>, <a href="tbResList.php?qv=118&tsv=35&wNotes=on">cMyc↓</a>, <a href="tbResList.php?qv=118&tsv=175&wNotes=on&word=LDH">LDHA↓</a>, <a href="tbResList.php?qv=118&tsv=773&wNotes=on">HK2↓</a>, <a href="tbResList.php?qv=118&tsv=356&wNotes=on">GRP78↑</a>, <br> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - inhibits <a href="tbResList.php?qv=118&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=118&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=118&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=118&wNotes=on&word=NOTCH">Notch↓</a>, <a href="tbResList.php?qv=118&tsv=361&wNotes=on">PDGF↓</a>, <a href="tbResList.php?qv=118&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, <a href="tbResList.php?qv=118&&wNotes=on&word=ITG">Integrins↓</a>, <br> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=118&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=118&tsv=4&wNotes=on">AKT↓</a>, <a href="tbResList.php?qv=118&wNotes=on&word=STAT">STAT↓</a>, <a href="tbResList.php?qv=118&tsv=377&wNotes=on">Wnt↓</a>, <a href="tbResList.php?qv=118&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=118&tsv=9&wNotes=on">AMPK</a>, <a href="tbResList.php?qv=118&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=118&tsv=168&wNotes=on">JNK</a>, <a href="tbResList.php?qv=118&word=Trx&wNotes=on">TrxR**</a>, - Shown to modulate the nuclear translocation of <a href="tbResList.php?qv=118&tsv=1132&wNotes=on&exSp=open&word=SREBP2">SREBP-2</a> (related to cholesterol).<br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=118&tsv=1106&wNotes=on">chemo-sensitization</a>, <a href="tbResList.php?qv=118&tsv=1171&wNotes=on">chemoProtective</a>, <a href="tbResList.php?qv=118&tsv=1107&wNotes=on">RadioSensitizer</a>, <a href="tbResList.php?qv=118&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <a href="tbResList.php?qv=118&tsv=1105&wNotes=on">Neuroprotective</a>, <a href="tbResList.php?qv=118&tsv=1175&wNotes=on">Renoprotection</a>, <a href="tbResList.php?qv=118&tsv=1179&wNotes=on">Hepatoprotective</a>, <a href="tbResList.php?&qv=118&tsv=1188&wNotes=on">CardioProtective</a>, <br> <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=118&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br>
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Lyco
Lycopene
NP
<b>Lycopene</b> is a naturally occurring carotenoid found predominantly in tomatoes and other red fruits and vegetables. <br> <br> Antioxidant Properties:<br> -Lycopene is a powerful antioxidant. It helps neutralize free radicals, which can reduce oxidative stress—a factor implicated in cancer development. Possible <a href="https://nestronics.ca/dbx/tbResEdit.php?rid=3273">concern</a> about interfering with chemotherapy and radiation therapy. However this <a href="https://nestronics.ca/dbx/tbResEdit.php?rid=3281">review </a>disagrees.<br> Inflammation Reduction:<br> -Some studies suggest that lycopene may help lower levels of inflammation, another process linked to cancer progression<br> <br> At supraphysiological or extremely high concentrations, lycopene may have the potential to switch from an antioxidant to a prooxidant role<br> -The prooxidant effect of lycopene has been observed under conditions of high oxygen tension. In vitro studies have suggested that in environments with elevated oxygen levels, lycopene might promote rather than neutralize the production of reactive oxygen species (ROS).<br> -The presence of metal ions (such as iron or copper) in the environment can catalyze reactions where antioxidants, including lycopene, contribute to oxidative processes. These metals can interact with lycopene, potentially leading to the formation of radicals.<br> <br> The mevalonate pathway produces cholesterol and a variety of isoprenoids, which are important for maintaining cell membrane integrity, protein prenylation, and other essential cellular functions.<br> -One of the primary enzymes in this pathway is HMG-CoA reductase (3-hydroxy-3-methylglutaryl-coenzyme A reductase), which is the target of statin drugs used for lowering cholesterol. Some studies suggest that lycopene might downregulate the activity of HMG-CoA reductase or other enzymes in the mevalonate pathway. By doing so, lycopene could potentially reduce the synthesis of cholesterol and isoprenoids that are necessary for rapid cell proliferation—an especially relevant aspect in cancer cells.<br> <br> Lycopene typically used in a 100mg/day range for cancer (inhibition of the the Melavonate Pathway)<br> -also has <a href="tbResList.php?qv=119&tsv=10&wNotes=on&exSp=open">antiplatelet </a>aggregation capability.<br> <br> -Note <a href="tbResList.php?qv=119&tsv=1109&wNotes=on&exSp=open">half-life</a> 16–20 days.<br> <a href="tbResList.php?qv=119&tsv=792&wNotes=on&exSp=open">BioAv</a> Heat processing, especially when combined with a small amount of fat, significantly enhances lycopene’s bioaccessibility and absorption. (20% under optimal conditions) <br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - <a href="tbResList.php?qv=119&tsv=275&wNotes=on">ROS</a> usually goes down, but may go up or down depending on dose and environment<br> <!-- - ROS↑ related: <a href="tbResList.php?qv=119&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?qv=119&tsv=103&wNotes=on">ER Stress↑</a>, <a href="tbResList.php?qv=119&tsv=459&wNotes=on">UPR↑</a>, <a href="tbResList.php?qv=119&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=119&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>, <a href="tbResList.php?qv=119&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?qv=119&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?qv=119&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?qv=119&tsv=239&wNotes=on">cl-PARP↑</a>, <a href="tbResList.php?qv=119&wNotes=on&word=HSP">HSP↓</a>, <a href="tbResList.php?qv=119&wNotes=on&word=Prx">Prx</a>, <br> <!-- <!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, --> <!-- - Lowers AntiOxidant defense in Cancer Cells: <a href="tbResList.php?qv=119&tsv=226&wNotes=on&word=NRF2↓">NRF2↓</a>, <a href="tbResList.php?qv=119&word=Trx&wNotes=on">TrxR↓**</a>, <a href="tbResList.php?qv=119&tsv=298&wNotes=on&word=SOD↓">SOD↓</a>, <a href="tbResList.php?qv=119&tsv=137&wNotes=on&word=GSH↓">GSH↓</a> <a href="tbResList.php?qv=119&tsv=46&wNotes=on">Catalase↓</a> <a href="tbResList.php?qv=119&tsv=597&wNotes=on">HO1↓</a> <a href="tbResList.php?qv=119&wNotes=on&word=GPx">GPx↓</a> <br> --> - Raises <a href="tbResList.php?qv=119&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?qv=119&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>, <a href="tbResList.php?qv=119&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?qv=119&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?qv=119&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?qv=119&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?qv=119&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?qv=119&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?qv=119&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, <a href="tbResList.php?qv=119&tsv=235&wNotes=on&word=p38↓">p38↓</a>, Pro-Inflammatory Cytokines : <a href="tbResList.php?qv=119&tsv=908&wNotes=on&word=NLRP3↓">NLRP3↓</a>, <a href="tbResList.php?qv=119&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, <a href="tbResList.php?qv=119&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?qv=119&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <a href="tbResList.php?qv=119&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a> <br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓ inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.--> - inhibit Growth/Metastases : <!-- <a href="tbResList.php?qv=119&tsv=604&wNotes=on">TumMeta↓</a>, --> <!-- <a href="tbResList.php?qv=119&tsv=323&wNotes=on">TumCG↓</a>, --> <a href="tbResList.php?qv=119&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=119&tsv=204&wNotes=on">MMPs↓</a>, <!-- <a href="tbResList.php?qv=119&tsv=201&wNotes=on">MMP2↓</a>, --> <a href="tbResList.php?qv=119&tsv=203&wNotes=on">MMP9↓</a>, <!-- <a href="tbResList.php?qv=119&tsv=308&wNotes=on">TIMP2</a>, --> <a href="tbResList.php?qv=119&tsv=415&wNotes=on">IGF-1↓</a>, <a href="tbResList.php?qv=119&tsv=428&wNotes=on">uPA↓</a>, <a href="tbResList.php?qv=119&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=119&tsv=1284&wNotes=on">ROCK1↓</a>, <a href="tbResList.php?qv=119&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?qv=119&tsv=273&wNotes=on">RhoA↓</a>, <a href="tbResList.php?qv=119&tsv=214&wNotes=on">NF-κB↓</a>, <!-- <a href="tbResList.php?qv=119&tsv=79&wNotes=on">CXCR4↓</a>, --> <!-- <a href="tbResList.php?qv=119&tsv=1247&wNotes=on">SDF1↓</a>, --> <!-- <a href="tbResList.php?qv=119&tsv=304&wNotes=on">TGF-β↓</a>, --> <!-- <a href="tbResList.php?qv=119&tsv=719&wNotes=on">α-SMA↓</a>, --> <a href="tbResList.php?qv=119&tsv=105&wNotes=on">ERK↓</a> <!-- <a href="tbResList.php?qv=119&tsv=1178&wNotes=on">MARK4↓</a> --> <!-- contributing to tumor growth, invasion, and metastasis--> <br> <!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, --> - reactivate genes thereby inhibiting cancer cell growth : <!-- <a href="tbResList.php?qv=119&tsv=140&wNotes=on">HDAC↓</a>, --> <!-- <a href="tbResList.php?qv=119&wNotes=on&word=DNMT">DNMTs↓</a>, --> <a href="tbResList.php?qv=119&tsv=108&wNotes=on">EZH2↓</a>, <a href="tbResList.php?qv=119&tsv=236&wNotes=on">P53↑</a>, <!-- <a href="tbResList.php?qv=119&wNotes=on&word=HSP">HSP↓</a>, --> <a href="tbResList.php?qv=119&tsv=506&wNotes=on">Sp proteins↓</a>, <!-- <a href="tbResList.php?qv=119&wNotes=on&word=TET">TET↑</a> --> <br> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?qv=119&tsv=322&wNotes=on">TumCCA↑</a>, <a href="tbResList.php?qv=119&tsv=73&wNotes=on">cyclin D1↓</a>, <a href="tbResList.php?qv=119&tsv=378&wNotes=on">cyclin E↓</a>, <a href="tbResList.php?qv=119&tsv=467&wNotes=on">CDK2↓</a>, <a href="tbResList.php?qv=119&tsv=894&wNotes=on">CDK4↓</a>, <!-- <a href="tbResList.php?qv=119&tsv=895&wNotes=on">CDK6↓</a>, --> <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?qv=119&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?qv=119&tsv=324&wNotes=on">TumCI↓</a>, <a href="tbResList.php?qv=119&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <!-- encourages invasion, proliferation, EMT, and angiogenesis --> <a href="tbResList.php?qv=119&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?qv=119&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=119&tsv=96&wNotes=on">EMT↓</a>, <!-- <a href="tbResList.php?qv=119&wNotes=on&word=TOP">TOP1↓</a>, --> <!-- <a href="tbResList.php?qv=119&tsv=657&wNotes=on">TET1</a>, --> <br> <!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS --> <!-- - inhibits <a href="tbResList.php?qv=119&tsv=129&wNotes=on">glycolysis</a> /<a href="tbResList.php?qv=119&tsv=947&wNotes=on">Warburg Effect</a> and <a href="tbResList.php?qv=119&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> : <a href="tbResList.php?qv=119&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=119&tsv=772&wNotes=on">PKM2↓</a>, <a href="tbResList.php?qv=119&tsv=35&wNotes=on">cMyc↓</a>, <a href="tbResList.php?qv=119&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>, <a href="tbResList.php?qv=119&tsv=906&wNotes=on">LDH↓</a>, <a href="tbResList.php?qv=119&tsv=175&wNotes=on&word=LDH">LDHA↓</a>, <a href="tbResList.php?qv=119&tsv=773&wNotes=on">HK2↓</a>, <a href="tbResList.php?qv=119&wNotes=on&word=PFK">PFKs↓</a>, <a href="tbResList.php?qv=119&wNotes=on&word=PDK">PDKs↓</a>, <a href="tbResList.php?qv=119&tsv=847&wNotes=on">ECAR↓</a>, <a href="tbResList.php?qv=119&tsv=230&wNotes=on">OXPHOS↓</a>, <a href="tbResList.php?qv=119&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=119&tsv=1278&wNotes=on">Glucose↓</a>, <a href="tbResList.php?qv=119&tsv=623&wNotes=on">GlucoseCon↓</a> <br> --> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - inhibits <a href="tbResList.php?qv=119&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=119&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=119&tsv=143&wNotes=on">HIF-1α↓</a>, <!-- <a href="tbResList.php?qv=119&wNotes=on&word=NOTCH">Notch↓</a>, --> <!-- <a href="tbResList.php?qv=119&wNotes=on&word=FGF">FGF↓</a>, --> <!-- <a href="tbResList.php?qv=119&wNotes=on&word=PDGF">PDGF↓</a>, --> <!-- <a href="tbResList.php?qv=119&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, --> <a href="tbResList.php?qv=119&&wNotes=on&word=ITG">Integrins↓</a>, <br> <!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, --> <!-- - inhibits Cancer Stem Cells : <a href="tbResList.php?qv=119&tsv=795&wNotes=on">CSC↓</a>, <a href="tbResList.php?qv=119&tsv=524&wNotes=on">CK2↓</a>, <a href="tbResList.php?qv=119&tsv=141&wNotes=on">Hh↓</a>, <a href="tbResList.php?qv=119&tsv=434&wNotes=on">GLi↓</a>, <a href="tbResList.php?qv=119&tsv=124&wNotes=on">GLi1↓</a>, <a href="tbResList.php?qv=119&tsv=677&wNotes=on">CD133↓</a>, <a href="tbResList.php?qv=119&tsv=655&wNotes=on">CD24↓</a>, <a href="tbResList.php?qv=119&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=119&tsv=357&wNotes=on">n-myc↓</a>, <a href="tbResList.php?qv=119&tsv=656&wNotes=on">sox2↓</a>, <a href="tbResList.php?qv=119&wNotes=on&word=NOTCH">Notch2↓</a>, <a href="tbResList.php?qv=119&tsv=1024&wNotes=on">nestin↓</a>, <a href="tbResList.php?qv=119&tsv=508&wNotes=on">OCT4↓</a>, <br> --> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=119&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=119&tsv=4&wNotes=on">AKT↓</a>, <a href="tbResList.php?qv=119&wNotes=on&word=JAK">JAK↓</a>, <a href="tbResList.php?qv=119&wNotes=on&word=STAT">STAT↓</a>, <a href="tbResList.php?qv=119&tsv=377&wNotes=on">Wnt↓</a>, <a href="tbResList.php?qv=119&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=119&tsv=9&wNotes=on">AMPK</a>, <!-- <a href="tbResList.php?qv=119&tsv=475&wNotes=on">α↓</a>, --> <a href="tbResList.php?qv=119&tsv=105&wNotes=on">ERK↓</a>, <!-- <a href="tbResList.php?qv=119&tsv=1014&wNotes=on">5↓</a>, --> <a href="tbResList.php?qv=119&tsv=168&wNotes=on">JNK</a>, - <a href="tbResList.php?qv=119&wNotes=on&word=SREBP">SREBP</a> (related to cholesterol).<br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=119&tsv=1106&wNotes=on">chemo-sensitization</a>, <a href="tbResList.php?qv=119&tsv=1171&wNotes=on">chemoProtective</a>, <a href="tbResList.php?qv=119&tsv=1107&wNotes=on">RadioSensitizer</a>, <a href="tbResList.php?qv=119&tsv=1185&wNotes=on">RadioProtective</a>, <a href="tbResList.php?qv=119&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <a href="tbResList.php?qv=119&tsv=1105&wNotes=on">Neuroprotective</a>, <a href="tbResList.php?qv=119&tsv=557&wNotes=on">Cognitive</a>, <a href="tbResList.php?qv=119&tsv=1175&wNotes=on">Renoprotection</a>, <a href="tbResList.php?qv=119&tsv=1179&wNotes=on">Hepatoprotective</a>, <a href="tbResList.php?&qv=119&tsv=1188&wNotes=on">CardioProtective</a>, <br> <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=119&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br>
120
-
Mg
Magnesium
NP
<b>Mineral</b> for normal bone structure. Found in nuts, legumes, fiber rich whole grains, low-fat dairy products, greens - spinach, swiss chard, collard greens.<br> RDA. 51+ years male420 mg. Female 320 mg<br> Pumpkin seeds (hulled, roasted): 1 oz = 150 mg of magnesium<br> Peanuts (dry roasted): 1 oz = 49 mg of magnesium.<br> Shredded wheat (plain, unfrosted): 1 cup = 56 mg of magnesium.<br> Milk (nonfat): 1 cup = 24 to 27 mg of magnesium<br> Yogurt (plain, low fat): 8 oz = 42 mg of magnesium.<br> Dark chocolate (70%-85% cocoa): 1 oz = 64 milligrams of magnesium.<br> Water saskatoon 19mg/L<br> <br> Magnesium acts as a natural calcium antagonist<br> Magnesium deficiency contributes to an exaggerated response to immune stress and oxidative stress is the consequence of the inflammatory response.<br> Simultaneously, magnesium ion deficiency, which antagonize calcium ions, increases intracellular calcium overload, activating numerous calcium-dependent kinases and proteins, such as nitric oxide synthase and calcium-dependent calcium-binding proteins, further augmenting ROS production.<br> <br> Magnesium (Mg) is an essential mineral that plays a crucial role in various cellular processes, including energy production, DNA synthesis, and cell signaling. <br> -Magnesium can inhibit the growth and proliferation of cancer cells by regulating the activity of various enzymes and signaling pathways.<br> -Magnesium can induce apoptosis (programmed cell death) in cancer cells, which can help to prevent tumor growth and metastasis.<br> -Mg deficiency has been linked to an increased risk of cancer.<br> -May improve Ascorbic Acid (IV) efficacy.<br>
192
-
MFrot
Magnetic Field Rotating
T
<b>Rotary Magnetic field</b> can be generated by a spinning magnet or magnets. Or it can be implemented with 2 or more coils, power with a phase shift between them (90 deg for 2 coil implementation) (60deg for 3 coil implementation)<br> Targets affected are mostly the same as for <a href="tbResList.php?qv=172&exPr=open">Magnet fields</a><br> Main differences<br> - may enhance the EPR effect allowing targeting of drugs to cancer cells<br> - acts as wireless stirrer, especially on magnetic particles(inducing eddy currents in water media)<br> - research for use in nano surgery, and mechanical destruction of cancer cells<br> - continue to highlight ability to raise ROS in cancer cell and lower ROS in normal cells<br> - RMF may be responsible for Ca2+ distribution to pass across the plasma membrane(differental affected for cancer and normal cells) <br> <br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - induce <a href="tbResList.php?qv=192&tsv=275&wNotes=on">ROS</a> production in cancer cells, while decreasing ROS in normal cells. Ca2+ is critical and the Ca2+ balance is increased in cancer cells while decreased in normal cells (example for wound healing)<br> - ROS↑ related: <a href="tbResList.php?qv=192&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <!-- <a href="tbResList.php?qv=192&tsv=103&wNotes=on">ER Stress↑</a>, --> <!-- <a href="tbResList.php?qv=192&tsv=459&wNotes=on">UPR↑</a>, --> <!-- <a href="tbResList.php?qv=192&tsv=356&wNotes=on">GRP78↑</a>, --> <a href="tbResList.php?qv=192&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>, <a href="tbResList.php?qv=192&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?qv=192&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?qv=192&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?qv=192&tsv=239&wNotes=on">cl-PARP↑</a>, <a href="tbResList.php?qv=192&wNotes=on&word=HSP">HSP↓</a>, <a href="tbResList.php?qv=192&wNotes=on&word=Prx">Prx</a>,<!-- mitochondrial antioxidant enzyme--> <br> <!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, --> <!-- - Lowers AntiOxidant defense in Cancer Cells: <a href="tbResList.php?qv=192&tsv=226&wNotes=on&word=NRF2↓">NRF2↓</a>, <a href="tbResList.php?qv=192&word=Trx&wNotes=on">TrxR↓**</a>, <a href="tbResList.php?qv=192&tsv=298&wNotes=on&word=SOD↓">SOD↓</a>, <a href="tbResList.php?qv=192&tsv=137&wNotes=on&word=GSH↓">GSH↓</a> <a href="tbResList.php?qv=192&tsv=46&wNotes=on">Catalase↓</a> <a href="tbResList.php?qv=192&tsv=597&wNotes=on">HO1↓</a> <a href="tbResList.php?qv=192&wNotes=on&word=GPx">GPx↓</a> <br> --> - Raises <a href="tbResList.php?qv=192&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?qv=192&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>, <a href="tbResList.php?qv=192&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?qv=192&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?qv=192&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?qv=192&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <!-- genes involved in the oxidative stress-antioxidant defense system PRNP, NQO1, and GCLM --> <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?qv=192&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?qv=192&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?qv=192&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, <a href="tbResList.php?qv=192&tsv=235&wNotes=on&word=p38↓">p38↓</a>, Pro-Inflammatory Cytokines : <!-- <a href="tbResList.php?qv=192&tsv=908&wNotes=on&word=NLRP3↓">NLRP3↓</a>, --> <!-- <a href="tbResList.php?qv=192&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, --> <a href="tbResList.php?qv=192&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?qv=192&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <!-- <a href="tbResList.php?qv=192&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a> --> <br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓ inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.--> - inhibit Growth/Metastases : <a href="tbResList.php?qv=192&tsv=604&wNotes=on">TumMeta↓</a>, <a href="tbResList.php?qv=192&tsv=323&wNotes=on">TumCG↓</a>, <!-- <a href="tbResList.php?qv=192&tsv=96&wNotes=on">EMT↓</a>, --> <a href="tbResList.php?qv=192&tsv=204&wNotes=on">MMPs↓</a>, <a href="tbResList.php?qv=192&tsv=201&wNotes=on">MMP2↓</a>, <a href="tbResList.php?qv=192&tsv=203&wNotes=on">MMP9↓</a>, <!-- <a href="tbResList.php?qv=192&tsv=308&wNotes=on">TIMP2</a>, --> <a href="tbResList.php?qv=192&tsv=415&wNotes=on">IGF-1↓</a>, <!-- <a href="tbResList.php?qv=192&tsv=428&wNotes=on">uPA↓</a>, --> <!-- <a href="tbResList.php?qv=192&tsv=334&wNotes=on">VEGF↓</a>, --> <!-- <a href="tbResList.php?qv=192&tsv=1284&wNotes=on">ROCK1↓</a>, --> <!-- <a href="tbResList.php?qv=192&tsv=110&wNotes=on">FAK↓</a>, --> <a href="tbResList.php?qv=192&tsv=273&wNotes=on">RhoA↓</a>, <a href="tbResList.php?qv=192&tsv=214&wNotes=on">NF-κB↓</a>, <!-- <a href="tbResList.php?qv=192&tsv=79&wNotes=on">CXCR4↓</a>, --> <!-- <a href="tbResList.php?qv=192&tsv=1247&wNotes=on">SDF1↓</a>, --> <a href="tbResList.php?qv=192&tsv=304&wNotes=on">TGF-β↓</a>, <!-- <a href="tbResList.php?qv=192&tsv=719&wNotes=on">α-SMA↓</a>, --> <a href="tbResList.php?qv=192&tsv=105&wNotes=on">ERK↓</a> <!-- <a href="tbResList.php?qv=192&tsv=1178&wNotes=on">MARK4↓</a> --> <!-- contributing to tumor growth, invasion, and metastasis--> <br> <!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, --> <!-- - reactivate genes thereby inhibiting cancer cell growth : <a href="tbResList.php?qv=192&tsv=140&wNotes=on">HDAC↓</a>, <a href="tbResList.php?qv=192&wNotes=on&word=DNMT">DNMTs↓</a>, <a href="tbResList.php?qv=192&tsv=108&wNotes=on">EZH2↓</a>, <a href="tbResList.php?qv=192&tsv=236&wNotes=on">P53↑</a>, <a href="tbResList.php?qv=192&wNotes=on&word=HSP">HSP↓</a>, <a href="tbResList.php?qv=192&tsv=506&wNotes=on">Sp proteins↓</a>, <a href="tbResList.php?qv=192&wNotes=on&word=TET">TET↑</a> <br> --> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?qv=192&tsv=322&wNotes=on">TumCCA↑</a>, <!-- <a href="tbResList.php?qv=192&tsv=73&wNotes=on">cyclin D1↓</a>, --> <!-- <a href="tbResList.php?qv=192&tsv=378&wNotes=on">cyclin E↓</a>, --> <!-- <a href="tbResList.php?qv=192&tsv=467&wNotes=on">CDK2↓</a>, --> <!-- <a href="tbResList.php?qv=192&tsv=894&wNotes=on">CDK4↓</a>, --> <!-- <a href="tbResList.php?qv=192&tsv=895&wNotes=on">CDK6↓</a>, --> <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?qv=192&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?qv=192&tsv=324&wNotes=on">TumCI↓</a>, <a href="tbResList.php?qv=192&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <!-- encourages invasion, proliferation, EMT, and angiogenesis --> <!-- <a href="tbResList.php?qv=192&tsv=110&wNotes=on">FAK↓</a>, --> <a href="tbResList.php?qv=192&tsv=105&wNotes=on">ERK↓</a>, <!-- <a href="tbResList.php?qv=192&tsv=96&wNotes=on">EMT↓</a>, --> <!-- <a href="tbResList.php?qv=192&wNotes=on&word=TOP">TOP1↓</a>, --> <!-- <a href="tbResList.php?qv=192&tsv=657&wNotes=on">TET1</a>, --> <br> <!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS --> <!-- - inhibits <a href="tbResList.php?qv=192&tsv=129&wNotes=on">glycolysis</a> /<a href="tbResList.php?qv=192&tsv=947&wNotes=on">Warburg Effect</a> and <a href="tbResList.php?qv=192&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> : <a href="tbResList.php?qv=192&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=192&tsv=772&wNotes=on">PKM2↓</a>, <a href="tbResList.php?qv=192&tsv=35&wNotes=on">cMyc↓</a>, <a href="tbResList.php?qv=192&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>, <a href="tbResList.php?qv=192&tsv=906&wNotes=on">LDH↓</a>, <a href="tbResList.php?qv=192&tsv=175&wNotes=on&word=LDH">LDHA↓</a>, <a href="tbResList.php?qv=192&tsv=773&wNotes=on">HK2↓</a>, <a href="tbResList.php?qv=192&wNotes=on&word=PFK">PFKs↓</a>, <a href="tbResList.php?qv=192&wNotes=on&word=PDK">PDKs↓</a>, <a href="tbResList.php?qv=192&tsv=847&wNotes=on">ECAR↓</a>, <a href="tbResList.php?qv=192&tsv=230&wNotes=on">OXPHOS↓</a>, <a href="tbResList.php?qv=192&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=192&tsv=1278&wNotes=on">Glucose↓</a>, <a href="tbResList.php?qv=192&tsv=623&wNotes=on">GlucoseCon↓</a> <br> --> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> <!-- - inhibits <a href="tbResList.php?qv=192&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=192&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=192&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=192&wNotes=on&word=NOTCH">Notch↓</a>, <a href="tbResList.php?qv=192&wNotes=on&word=FGF">FGF↓</a>, <a href="tbResList.php?qv=192&wNotes=on&word=PDGF">PDGF↓</a>, <a href="tbResList.php?qv=192&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, <a href="tbResList.php?qv=192&&wNotes=on&word=ITG">Integrins↓</a>, <br> --> <!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, --> <!-- - inhibits Cancer Stem Cells : <a href="tbResList.php?qv=192&tsv=795&wNotes=on">CSC↓</a>, <a href="tbResList.php?qv=192&tsv=524&wNotes=on">CK2↓</a>, <a href="tbResList.php?qv=192&tsv=141&wNotes=on">Hh↓</a>, <a href="tbResList.php?qv=192&tsv=434&wNotes=on">GLi↓</a>, <a href="tbResList.php?qv=192&tsv=124&wNotes=on">GLi1↓</a>, <a href="tbResList.php?qv=192&tsv=677&wNotes=on">CD133↓</a>, <a href="tbResList.php?qv=192&tsv=655&wNotes=on">CD24↓</a>, <a href="tbResList.php?qv=192&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=192&tsv=357&wNotes=on">n-myc↓</a>, <a href="tbResList.php?qv=192&tsv=656&wNotes=on">sox2↓</a>, <a href="tbResList.php?qv=192&wNotes=on&word=NOTCH">Notch2↓</a>, <a href="tbResList.php?qv=192&tsv=1024&wNotes=on">nestin↓</a>, <a href="tbResList.php?qv=192&tsv=508&wNotes=on">OCT4↓</a>, <br> --> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=192&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=192&tsv=4&wNotes=on">AKT↓</a>, <!-- <a href="tbResList.php?qv=192&wNotes=on&word=JAK">JAK↓</a>, --> <!-- <a href="tbResList.php?qv=192&wNotes=on&word=STAT">STAT↓</a>, --> <a href="tbResList.php?qv=192&tsv=377&wNotes=on">Wnt↓</a>, <!-- <a href="tbResList.php?qv=192&tsv=342&wNotes=on">β-catenin↓</a>, --> <a href="tbResList.php?qv=192&tsv=9&wNotes=on">AMPK</a>, <!-- <a href="tbResList.php?qv=192&tsv=475&wNotes=on">α↓</a>, --> <a href="tbResList.php?qv=192&tsv=105&wNotes=on">ERK↓</a>, <!-- <a href="tbResList.php?qv=192&tsv=1014&wNotes=on">5↓</a>, --> <a href="tbResList.php?qv=192&tsv=168&wNotes=on">JNK</a>, <!-- - <a href="tbResList.php?qv=192&wNotes=on&word=SREBP">SREBP</a> (related to cholesterol). --><br> <!-- SYNERGIES : --> - Synergies: <!-- <a href="tbResList.php?qv=192&tsv=1106&wNotes=on">chemo-sensitization</a>, --> <!-- <a href="tbResList.php?qv=192&tsv=1171&wNotes=on">chemoProtective</a>, --> <<!-- a href="tbResList.php?qv=192&tsv=1107&wNotes=on">RadioSensitizer</a>, --> <!-- <a href="tbResList.php?qv=192&tsv=1185&wNotes=on">RadioProtective</a>, --> <a href="tbResList.php?qv=192&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <a href="tbResList.php?qv=192&tsv=1105&wNotes=on">Neuroprotective</a>, <a href="tbResList.php?qv=192&tsv=557&wNotes=on">Cognitive</a>, <!-- <a href="tbResList.php?qv=192&tsv=1175&wNotes=on">Renoprotection</a>, --> <!-- <a href="tbResList.php?qv=192&tsv=1179&wNotes=on">Hepatoprotective</a>, --> <!-- <a href="tbResList.php?&qv=192&tsv=1188&wNotes=on">CardioProtective</a>, --> <br> <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=192&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br>
172
-
MF
Magnetic Fields
T
Therapy
<b>Magnetic Fields</b> can be Static, or pulsed. The most common therapy is a pulsed magnetic field in the uT or mT range.<br> The main pathways affected are:<br> Calcium Signaling: -influence the activity of voltage-gated calcium channels.<br> Oxidative Stress and Reactive Oxygen Species (ROS) Pathways<br> Heat Shock Proteins (HSPs) and Cellular Stress Responses<br> Cell Proliferation and Growth Signaling: MAPK/ERK pathway.<br> Gene Expression and Epigenetic Modifications: NF-κB<br> Angiogenesis Pathways: VEGF (improving VEGF for normal cells)<br> PEMF was found to have a 2-fold increase in drug uptake compared to traditional electrochemotherapy in rat melanoma models<br> <br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - most reports have <a href="tbResList.php?qv=172&tsv=275&wNotes=on">ROS</a> production increasing in cancer cells , while decreasing in normal cells.<br> - ROS↑ related: <a href="tbResList.php?qv=172&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?qv=172&tsv=103&wNotes=on">ER Stress↑</a>, <a href="tbResList.php?qv=172&tsv=459&wNotes=on">UPR↑</a>, <a href="tbResList.php?qv=172&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=172&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>, <a href="tbResList.php?qv=172&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?qv=172&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?qv=172&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?qv=172&tsv=239&wNotes=on">cl-PARP↑</a>, <a href="tbResList.php?qv=172&wNotes=on&word=HSP">HSP↓</a>, <a href="tbResList.php?qv=172&wNotes=on&word=Prx">Prx</a>,<!-- mitochondrial antioxidant enzyme--> <br> <!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, --> <!-- - Lowers AntiOxidant defense in Cancer Cells: <a href="tbResList.php?qv=172&tsv=226&wNotes=on&word=NRF2↓">NRF2↓</a>, <a href="tbResList.php?qv=172&word=Trx&wNotes=on">TrxR↓**</a>, <a href="tbResList.php?qv=172&tsv=298&wNotes=on&word=SOD↓">SOD↓</a>, <a href="tbResList.php?qv=172&tsv=137&wNotes=on&word=GSH↓">GSH↓</a> <a href="tbResList.php?qv=172&tsv=46&wNotes=on">Catalase↓</a> <a href="tbResList.php?qv=172&tsv=597&wNotes=on">HO1↓</a> <a href="tbResList.php?qv=172&wNotes=on&word=GPx">GPx↓</a> <br> --> - Raises <a href="tbResList.php?qv=172&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?qv=172&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>, <a href="tbResList.php?qv=172&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?qv=172&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?qv=172&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?qv=172&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <!-- genes involved in the oxidative stress-antioxidant defense system PRNP, NQO1, and GCLM --> <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?qv=172&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?qv=172&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?qv=172&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, <!-- <a href="tbResList.php?qv=172&tsv=235&wNotes=on&word=p38↓">p38↓</a>, --> Pro-Inflammatory Cytokines : <a href="tbResList.php?qv=172&tsv=908&wNotes=on&word=NLRP3↓">NLRP3↓</a>, <a href="tbResList.php?qv=172&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, <a href="tbResList.php?qv=172&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?qv=172&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <a href="tbResList.php?qv=172&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a> <br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓ inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.--> - inhibit Growth/Metastases : <a href="tbResList.php?qv=172&tsv=604&wNotes=on">TumMeta↓</a>, <a href="tbResList.php?qv=172&tsv=323&wNotes=on">TumCG↓</a>, <!-- <a href="tbResList.php?qv=172&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=172&tsv=204&wNotes=on">MMPs↓</a>, <a href="tbResList.php?qv=172&tsv=201&wNotes=on">MMP2↓</a>, <a href="tbResList.php?qv=172&tsv=203&wNotes=on">MMP9↓</a>, <a href="tbResList.php?qv=172&tsv=308&wNotes=on">TIMP2</a>, <a href="tbResList.php?qv=172&tsv=415&wNotes=on">IGF-1↓</a>, <a href="tbResList.php?qv=172&tsv=428&wNotes=on">uPA↓</a>, --> <a href="tbResList.php?qv=172&tsv=334&wNotes=on">VEGF↓</a>(mostly regulated up in normal cells), <!-- <a href="tbResList.php?qv=172&tsv=1284&wNotes=on">ROCK1↓</a>, <a href="tbResList.php?qv=172&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?qv=172&tsv=273&wNotes=on">RhoA↓</a>, <a href="tbResList.php?qv=172&tsv=214&wNotes=on">NF-κB↓</a>, <a href="tbResList.php?qv=172&tsv=79&wNotes=on">CXCR4↓</a>, <a href="tbResList.php?qv=172&tsv=1247&wNotes=on">SDF1↓</a>, <a href="tbResList.php?qv=172&tsv=304&wNotes=on">TGF-β↓</a>, <a href="tbResList.php?qv=172&tsv=719&wNotes=on">α-SMA↓</a>, <a href="tbResList.php?qv=172&tsv=105&wNotes=on">ERK↓</a> <a href="tbResList.php?qv=172&tsv=1178&wNotes=on">MARK4↓</a> --> <!-- contributing to tumor growth, invasion, and metastasis--> <br> <!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, --> <!-- - reactivate genes thereby inhibiting cancer cell growth : <a href="tbResList.php?qv=172&tsv=140&wNotes=on">HDAC↓</a>, <a href="tbResList.php?qv=172&wNotes=on&word=DNMT">DNMTs↓</a>, <a href="tbResList.php?qv=172&tsv=108&wNotes=on">EZH2↓</a>, <a href="tbResList.php?qv=172&tsv=236&wNotes=on">P53↑</a>, <a href="tbResList.php?qv=172&wNotes=on&word=HSP">HSP↓</a>, <a href="tbResList.php?qv=172&tsv=506&wNotes=on">Sp proteins↓</a>, <a href="tbResList.php?qv=172&wNotes=on&word=TET">TET↑</a> <br> --> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?qv=172&tsv=322&wNotes=on">TumCCA↑</a>, <!-- <a href="tbResList.php?qv=172&tsv=73&wNotes=on">cyclin D1↓</a>, <a href="tbResList.php?qv=172&tsv=378&wNotes=on">cyclin E↓</a>, <a href="tbResList.php?qv=172&tsv=467&wNotes=on">CDK2↓</a>, <a href="tbResList.php?qv=172&tsv=894&wNotes=on">CDK4↓</a>, <a href="tbResList.php?qv=172&tsv=895&wNotes=on">CDK6↓</a>, --> <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?qv=172&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?qv=172&tsv=324&wNotes=on">TumCI↓</a>, <a href="tbResList.php?qv=172&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <!-- encourages invasion, proliferation, EMT, and angiogenesis --> <!-- <a href="tbResList.php?qv=172&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?qv=172&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=172&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=172&wNotes=on&word=TOP">TOP1↓</a>, <a href="tbResList.php?qv=172&tsv=657&wNotes=on">TET1</a>, --> <br> <!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS --> - inhibits <a href="tbResList.php?qv=172&tsv=129&wNotes=on">glycolysis</a> /<a href="tbResList.php?qv=172&tsv=947&wNotes=on">Warburg Effect</a> and <a href="tbResList.php?qv=172&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> : <a href="tbResList.php?qv=172&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=172&tsv=772&wNotes=on">PKM2↓</a>, <!-- <a href="tbResList.php?qv=172&tsv=35&wNotes=on">cMyc↓</a>, --> <a href="tbResList.php?qv=172&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>, <a href="tbResList.php?qv=172&tsv=906&wNotes=on">LDH↓</a>, <!-- <a href="tbResList.php?qv=172&tsv=175&wNotes=on&word=LDH">LDHA↓</a>, --> <a href="tbResList.php?qv=172&tsv=773&wNotes=on">HK2↓</a>, <a href="tbResList.php?qv=172&wNotes=on&word=PFK">PFKs↓</a>, <a href="tbResList.php?qv=172&wNotes=on&word=PDK">PDKs↓</a>, <a href="tbResList.php?qv=172&tsv=847&wNotes=on">ECAR↓</a>, <a href="tbResList.php?qv=172&tsv=230&wNotes=on">OXPHOS↓</a>, <a href="tbResList.php?qv=172&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=172&tsv=1278&wNotes=on">Glucose↓</a>, <a href="tbResList.php?qv=172&tsv=623&wNotes=on">GlucoseCon↓</a> <br> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - inhibits <a href="tbResList.php?qv=172&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=172&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=172&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=172&wNotes=on&word=NOTCH">Notch↓</a>, <a href="tbResList.php?qv=172&wNotes=on&word=FGF">FGF↓</a>, <a href="tbResList.php?qv=172&wNotes=on&word=PDGF">PDGF↓</a>, <a href="tbResList.php?qv=172&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, <a href="tbResList.php?qv=172&&wNotes=on&word=ITG">Integrins↓</a>, <br> <!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, --> <!-- - inhibits Cancer Stem Cells : <a href="tbResList.php?qv=172&tsv=795&wNotes=on">CSC↓</a>, <a href="tbResList.php?qv=172&tsv=524&wNotes=on">CK2↓</a>, <a href="tbResList.php?qv=172&tsv=141&wNotes=on">Hh↓</a>, <a href="tbResList.php?qv=172&tsv=434&wNotes=on">GLi↓</a>, <a href="tbResList.php?qv=172&tsv=124&wNotes=on">GLi1↓</a>, <a href="tbResList.php?qv=172&tsv=677&wNotes=on">CD133↓</a>, <a href="tbResList.php?qv=172&tsv=655&wNotes=on">CD24↓</a>, <a href="tbResList.php?qv=172&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=172&tsv=357&wNotes=on">n-myc↓</a>, <a href="tbResList.php?qv=172&tsv=656&wNotes=on">sox2↓</a>, <a href="tbResList.php?qv=172&wNotes=on&word=NOTCH">Notch2↓</a>, <a href="tbResList.php?qv=172&tsv=1024&wNotes=on">nestin↓</a>, <a href="tbResList.php?qv=172&tsv=508&wNotes=on">OCT4↓</a>, <br> --> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=172&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=172&tsv=4&wNotes=on">AKT↓</a>, <!-- <a href="tbResList.php?qv=172&wNotes=on&word=JAK">JAK↓</a>, --> <a href="tbResList.php?qv=172&wNotes=on&word=STAT">STAT↓</a>, <a href="tbResList.php?qv=172&tsv=377&wNotes=on">Wnt↓</a>, <a href="tbResList.php?qv=172&tsv=342&wNotes=on">β-catenin↓</a>, <!-- <a href="tbResList.php?qv=172&tsv=9&wNotes=on">AMPK</a>, --> <!-- <a href="tbResList.php?qv=172&tsv=475&wNotes=on">α↓</a>, --> <a href="tbResList.php?qv=172&tsv=105&wNotes=on">ERK↓</a>, <!-- <a href="tbResList.php?qv=172&tsv=1014&wNotes=on">5↓</a>, --> <a href="tbResList.php?qv=172&tsv=168&wNotes=on">JNK</a>, - <a href="tbResList.php?qv=172&wNotes=on&word=SREBP">SREBP</a> (related to cholesterol).<br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=172&tsv=1106&wNotes=on">chemo-sensitization</a>, <a href="tbResList.php?qv=172&tsv=1171&wNotes=on">chemoProtective</a>, <a href="tbResList.php?qv=172&tsv=1233&wNotes=on">cytoProtective</a>, <a href="tbResList.php?qv=172&tsv=1107&wNotes=on">RadioSensitizer</a>, <a href="tbResList.php?qv=172&tsv=1185&wNotes=on">RadioProtective</a>, <a href="tbResList.php?qv=172&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <a href="tbResList.php?qv=172&tsv=1105&wNotes=on">Neuroprotective</a>, <!-- <a href="tbResList.php?qv=172&tsv=557&wNotes=on">Cognitive</a>, --> <!-- <a href="tbResList.php?qv=172&tsv=1175&wNotes=on">Renoprotection</a>, --> <a href="tbResList.php?qv=172&tsv=1179&wNotes=on">Hepatoprotective</a>, <a href="tbResList.php?&qv=172&tsv=1188&wNotes=on">CardioProtective</a>, <br> <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=172&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br>
236
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MNPs
magnetic nanoparticles
NP
<b>MNPs</b> often used in combination with Magnetic field for thermal effects, or cell disruption.<br>
121
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MAG
Magnolol
NP
<b>Lignan</b> found in bark of some magnolia species.<br>
322
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Matr
Matrine
NP
<b>Matrine</b> is a naturally occurring alkaloid primarily isolated from the root of Sophora flavescens, a traditional Chinese medicinal herb. <br> Matrine, an alkaloid extracted from Panax ginseng<br> <br> Pathways:<br> -cell cycle arrest <br> -many studies report that matrine exhibits selective toxicity towards cancer cells<br> -exhibits the ability to suppress HK2 2.0 μM<br>
333
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MCT
MCToil
NP
<b>MCT oils</b> typically consist of medium-chain fatty acids such as caprylic acid (C8) and capric acid (C10). Here are some examples and sources of MCT oils:<br> • Purified MCT Oil Products:<br> – Commercial MCT oils (e.g., Nature’s Way MCT Oil, Now Sports MCT Oil) are available as dietary supplements and are often used in both nutritional and pharmaceutical applications.<br> – These products are refined to contain mostly C8 and C10 fatty acids, which are known for their rapid digestion and absorption.<br> • Coconut Oil (Fractionated):<br> – Although traditional coconut oil contains a mix of medium-chain (and longer-chain) fatty acids, fractionated coconut oil has been processed to separate the medium-chain triglycerides (mainly C8 and C10).<br> – This fractionated form is liquid at room temperature and can serve a similar purpose as purified MCT oil in formulations.<br> - MCT oil is rapidly metabolized in the liver to produce ketone bodies, making it a common component of ketogenic diets.<br>
331
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meben
mebendazole
RD
<b>Mebendazole</b>—an anthelmintic (anti-parasitic) medication<br> Mebendazole is traditionally used to treat various parasitic worm infections (helminths).<br> <br> -Mebendazole has been found to disrupt microtubule formation in cells.<br> -It might interfere with angiogenesis (the formation of new blood vessels that tumors need to grow)<br> -Can inhibit the proliferation of various cancer cell lines (such as melanoma, colon cancer, and others)<br> -May work synergistically with established chemotherapeutic agents.<br>
122
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MEL
Melatonin
NP
<b>Hormone</b> in the body made by pineal gland.<br> • Melatonin is a potent antioxidant. It neutralizes reactive oxygen species (ROS) and reactive nitrogen species (RNS), which are involved in DNA damage and cancer progression.<br> • Melatonin has been shown to modulate apoptotic pathways by influencing mitochondrial permeability, cytochrome c release, and caspase activation.<br> • In several cancer cell models, melatonin appears to promote apoptosis in malignant cells while sparing normal cells.<br> <br> The most well-known indolamines are serotonin and melatonin, both of which play significant roles in regulating mood, sleep, and overall mental well-being.<br> <br> Melatonin doses (20 mg to even 40 mg per day), often given as an adjuvant treatment for cancer.<br> -The plasma half-life of melatonin is generally in the range of approximately 20 to 60 minutes<br> -It has been suggested that administering melatonin at the appropriate phase of the circadian cycle may enhance its anti-tumor activity and reduce the side effects of chemotherapy and radiation therapy.<br> <br> Bio-availability: Oral melatonin has a low and variable bio-availability (often estimated between 3% and 33%), which means that only a fraction of the ingested dose reaches the bloodstream unchanged.<br> <br> For proOxidant effect might need >10uM, which might be 100mg dose (assuming 10% bio-availability) Might also be required X10 levels?<br> -It remains unknown whether the pro-oxidant action exists in vivo. the vast majority of evidence indicates that melatonin is a potent antioxidant in vivo even at pharmacological concentrations.<br> <br> Interactions:<br> -Melatonin could potentially add to the blood pressure–lowering properties of antihypertensive drugs.<br> -Patients using insulin should be monitored for changes in blood glucose levels.<br> -Melatonin might interact with drugs like warfarin, aspirin, or clopidogrel.(antiplatelet)<br>
269
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Mel
Melitidin
NP
<b>Melitidin</b> is a naturally occurring compound found in certain plant extracts. Although it is more frequently discussed with respect to its cholesterol-lowering and antidiabetic properties, melitidin has structural characteristics that classify it among bioactive phytochemicals. Its antioxidant and anti-inflammatory actions have raised interest in the possibility that melitidin might also interfere with cellular events related to carcinogenesis.<br>
11
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MET
Metformin
RD
oral antidiabetic agent,
<b>Metformin</b> is a pleiotropic drug: attributed to its action on AMPK<br> Metformin directly inhibits Complex I of the electron transport chain (ETC) in mitochondria. This inhibition decreases mitochondrial ATP production and forces cells to rely more on glycolysis for energy.<br> Cancer cells, especially those with high energy demands, may be particularly sensitive to a drop in ATP levels. The inhibition of Complex I also increases the AMP/ATP ratio, setting the stage for the activation of downstream energy stress pathways.<br> AMPK activation results in the inhibition of the mammalian target of rapamycin (mTOR) pathway, a central regulator of protein synthesis and cellular growth. mTOR inhibition reduces cell proliferation and limits tissue growth, which can slow tumor progression.<br> <br> Metformin reduces circulating insulin levels, which in turn can decrease the activation of the insulin and insulin-like growth factor-1 (IGF-1) receptor pathways.<br> <br> ETC Inhibitors: Drugs that directly inhibit specific ETC complexes (e.g., Complex I inhibitors like metformin or phenformin) can increase electron leakage and ROS production.<br> <br> -known as OXPHOS inhibitor<br> <br>
223
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MTX
methotrexate
D
<b>Methotrexate</b> is a chemotherapy medication that has been used to treat various types of cancer.<br> Methotrexate works by:<br> Inhibiting dihydrofolate reductase (DHFR): Methotrexate binds to DHFR, an enzyme that is necessary for the production of tetrahydrofolate, a co-factor for DNA synthesis.<br> Interfering with DNA synthesis: By inhibiting DHFR, methotrexate prevents the production of tetrahydrofolate, which is necessary for DNA synthesis.<br> Inducing apoptosis: Methotrexate can induce apoptosis (programmed cell death) in cancer cells.<br>
294
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MeJa
Methyl Jasmonate
NP
<b>Methyl jasmonate (MeJa)</b> is a well-known plant stress hormone. <br> Pathways:<br> -Causes mitochondrial dysfunction by inducing the release of cytochrome c, which leads to caspase activation.<br> - ↓ glycolysis via hexokinase-VDAC disruption<br> - ↑ ROS in cancer cells<br> -MJ can lead to cell cycle arrest, thereby inhibiting the proliferation of cancer cells<br>
12
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M-Blu
Methylene blue
RD
<b>Methylene blue (MB)</b>, also known as methylthioninium chloride, is a thiazine dye that can be used as a medication, and can be administered orally, subcutaneously or intravenously.<br> Mainly used to treat methemoglobinemia by chemically reducing the ferric iron in hemoglobin to ferrous iron<br> Methylene blue is commonly used in medical practice, especially as a dye in microbiological staining<br> Antidote in cyanide poisoning: an oxidation-reduction indicator: an antiseptic<br> <br> Pathways:<br> -increases the oxygen consumption of normal tissues having aerobic glycolysis, and of tumors<br> - generate reactive oxygen species (ROS) upon light activation<br> -effects on mitochondrial metabolism may contribute to modulation of apoptosis and energy metabolism in cancer cells.<br> -can affect the generation of reactive oxygen species.<br> -Historically, it was used in patients with urinary tract infection <br> -MB has also been used as a tracer for cancer diagnosis and as a photosensitizer for cancer treatment <br> -methylene blue reverses Warburg effect<br> -can cross BBB and reach brain at concentrations 10 times higher than that in the circulation<br> -causes shift from shift from glycolysis to oxidative phosphorylation.<br> -reduces glutathione reductase GSR (an enzyme of glutathione metabolism) <br>
123
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MGO
Methylglyoxal
NP
<b><a href="https://en.wikipedia.org/wiki/Methylglyoxal">Methylglyoxal</b></a> is a reduced derivative of pyruvic acid that is produced by glycolysis and other metabolic pathways. It is involved in the formation of advanced glycation end products, DNA damage, and diabetes complications.<br> <br> -Methylglyoxal is specifically inhibits OXPHOS in cancer cells ?<br> -Methylglyoxal in cancer cells inhibits GAPDH, an essential enzyme acting in the glycolsis pathway. GAPDH inhibition depletes ATP profoundly depriving the cancer cells of energy. <br> -Activator of GABA A receptor<br> <br> <a href="https://www.cancertreatmentsresearch.com/methilglyoxal/" >Some research may indicate it can promote cancer growth.</a><br> <br> Dose: (30-40mg/day) 7.5mg/kg 4 times/day (plus 400mg Vit C) + VitB complex twice/day <br> -Combine with curcumin(8g/d)?<br> <br> Combine with:<br> Chitosan?<br> Creatine (30-60 mins before)<br> GLO1 inhibitors (Naringin, Curcumin)<br> Nrf2 inhibitors: (ex Ascorbic Acid)<br> GABA supplementation<br> Metformin?<br> <br> Avoid combination with DCA?<br> <br> Pathways<br> 1. Glyoxalase System Glyoxalase I and II: (glyoxalase system) which detoxifies methylglyoxal. In many cancers, the expression of glyoxalase I (and sometimes glyoxalase II) is upregulated. This allows tumor cells to tolerate higher MG levels resulting from their altered metabolism (often enhanced glycolysis), protecting them from dicarbonyl stress while simultaneously supporting their survival and proliferation.<br> <br> 2. Advanced Glycation End Products (AGEs) and RAGE Pathway<br> AGE Formation:-Supplemented MG can increase the formation of advanced glycation end products (AGEs) RAGE Activation:AGEs can lead to the activation of RAGEE, which include the activation of NF-κB and MAPK pathways. <br> <br> 3. NF-κB Signaling Pathway: The activation of NF-κB by MG-induced AGE-RAGE signaling <br> <br> 4. MAPK Pathway: can be activated as a result of MG-induced oxidative and dicarbonyl stress<br>. <br> 5. ROS Generation and Oxidative Stress<br> Methylglyoxal can raise intracellular ROS levels. (reinforcing the pro-tumorigenic environment.) -excessive ROS can be deleterious. <br> <br> Sources: <a href="https://www.scbt.com/p/methylglyoxal-solution-78-98-8" >Western or Chinese chemical suppliers under CAS number 78-98-8 </a> <br>
190
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MeSA
methylseleninic acid
NP
<b>Methylseleninic acid</b>, a widespread selenium-containing compound of organic nature.<br>
124
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MSM
Methylsulfonylmethane
NP
<b>Chemical</b> found in humans, animals and plants.<br>
327
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metroC
metronomic chemo
T
<b>Metronomic chemotherapy</b> refers to the therapeutic strategy of administering chemotherapeutic drugs at relatively low, minimally toxic doses on a frequent or continuous schedule without extended rest periods. This dosing regimen contrasts with traditional maximum tolerated dose (MTD) chemotherapy, which involves high doses given intermittently with breaks to allow patient recovery.<br> <br> -The drugs are given in lower doses and more frequently (often daily or multiple times a week) <br> -Aims to consistently impair tumor growth mechanisms and potentially minimize the chance for cancer cells to recover<br> -Aims to consistently impair tumor growth mechanisms and potentially minimize the chance for cancer cells to recover<br> -With a lower dose intensity, patients often experience fewer and less severe side effects<br>
125
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MT
Mistletoe
NP
<b>Semiparasitic plant</b> that grows on apple, oak, pine and elm trees.<br> Most bioactive ingredients of mistletoe have been identified and characterized such as lectins (I, II, and III), polypeptides (e.g., viscotoxins), and immunostimulatory glycoproteins (5–7). The extracts are also enriched in biologically active flavonoids, phenolic acids, sterols, lignans, terpenoids, and phenylpropanoids (8). There is strong evidence that the complete mistletoe extract is more potent than when isolated compounds are administered.<br>
126
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MCP
Modified Citrus Pectin
NP
<b>Obtained</b> from peels, seeds and pulp of citrus fruits.<br>
209
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Moringa
Moringa oleifera
NP
<b>The leaves, seeds, and pods of the Moringa oleifera plant</b> contain a variety of bioactive compounds, including flavonoids, phenolic acids, and saponins, which have been shown to have anti-inflammatory, antioxidant, and anti-proliferative effects.<br> Moringa oleifera extracts on various types of cancer: Breast, Lung, Colon, Prostate<br>
58
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MushCha
Mushroom Chaga
NP
<b>Fungus</b> that grows in birch trees. Available as a herbal tea. Type of mushroom.<br>
325
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mushLions
Mushroom Lion’s Mane
NP
<b>Lion’s Mane Mushroom (Hericium erinaceus)</b> is renowned for its potential health benefits, particularly in areas like neuroprotection, cognitive function, and immune support. <br> <br> -Most commonly cited mechanisms of Lion’s Mane is its ability to stimulate the synthesis of Nerve Growth Factor (NGF)<br> -Specific compounds such as hericenones and erinacines present in the mushroom are thought to be responsible for this effect.<br> -May inhibit NF-κB Pathway<br> -May lower the production of pro-inflammatory cytokines (e.g., TNF-α, IL-6)<br> -Neutralize free radicals, reducing oxidative stress<br> -Lion’s Mane influences gut health and, in turn, the gut-brain axis<br> -Anti-inflammatory responses, antioxidant protection<br> <br> -Mushrooms, including Lion’s Mane (Hericium erinaceus), contain ergosterol—a precursor to vitamin D. When exposed to ultraviolet (UV) light (such as sunlight), ergosterol is converted to vitamin D₂ (ergocalciferol).<br>
214
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MushMait
Mushroom Maitake
NP
enhance the immune system
<b>Maitake Mushroom (Grifola frondosa)</b> – This medicinal mushroom has immune-boosting properties. May have anti-cancer properties due to their rich content of polysaccharides, particularly beta-glucans, which are known to enhance the immune system.<br>
131
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MushPL
Mushroom Phellinus. linteus
NP
<b>Tropical mushroom.</b><br>
235
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MushReishi
Mushroom Reishi
NP
<b>Reishi mushroom (Ganoderma lucidum)</b><br> -Various compounds such as glycoproteins, polysaccharides, triterpenoids, meroterpenoids, sesquiterpenoids, steroids, alkaloids, benzopyran derivatives, and benzoic acid derivatives, and minerals such as potassium, calcium, phosphorus, magnesium, selenium, iron and zinc.<br> -Most important polysaccharides and triterpenes. <br> -Polysaccharides, especially beta-glucans (ability to support immune system function) <br> <br> Higher bioavailability in liquid form<br> <br> Pathways<br> -Enhances activity of natural killer (NK) cells, dendritic cells, and T lymphocytes -NF-κB Inhibition<br>
25
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MushShi
Mushroom Shiitake, AHCC
NP
immunoenhancer
<b>Mushroom Shiitake</b>, Active hexose correlated compound<br> Extracted from Basidiomycete mushrooms (eg, shiitake [Lentinula edodes]) that is purported to improve immune function.<br> Summary:<br> - Can significantly inhibit carcinogenesis and improve anti-tumor effects, thus increasing the effectiveness of cancer immunotherapy.<br> - Enhanced abundance of Akkermansia in the intestine of those who responded positively to the ICI(immune checkpoint inhibitors).<br> <br> -Eat fermented foods then fibre to maintain them. Fruits and vegs for fibre Chicory root for fibre (inulin which is main prebiotic)<br> <br> AHCC is mainly derived from the mycelium of Shiitake mushrooms.<br> • It is rich in polysaccharides that are believed to enhance immune function.<br> • The compound may influence various pathways in cancer, including boosting NK cell activity, modulating cytokine production, influencing the NF-kB inflammatory pathway, and reducing oxidative stress.<br> <br> Pathways:<br> -Stimulate cytokine production (e.g., interleukins, tumor necrosis factor) and enhance the function of macrophages and dendritic cells.<br> <a href="https://pubmed.ncbi.nlm.nih.gov/28727820/" > https://pubmed.ncbi.nlm.nih.gov/28727820/ </a> <br>
306
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mushTT
mushroom Turkey Tail
NP
<b>Turkey Tail (Trametes versicolor)</b><br> Key Compounds: Polysaccharide-K (PSK, also known as Krestin) and polysaccharide peptide (PSP).<br> <br> -Toll-Like Receptor (TLR) Activation<br> -Increased NK cell and cytotoxic T-cell activities<br> -Upregulation of IFN-γ<br>
127
-
Myr
Myricetin
NP
<b>Myricetin</b> is a naturally occurring flavonoid that has been the subject of extensive preclinical studies for its potential anticancer properties.<br> <br> Pathways:<br> -Inhibit the PI3K/Akt signaling pathway, which is often hyperactive in many cancers<br> -MAPK/ERK Pathway<br> -Inhibit NF‑κB activation<br> -Activate or enhance p53 signaling, thereby contributing to its anticancer effects -AK/STAT Signaling<br> -May inhibit angiogenesis (VEGF)<br> -Suppress the processes involved in metastasis, such as matrix metalloproteinase (MMP) activity<br> -Can exert antioxidant effects; however, in cancer cells, it sometimes induces oxidative stress beyond a threshold, contributing to apoptotic cell death.<br> -Inhibitory effects on mammalian TrxRs (thioredoxin reductase)<br>
183
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Myrrh
Myrrh
NP
<b>Myrrh</b> extract is a well-known medicinal plant with significant therapeutic benefits attributed to the activity of its diverse metabolites.<br>
128
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NarG
Naringin
NP
<b>Flavonoid glycoside</b>. Responsible for the bitterness of grapefruit.<br> Naringin is a flavonoid glycoside predominantly found in citrus fruits such as grapefruit and oranges. It is known for its antioxidant, anti-inflammatory, and potential anticancer properties.<br> -Antioxidant Activity<br> -Induction of Apoptosis<br> -Cell Cycle Arrest (often G1 or G2/M)<br> -Anti-inflammatory Effects<br> <br> -**a natural bioenhancer and reported to enhance the bioavailability of drugs by inhibiting cytochrome P450 and P-glycoprotein (P-gp)<br> -Usually paired with other bioflavonoids such as quercetin, hesperidin and rutin.<br> <br> -Mainly obtained from grapefruit<br> -Including enhanced solubility, improved bioavailability and targeted delivery.<br> -Antioxidant<br> -Inhibition of CYP19. Naringin suppresses the PI3K/AKT signalling pathway<br> -Wnt/β-catenin, PI3K/Akt, NF-ĸB, and TGF-β pathways<br> -Up-regulation of adenosine monophosphate-activated protein kinase (AMPK), and inhibition of gluconeogenesis<br> -Antioxidant effects, by modulating reactive oxygen species (ROS) levels and increasing superoxide dismutase (SOD)<br> -Naringenin can reduce carcinogenesis through pleiotropic processes such as antioxidative, apoptotic-inducing ROS generation, and cell cycle arrest<br> -Revealed new mechanisms underlying the hypolipidemic effects of naringin and naringenin, including regulation of lipid digestion, reverse cholesterol transport, and low-density lipoprotein receptor expression<br> -Low bioavailability (approximately 8.8%) when administered orally<br>
187
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NRF
nelfinavir/Viracept
RD
<b>NRF</b> is an antiretroviral medication used in the treatment of HIV/AIDS.<br> Nelfinavir belongs to the class of drugs known as protease inhibitors and like other PIs is almost always used in combination with other antiretroviral drugs.<br>
13
-
NCL
Niclosamide (Niclocide)
RD
<b>Used</b> to treat tapeworm infestations.<br>
268
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NAD
nicotinamide adenine dinucleotide
NP
<b>(Nicotinamide adenine dinucleotide)</b> is a vital coenzyme found in all living cells.<br> • It exists in two forms: oxidized (NAD⁺) and reduced (NADH), playing central roles in redox reactions, energy metabolism, and various signaling pathways.<br> • NAD⁺ is essential for critical cellular processes, including ATP production, DNA repair (via enzymes like PARPs), and regulation of sirtuins (a family of NAD⁺-dependent deacetylases involved in cellular stress responses and longevity).<br> <br> NAD⁺ is integral to energy metabolism, redox balance, DNA repair, and cellular regulatory functions—processes that are often dysregulated in cancer.<br> <br> <a href="https://medicorcancer.com/wp-content/uploads/Momentum-DCA-Brochure.pdf"> Medicor Cancer Centres offers it: </a><br> <br> -involved in glycolysis, the tricarboxylic acid (TCA) cycle, and oxidative phosphorylation.<br> -NMN is a precursor to nicotinamide adenine dinucleotide (NAD+)<br> -alternative form of vitamin B, amide of nicotinic acid<br> -NAD+ levels decline as we age<br> -high dose NMN promotes ferroptosis through NAM-mediated SIRT1-AMPK-ACC signaling<br> -At low doses (10 and 20 mM) and prolonged exposure (48 h), NMN increased cell proliferation, but it induced the suppression of cell proliferation at the high dose (100 mM)<br> -VitB3 and niacin are precursors for the synthesis of NAD in the body<br> <br>
250
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Nimb
Nimbolide
NP
<b>Nimbolide</b> is a compound found in the neem tree (Azadirachta indica) and has been studied for its potential anti-cancer properties. It is a type of limonoid, a class of compounds that are commonly found in citrus fruits and other plants.<br> <br> Research has shown that nimbolide has anti-proliferative and pro-apoptotic effects on various types of cancer cells, including breast, lung, colon, and prostate cancer cells. It has also been shown to inhibit the growth of cancer cells by inducing cell cycle arrest and apoptosis (programmed cell death).<br> <br> Some of the ways in which nimbolide may help to prevent or treat cancer include:<br> -Inhibiting the activity of certain enzymes that are involved in cancer cell growth and survival<br> -Inducing the production of reactive oxygen species (ROS) that can damage cancer cells<br> -Inhibiting the formation of new blood vessels that are needed to support the growth of cancer cells<br> -Enhancing the effectiveness of chemotherapy and radiation therapy<br>
22
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NIV
nivolumab
IM
Immunomodulatory antibodies
<b>Two</b> different inhibitory pathways that block antitumor T cell responses. <br>
297
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Nos
Noscapine
NP
<b>Noscapine</b> is a natural product. It is an isoquinoline alkaloid derived from the opium poppy (Papaver somniferum), although unlike some opium alkaloids, it does not have narcotic effects.<br> -Historically, it has been used as an antitussive (cough suppressant) due to its antitussive properties without causing the sedation associated with opiates.<br> <br> Pathways:<br> -Mitochondrial stress, release of cytochrome c, and activation of caspases (such as caspase-3), leading to cellular apoptosis.<br> -Inhibit angiogenesis<br> -Interfere with the NF-κB signaling pathway<br> <br> -Noscapine can enhance the effects of traditional chemotherapeutics when used in combination. It may help overcome drug resistance by modulating cell cycle regulators and apoptosis-related proteins.<br>
199
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Octr
octreotide
D
<b>Octreotide</b>, sold under the brand name Sandostatin among others, is an octapeptide that mimics natural somatostatin pharmacologically, though it is a more potent inhibitor of growth hormone, glucagon, and insulin than the natural hormone.<br> Octreotide works by binding to somatostatin receptors on the surface of cancer cells, which can help to slow down the growth and proliferation of these cells.<br>
14
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OLST
Orlistat
RD
<b>Inhibits</b> lipase and is used to facilitate weight loss.<br>
261
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OA
Oroxylin A
NP
<b>Oroxylin A</b> is a naturally occurring flavonoid, a type of polyphenolic compound known for its various bioactive properties.<br> Scutellaria baicalensis (Baikal skullcap): One of the primary sources of Oroxylin A, this traditional medicinal herb has been used in Chinese medicine for its anti-inflammatory and anti-cancer properties.<br> <br> Oroxylin A has been shown to impact various cellular signaling pathways, such as the NF-κB, PI3K/Akt, and MAPK pathways.<br>
129
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OA
Oroxylin-A
NP
<b>O-methylated flavone</b>, a chemical compound that can be found in the medicinal plants Scutellaria baicalensis [1] and Scutellaria lateriflora, [2] [3] and the Oroxylum indicum tree. [4]<br>
253
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Osi
Osimertinib
D
<b>Osimertinib</b> works by selectively inhibiting the activity of EGFR, which is a protein that plays a critical role in the growth and survival of cancer cells. By blocking the activity of EGFR, osimertinib prevents the growth and proliferation of cancer cells, leading to tumor shrinkage and improved survival.<br> Osimertinib has been shown to be effective in patients with NSCLC who have specific EGFR mutations. In the AURA3 trial, osimertinib significantly improved progression-free survival (PFS) compared with platinum-based chemotherapy. In the FLAURA trial, osimertinib significantly improved PFS and overall survival (OS) compared with erlotinib or gefitinib.<br>
213
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OXA
Oxaliplatin
D
<b>Oxaliplatin</b> is a chemotherapy medication used to treat mainly colorectal cancer. It is a platinum-based drug that works by interfering with the DNA of cancer cells, preventing them from reproducing and eventually leading to cell death.<br> <br> Oxaliplatin is often used in combination with other chemotherapy medications, such as 5-fluorouracil (5-FU) and leucovorin to treat CRC.<br>
239
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OAA
oxaloacetate
NP
</b>Oxaloacetate</b> is a four-carbon dicarboxylic acid that plays a crucial role in the citric acid cycle (Krebs cycle), which is essential for cellular respiration and energy production. oxaloacetate may have tumor-suppressive properties. <br> <br> In the citric acid cycle, oxaloacetate is formed from the condensation of acetyl-CoA and oxaloacetate itself, and it plays a crucial role in the metabolism of carbohydrates, fats, and proteins. It is involved in energy production and the synthesis of various biomolecules.<br> <br> Oxaloacetate can also be produced through other metabolic pathways, such as gluconeogenesis and the transamination of aspartate<br> Oxaloacetate can be derived from several sources and metabolic pathways in the body. Here are the primary sources of oxaloacetate:<br> <br> Citric Acid Cycle (Krebs Cycle):<br> Oxaloacetate is a key intermediate in the citric acid cycle, where it is formed from the condensation of acetyl-CoA and oxaloacetate itself. It is also regenerated at the end of the cycle after the conversion of succinate to fumarate and then to malate.<br> Gluconeogenesis:<br> During gluconeogenesis, which is the process of synthesizing glucose from non-carbohydrate precursors, oxaloacetate is produced from pyruvate through the action of the enzyme pyruvate carboxylase. This pathway is particularly important during fasting or intense exercise.<br> <br> • Oxaloacetate is a central metabolite in energy metabolism with links to multiple pathways altered in cancer cells (e.g., the TCA cycle, glycolysis, anaplerosis, redox balance, and nucleotide synthesis).<br>
173
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Oxy
Oxygen, Hyperbaric
T
Therapy
<b>Hyperbaric oxygen (HBO) therapy</b> is a treatment where patients breathe 100% oxygen inside a pressurized chamber. This approach increases the oxygen concentration in the blood and tissues.<br> <br> Enhanced Oxygenation of Tumors:<br> -Many tumors are hypoxic (low in oxygen), which can make them more resistant to radiation and some forms of chemotherapy. Enhanced oxygenation through HBO may help overcome this hypoxia.<br> Increased oxygen levels can lead to the formation of reactive oxygen species (ROS), which may damage cancer cells and sensitize them to treatment.<br> <br> Synergistic Effects with Radiation Therapy:<br> -Oxygen acts as a radiosensitizer. Radiation-induced DNA damage can be more effective in the presence of oxygen, potentially improving the efficacy of radiotherapy.<br> Some studies have explored combining HBO with radiotherapy to overcome radioresistance in hypoxic tumor regions.<br> <br> Improved Delivery of Chemotherapeutic Agents:<br> -Elevated tissue oxygenation might enhance the delivery and efficacy of certain chemotherapeutic drugs, although this area is still under investigation.<br> <br> Potential Immune Modulation:<br> -There is ongoing research into whether HBO can modulate the tumor microenvironment in a way that is more favorable for anti-tumor immune responses.<br> <br> Possible problems:<br> -Implanted device (such as an insulin pump or pacemaker)<br> -Avoid with recent perforated ear drum<br> -Pneumothorax<br> -Wait for 4 wks after chemo?<br>
323
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PA
Pachymic acid
NP
<b>Pachymic acid</b> is a lanostane-type triterpenoid predominantly extracted from the sclerotium of the fungus Poria cocos (also known as Fu Ling in Traditional Chinese Medicine).<br> <br> Pachymic acid (PA) is a triterpene found in Poria, and molecular docking revealed that PA has a much higher affinity for HK II than G6P (molecular docking scores of 8.18 and 5.31, respectively)<br>
182
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PacT
Paclitaxel
D
<b>Paclitaxel</b> (brand name Taxol) is a chemotherapy medication used to treat ovarian cancer, esophageal cancer, breast cancer, lung cancer, Kaposi's sarcoma, cervical cancer, and pancreatic cancer. Administered by intravenous injection.<br> Derived from a natural product, Taxol (from Pacific Yew Tree).<br>
246
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Pap
papain
NP
<b>Papain</b> is a proteolytic enzyme found in papaya fruit. It has been studied for its potential anti-cancer properties.<br> • Inhibiting cancer cell growth: Papain has been shown to inhibit the growth of cancer cells in laboratory studies.<br> • Inducing apoptosis: Papain can induce apoptosis (programmed cell death) in cancer cells, which can help to reduce tumor size.<br> • Anti-angiogenic activity: Papain has been shown to inhibit the formation of new blood vessels, which is necessary for tumor growth.<br> • Immune system modulation: Papain may help to stimulate the immune system to attack cancer cells.<br>
8
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Part
Parthenolide
NP
<b>Parthenolide</b> is a naturally occurring sesquiterpene lactone derived from the medicinal plant feverfew (Tanacetum parthenium). <br> -Micheliolide (MCL) is converted readily from parthenolide (PTL), and has better stability and solubility than PTL<br> -Parthenolide is a natural compound used to treat migraines and arthritis and found to act as a potent NF-κB signaling inhibitor.<br> <br> Main activities include:<br> -Inhibition of NF-κB Signaling:<br> -Induction of Oxidative Stress (ROS): oxidative stress can overwhelm the antioxidant defenses of the cancer cells, leading to cellular damage and death<br> -Parthenolide can interfere with STAT3 signaling, inhibiting the transcription of genes that favor tumor growth and resistance to apoptosis.<br> -Modulation of the MAPK/ERK Pathway:<br> -Impact on the JNK Pathway:<br> -Parthenolide has been shown to target cancer stem cells<br>
311
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PawPaw
Paw Paw
NP
<b>Paw Paw Cell Reg</b><br> -Extract is from the twigs of Asimina triloba tree<br> -Contains unique biological compounds called acetogenins, that were found to affect cells in the body that need and use higher ATP energy than normal cells. <br> <a href="https://healthy-sunshine.com/paw-paw-cell-reg-180-caps/" >Paw Paw Cell Reg </a>
23
-
Pem
pembrolizumab
IM
Immunomodulatory antibodies
<b>Two</b> different inhibitory pathways that block antitumor T cell responses. <br>
130
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P
Peppermint
NP
<b>Cross</b> between watermint and spearmint. Cultivated for oil, leaves and flavor.<br>
336
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Per
Perilla
NP
<b>Perilla<b> (commonly Perilla frutescens) is an herb used traditionally in various Asian cuisines and traditional medicine. It contains several bioactive compounds including flavonoids, phenolic acids, and fatty acids, which have been studied for their antioxidant, anti-inflammatory, and antimicrobial properties.</br>
174
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pH-AT
pH-Alkalization Therapy
T
Therapy
<b>pH-alkalization therapy</b> is a term used to describe strategies aimed at altering the pH (or acidity/alkalinity) of the tumor microenvironment in an effort to inhibit cancer growth and spread.<br> <br> -Normal tissues have a higher extracellular pH than intracellular pH, in cancer is exactly the opposite (inversion of the pH gradient).<br> <br> -Acidic Microenvironment: Many tumors exhibit an acidic microenvironment. This is largely due to the high rate of glycolysis (often referred to as the Warburg effect), even in the presence of oxygen, leading to lactate production. Acidification is thought to promote invasion, metastasis, and resistance to certain chemotherapies.<br> <br> -The basic premise behind pH-alkalization therapy is that by increasing the pH (making the environment less acidic), one might impair cancer cells’ adaptive advantage, reduce their proliferative and invasive capabilities, and perhaps render them more susceptible to standard treatments.<br> -Various approaches have been proposed to achieve a more alkaline microenvironment, such as dietary modifications (e.g., an "alkaline diet"), supplements (like bicarbonate), or drugs designed to interfere with proton pumps or transporters on cancer cells.<br> <br> -Most experts view pH-alkalization strategies as potentially complementary to conventional therapies (e.g., chemotherapy, radiotherapy, immunotherapy), rather than as a standalone cure for cancer.<br> <br> Natural Products with possible effect:<br> Fruits<br> -Lemons and Limes:acidic in their natural state, often considered alkalizing after digestion -Watermelon: High water content and alkaline minerals.<br> -Berries: Blueberries, raspberries, and strawberries antioxidants and have alkalizing minerals.<br> -Avocado: Provides healthy fats and may have an alkalizing effect.<br> Vegetables<br> -Leafy Greens: Spinach, kale, swiss chard, and collard greens (chlorophyll, to help reduce acidity.)<br> -Broccoli and Cauliflower: Cruciferous vegetables with a good mineral profile to support alkalinity.<br> -Cucumber: High water content and mild alkalizing properties.<br> -Celery: Often recommended for its hydrating and alkalizing effect.<br> Nuts & Seeds<br> -Almonds: Considered one of the more alkaline nuts.<br> -Flaxseeds and Chia Seeds: Rich in omega-3s and other minerals that may contribute positively.<br> -Legumes & Grains Quinoa: lower acid load compared to some other grains.<br> -Lentils:Provide protein and fiber while being relatively alkaline in nature.<br> Others<br> -Herbal Teas: Teas made from herbs like ginger or chamomile may support a balanced internal environment.<br> -Coconut Water: Rich in electrolytes and naturally alkaline.<br> -Baking Soda (Sodium Bicarbonate):<br> -Green Juices: Juices or smoothies made predominantly from leafy greens and vegetables can help maintain a mineral balance that leans toward alkalinity.<br> <br> <a href=https://www.amazon.ca/dp/B01ATZG6M6?ref_=cb_interstitial_us_ca_desktop_unrec_location_unk_dp_dp&th=1" >Basentabs food supplements that are strongly alkaline </a> <br>
15
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PB
Phenylbutyrate
RD
<b>Used</b> to treat urea cycle disorders<br> Sodium phenylbutyrate helps remove ammonia from the body.<br> -Phenyl-butyrate (PB)4 is an aromatic fatty acid that is converted in vivo to phenylacetate (PA) by β-oxidation in liver and kidney mitochondria.<br> -In human body, phenylbutyrate is oxidized to phenylacetate, which is in turn conjugated with glutamine and eliminated in urine as phenylacetylglutamine, thereby mediating elimination of waste nitrogen<br> -Phenylbutyrate is one of the first drugs encountered in cancer therapy as a histone deacetylase inhibitor (HDACI).<br> -Butyric acid is one of the short-chain fatty acids produced by the gut microbiota through the fermentation of dietary fiber. Butyrate is primarily recognized for its beneficial effects in the colon and is tightly linked to gut health. <br> -Phenylbutyrate is a derivative of butyrate that has been chemically modified by the addition of a phenyl group. This structural change increases its lipophilicity (fat solubility) and alters its metabolic fate and biological activity. This allows it to be used as a systemic drug, in contrast to the locally produced butyrate in the gut, which is rapidly metabolized by colonocytes<br> <br> Pathways:<br> -Histone deacetylase (HDAC) inhibitor<br> -ER stress inhibitor (at least in normal cell)<br> -Can act as a chemical chaperone, helping to reduce ER stress by facilitating proper protein folding.<br> -Modulation of NF-κB Signaling<br> -Changes in pathways such as PI3K/Akt/mTOR and MAPK.<br> -Some preclinical investigations have reported that treatment with phenylbutyrate leads to mitochondrial dysfunction and endoplasmic reticulum (ER) stress, both of which can result in an increase of ROS within cancer cells. <br> <br> Note: Sodium butyrate (NaBu) vs Sodium phenylbutyrate<br> -Sodium butyrate is primarily a research tool with limited clinical application, whereas phenylbutyrate is used clinically<br> -Phenylbutyrate typically exhibits improved pharmacokinetics and is more amenable to systemic use compared to sodium butyrate.<br> -Both compounds act as HDAC inhibitors, phenylbutyrate additionally modulates ER stress and mitochondrial function, leading to potentially greater ROS production in certain cancer cells.<br> <br> <a href="https://www.purepba.com/shop/">https://www.purepba.com/shop/ </a>
175
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PDT
Photodynamic Therapy
T
Therapy
<b>Photodynamic therapy</b> is a form of phototherapy involving light and a photosensitizing chemical substance used in conjunction with molecular oxygen to elicit cell death. <br>
132
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PFB
Physalin F & B
NP
Anti-inflammatory, immunomodulatory
<b>From</b> Physalis minima
133
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PI
Piperine
NP
<b>Compound</b> of black pepper that boosts bioavailability of curcumin<br>
134
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PL
Piperlongumine
NP
<b>Piperlongumine</b> (also called Piplartine), an alkaloid from long pepper fruit<br> -Piperlongumine is a bioactive alkaloid derived from the long pepper (Piper longum) <br> – Piperlongumine has been shown to selectively increase ROS levels in cancer cells.<br> -NLRP3 inhibitor?<br> -TrxR inhibitor (major antioxidant system) to increase ROS in cancer cells<br> -ic50 cancer cells maybe 2-10uM, normal cells maybe exceeding 20uM.<br> <br> Available from mcsformulas.com <br> -(Long Pepper, 500mg/Capsule)- 1 capsule 3 times daily with food<br> -Piperlongumine Pro Liposomal, 40 mg-take 1 capsule daily with plenty of water, after a meal<br> <br> -Note <a href="tbResList.php?qv=134&tsv=1109&wNotes=on&exSp=open">half-life</a> 30–60 minutes<br> <a href="tbResList.php?qv=134&tsv=792&wNotes=on&exSp=open">BioAv</a> poor aqueous solubility and bioavailability <br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - induce <a href="tbResList.php?qv=134&tsv=275&wNotes=on">ROS</a> production in cancer cells likely at any dose. Effect on normal cells is inconclusive.<br> - ROS↑ related: <a href="tbResList.php?qv=134&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?qv=134&tsv=103&wNotes=on">ER Stress↑</a>, <a href="tbResList.php?qv=134&tsv=459&wNotes=on">UPR↑</a>, <!--<a href="tbResList.php?qv=134&tsv=356&wNotes=on">GRP78↑</a>,--> <!--<a href="tbResList.php?qv=134&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>, ,--> <a href="tbResList.php?qv=134&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?qv=134&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?qv=134&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?qv=134&tsv=239&wNotes=on">cl-PARP↑</a>, <!--<a href="tbResList.php?qv=134&wNotes=on&word=HSP">HSP↓</a>, --> <a href="tbResList.php?qv=134&wNotes=on&word=Prx">Prx</a>,<!-- mitochondrial antioxidant enzyme--> <br> <!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, --> - Lowers some AntiOxidant markers/ defense in Cancer Cells: <a href="tbResList.php?qv=134&tsv=226&wNotes=on&word=NRF2"> but mostly raises NRF2 </a>(raises antiO defense), <a href="tbResList.php?qv=134&word=Trx&wNotes=on">TrxR↓</a>(*important),<!-- major antioxidant system --> <!--<a href="tbResList.php?qv=134&tsv=298&wNotes=on&word=SOD↓">SOD↓</a>,--> <a href="tbResList.php?qv=134&tsv=137&wNotes=on&word=GSH↓">GSH↓</a> <a href="tbResList.php?qv=134&tsv=46&wNotes=on">Catalase↓</a> <a href="tbResList.php?qv=134&tsv=597&wNotes=on">HO1↓</a> <a href="tbResList.php?qv=134&wNotes=on&word=GPx">GPx↓</a> <br> - Very little indication of raising <a href="tbResList.php?qv=134&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <!--<a href="tbResList.php?qv=134&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>,--> <!--<a href="tbResList.php?qv=134&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>,--> <!--<a href="tbResList.php?qv=134&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>,--> <a href="tbResList.php?qv=134&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <!--<a href="tbResList.php?qv=134&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>,--> <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?qv=134&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?qv=134&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?qv=134&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, <a href="tbResList.php?qv=134&tsv=235&wNotes=on&word=p38">conversely p38↑</a>, Pro-Inflammatory Cytokines : <a href="tbResList.php?qv=134&tsv=908&wNotes=on&word=NLRP3↓">NLRP3↓</a>, <a href="tbResList.php?qv=134&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, <a href="tbResList.php?qv=134&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?qv=134&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <a href="tbResList.php?qv=134&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a> <br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓ inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.--> - inhibit Growth/Metastases : <a href="tbResList.php?qv=134&tsv=604&wNotes=on">TumMeta↓</a>, <a href="tbResList.php?qv=134&tsv=323&wNotes=on">TumCG↓</a>, <a href="tbResList.php?qv=134&tsv=96&wNotes=on">EMT↓</a>, <!--<a href="tbResList.php?qv=134&tsv=204&wNotes=on">MMPs↓</a>,--> <a href="tbResList.php?qv=134&tsv=201&wNotes=on">MMP2↓</a>, <a href="tbResList.php?qv=134&tsv=203&wNotes=on">MMP9↓</a>, <!--<a href="tbResList.php?qv=134&tsv=308&wNotes=on">TIMP2</a>,--> <!--<a href="tbResList.php?qv=134&tsv=415&wNotes=on">IGF-1↓</a>,--> <!--<a href="tbResList.php?qv=134&tsv=428&wNotes=on">uPA↓</a>, --> <a href="tbResList.php?qv=134&tsv=334&wNotes=on">VEGF↓</a>, <!--<a href="tbResList.php?qv=134&tsv=1284&wNotes=on">ROCK1↓</a>, --> <!--<a href="tbResList.php?qv=134&tsv=110&wNotes=on">FAK↓</a>, --> <!--<a href="tbResList.php?qv=134&tsv=273&wNotes=on">RhoA↓</a>, --> <a href="tbResList.php?qv=134&tsv=214&wNotes=on">NF-κB↓</a>, <a href="tbResList.php?qv=134&tsv=79&wNotes=on">CXCR4↓</a>, <!--<a href="tbResList.php?qv=134&tsv=1247&wNotes=on">SDF1↓</a>,--> <!--<a href="tbResList.php?qv=134&tsv=304&wNotes=on">TGF-β↓</a>,--> <!--<a href="tbResList.php?qv=134&tsv=719&wNotes=on">α-SMA↓</a>,--> <a href="tbResList.php?qv=134&tsv=105&wNotes=on">ERK↓</a> <br> <!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, --> - reactivate genes thereby inhibiting cancer cell growth : <a href="tbResList.php?qv=134&tsv=140&wNotes=on">HDAC↓</a>(few reports), <a href="tbResList.php?qv=134&tsv=85&wNotes=on">DNMT1↓</a>, <a href="tbResList.php?qv=134&tsv=86&wNotes=on">DNMT3A↓</a>, <a href="tbResList.php?qv=134&tsv=108&wNotes=on">EZH2↓</a>, <a href="tbResList.php?qv=134&tsv=236&wNotes=on">P53↑</a>, <a href="tbResList.php?qv=134&wNotes=on&word=HSP">HSP↓</a>, <a href="tbResList.php?qv=134&tsv=506&wNotes=on">Sp proteins↓</a>, <br> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?qv=134&tsv=322&wNotes=on">TumCCA↑</a>, <a href="tbResList.php?qv=134&tsv=73&wNotes=on">cyclin D1↓</a>, <!--<a href="tbResList.php?qv=134&tsv=378&wNotes=on">cyclin E↓</a>,--> <a href="tbResList.php?qv=134&tsv=467&wNotes=on">CDK2↓</a>, <a href="tbResList.php?qv=134&tsv=894&wNotes=on">CDK4↓</a>, <a href="tbResList.php?qv=134&tsv=895&wNotes=on">CDK6↓</a>, <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?qv=134&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?qv=134&tsv=324&wNotes=on">TumCI↓</a>, <!--<a href="tbResList.php?qv=134&tsv=110&wNotes=on">FAK↓</a>,--> <a href="tbResList.php?qv=134&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=134&tsv=96&wNotes=on">EMT↓</a>, <!--<a href="tbResList.php?qv=134&tsv=1117&wNotes=on">TOP1↓</a>,--> <!--<a href="tbResList.php?qv=134&tsv=657&wNotes=on">TET1↓</a>,--> <br> <!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS --> - small indication of inhibiting <a href="tbResList.php?qv=134&tsv=129&wNotes=on">glycolysis</a> <!--/<a href="tbResList.php?qv=134&tsv=947&wNotes=on">Warburg Effect</a> and <a href="tbResList.php?qv=134&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> -->: <a href="tbResList.php?qv=134&tsv=143&wNotes=on">HIF-1α↓</a>, <!--<a href="tbResList.php?qv=134&tsv=772&wNotes=on">PKM2↓</a>, --> <a href="tbResList.php?qv=134&tsv=35&wNotes=on">cMyc↓</a>, <!--<a href="tbResList.php?qv=134&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>, --> <a href="tbResList.php?qv=134&tsv=906&wNotes=on">LDH↓</a>, <!--<a href="tbResList.php?qv=134&tsv=175&wNotes=on&word=LDH">LDHA↓</a>, --> <a href="tbResList.php?qv=134&tsv=773&wNotes=on">HK2↓</a>, <!-- <a href="tbResList.php?qv=134&wNotes=on&word=PFK">PFKs↓</a>, <a href="tbResList.php?qv=134&wNotes=on&word=PDK">PDKs↓</a>, <a href="tbResList.php?qv=134&tsv=847&wNotes=on">ECAR↓</a>, <a href="tbResList.php?qv=134&tsv=230&wNotes=on">OXPHOS↓</a>, <a href="tbResList.php?qv=134&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=134&tsv=1278&wNotes=on">Glucose↓</a>, <a href="tbResList.php?qv=134&tsv=623&wNotes=on">GlucoseCon↓</a> --> <br> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - inhibits <a href="tbResList.php?qv=134&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=134&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=134&tsv=143&wNotes=on">HIF-1α↓</a>, <!--<a href="tbResList.php?qv=134&wNotes=on&word=NOTCH">Notch↓</a>,--> <!--<a href="tbResList.php?qv=134&wNotes=on&word=FGF">FGF↓</a>,--> <!--<a href="tbResList.php?qv=134&tsv=361&wNotes=on">PDGF↓</a>,--> <a href="tbResList.php?qv=134&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, <!--<a href="tbResList.php?qv=134&&wNotes=on&word=ITG">Integrins↓</a>, --> <br> <!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, - inhibits Cancer Stem Cells : <a href="tbResList.php?qv=134&tsv=795&wNotes=on">CSC↓</a>, <a href="tbResList.php?qv=134&tsv=524&wNotes=on">CK2↓</a>, <a href="tbResList.php?qv=134&tsv=141&wNotes=on">Hh↓</a>, <a href="tbResList.php?qv=134&tsv=434&wNotes=on">GLi↓</a>, <a href="tbResList.php?qv=134&tsv=124&wNotes=on">GLi1↓</a>, <a href="tbResList.php?qv=134&tsv=677&wNotes=on">CD133↓</a>, <a href="tbResList.php?qv=134&tsv=655&wNotes=on">CD24↓</a>, <a href="tbResList.php?qv=134&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=134&tsv=357&wNotes=on">n-myc↓</a>, <a href="tbResList.php?qv=134&tsv=656&wNotes=on">sox2↓</a>, <a href="tbResList.php?qv=134&tsv=222&wNotes=on">notch2↓</a>, <a href="tbResList.php?qv=134&tsv=1024&wNotes=on">nestin↓</a>, <a href="tbResList.php?qv=134&tsv=508&wNotes=on">OCT4↓</a>, <br> --> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=134&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=134&tsv=4&wNotes=on">AKT↓</a>, <a href="tbResList.php?qv=134&wNotes=on&word=JAK">JAK↓</a>, <a href="tbResList.php?qv=134&wNotes=on&word=STAT">STAT↓</a>, <!--<a href="tbResList.php?qv=134&tsv=377&wNotes=on">Wnt↓</a>, --> <a href="tbResList.php?qv=134&tsv=342&wNotes=on">β-catenin↓</a>, <!--<a href="tbResList.php?qv=134&tsv=9&wNotes=on">AMPK</a>, --> <!--<a href="tbResList.php?qv=134&tsv=475&wNotes=on">α↓</a>, --> <a href="tbResList.php?qv=134&tsv=105&wNotes=on">ERK↓</a>, <!--<a href="tbResList.php?qv=134&tsv=1014&wNotes=on">5↓</a>, --> <a href="tbResList.php?qv=134&tsv=168&wNotes=on">JNK</a>, <br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=134&tsv=1106&wNotes=on">chemo-sensitization</a>, <!--<a href="tbResList.php?qv=134&tsv=1171&wNotes=on">chemoProtective</a>, --> <a href="tbResList.php?qv=134&tsv=1107&wNotes=on">RadioSensitizer</a>, <!--<a href="tbResList.php?qv=134&tsv=1185&wNotes=on">RadioProtective</a>, --> <a href="tbResList.php?qv=134&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <a href="tbResList.php?qv=134&tsv=1105&wNotes=on">Neuroprotective</a>, <a href="tbResList.php?qv=134&tsv=557&wNotes=on">Cognitive</a>, <!--<a href="tbResList.php?qv=134&tsv=1175&wNotes=on">Renoprotection</a>, --> <a href="tbResList.php?qv=134&tsv=1179&wNotes=on">Hepatoprotective</a>, <a href="tbResList.php?&qv=134&tsv=1188&wNotes=on">CardioProtective</a>, <br> <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=134&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br>
135
-
PIT
Pitavastatin
NP
Statin
<b>Higher</b> choice statin over Atorvastatin.<br>
299
-
Plum
Plumbagin
NP
<b>Plumbagin</b> (5-hydroxy-2-methyl-1,4-naphthoquinone) is a naturally occurring naphthoquinone derivative.<br> <br> –Plumbagin can undergo redox cycling to generate reactive oxygen species (ROS)<br> -apototosis, activation of caspases, modulation of Bax, Bcl‑2, loss of MMP.<br> -Cell cycle arrest in cancer cells, often at the G0/G1, or G2/M phases.<br> -May inhibit NF‑κB activation<br> – MAPK Pathways<br> – PI3K/Akt Pathway<br> -Downregulation of (VEGF) and matrix metalloproteinases (MMPs).<br> <br> -Seems capable of raising ROS in normal and cancer cells (#2004)<br> <br> -ic50 cancer cells 1-10uM, normal cells >10uM<br>
136
-
PACs
Proanthocyanidins
NP
<b>Polyphenols</b> found in cranberry, blueberry, and grape seeds.<br> <br> Proanthocyanidin B2 (PB2) is a type of dimer flavonoid that is found in grape seed, pine bark, wine, and tea leaves [17]. PB2 has been shown to possess various bioactivities, including anti-oxidant, anti-inflammation, and anti-obesity activities, and it has also shown efficacy in the treatment of cancer, cardiovascular disease, type 2 diabetes, ulcerative colitis, as well as acute liver injury. <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC6525465/"> PKM2 is the target of proanthocyanidin B2 </a><br> <br> PB2 also suppressed glucose uptake and lactate levels via the direct inhibition of the key glycolytic enzyme, PKM2.<br>
256
-
ProBio
probiotics
NP
<b>Probiotics</b> contain live bacteria the supplements the gastrointestinal flora. (Which can be affected from infection or antibiotics drugs.)<br> Some studies have suggested that gut microbiota—including Bifidobacterium species—can affect systemic immunity. This is important because the state of the immune system influences the body’s ability to fight cancer and also the response to immunotherapies.<br> Preclinical investigations have demonstrated that certain Bifidobacterium strains may help improve responses to immune checkpoint inhibitors in animal models. <br> There has been emerging research looking into discrete strains or formulations of Bifidobacterium longum (sometimes labeled with additional identifiers such as RAPO) that may have unique properties or enhanced effects.<br>
137
-
PBG
Propolis -bee glue
NP
Compound
<b>Brazilian Green Propolis</b> often considered best<br> • Derived from Baccharis dracunulifolia, this type is rich in artepillin C.<br> • It has been widely researched for its anticancer, anti-inflammatory, and antioxidant properties.<br> -Propolis common researched flavonoids :chrysin, pinocembrin, galangin, pinobanksin(Pinocembrin)<br> -most representative phenolic acids were caffeic acid, p-coumaric acid, and ferulic acid, as well as their derivatives, DMCA and caffeic acid prenyl, benzyl, phenylethyl (CAPE), and cinnamyl esters<br> -One of the most studied active compounds of a poplar-type propolis is caffeic acid phenethyl ester (CAPE)<br> -caffeic acid phenethyl ester (CAPE), galangin, chrysin, nemorosone, propolin G, artepillin C, cardanol, pinocembrin, pinobanksin, chicoric acid, and phenolic acids (caffeic acid, ferulic acid, and coumaric acid), as well as luteolin, apigenin, myricetin, naringenin, kaempferol, quercetin, polysaccharides, tannins, terpenes, sterols, and aldehydes -content highly variable based on location and extraction<br> Two main factors of interest:<br> 1. affects interstitual fluild pH<br> 2. high concentration raises ROS (Reactive Oxygen Species), while low concentration may reduce ROS<br> <br> - Artepillin-C (major phenolic compounds found in Brazilian green propolis (BGP))<br> - caffeic acid major source<br> <br> <a href="https://pubmed.ncbi.nlm.nih.gov/37864895/"> Do not combine with 2DG </a> <br> <br> Pathways:<br> -Propolis compounds (e.g., artepillin C, caffeic acid phenethyl ester [CAPE]) can trigger apoptosis (programmed cell death) in cancer cells.<br> -Propolis has been shown to inhibit NF‑κB activation.<br> -Propolis extracts can cause cell cycle arrest at specific checkpoints (e.g., G0/G1 or G2/M phases).<br> -Enhance the body’s antitumor immune responses, for example by activating natural killer (NK) cells and modulating cytokine profiles.<br> <br> -Note <a href="tbResList.php?qv=137&tsv=1109&wNotes=on&exSp=open">half-life</a> no standard, high variablity of content.<br> <a href="tbResList.php?qv=137&tsv=792&wNotes=on&exSp=open">BioAv</a> poor water solubility, and low oral bioavailability. <br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - high concentration may induce <a href="tbResList.php?qv=137&tsv=275&wNotes=on">ROS</a> production, while low concentrations mya low it. This may apply to both normal and cancer cells. <a href="https://nestronics.ca/dbx/tbResEdit.php?rid=3251">Normal Cells Example.</a> (Also not sure if high level are acheivable in vivo due to bioavailability)<br> - ROS↑ related: <a href="tbResList.php?qv=137&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?qv=137&tsv=103&wNotes=on">ER Stress↑</a>, <a href="tbResList.php?qv=137&tsv=459&wNotes=on">UPR↑</a>, <a href="tbResList.php?qv=137&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=137&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>, <a href="tbResList.php?qv=137&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?qv=137&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?qv=137&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?qv=137&tsv=239&wNotes=on">cl-PARP↑</a>, <a href="tbResList.php?qv=137&wNotes=on&word=HSP">HSP↓</a>, <a href="tbResList.php?qv=137&wNotes=on&word=Prx">Prx</a>,<!-- mitochondrial antioxidant enzyme--> <br> <!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, --> <!-- - Lowers AntiOxidant defense in Cancer Cells: <a href="tbResList.php?qv=137&tsv=226&wNotes=on&word=NRF2↓">NRF2↓</a>, <a href="tbResList.php?qv=137&word=Trx&wNotes=on">TrxR↓**</a>,<!-- major antioxidant system --> <a href="tbResList.php?qv=137&tsv=298&wNotes=on&word=SOD↓">SOD↓</a>, <a href="tbResList.php?qv=137&tsv=137&wNotes=on&word=GSH↓">GSH↓</a> <a href="tbResList.php?qv=137&tsv=46&wNotes=on">Catalase↓</a> <a href="tbResList.php?qv=137&tsv=597&wNotes=on">HO1↓</a> <a href="tbResList.php?qv=137&wNotes=on&word=GPx">GPx↓</a> --> <br> - Raises <a href="tbResList.php?qv=137&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?qv=137&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>, <a href="tbResList.php?qv=137&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?qv=137&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?qv=137&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?qv=137&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?qv=137&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?qv=137&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?qv=137&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, <!-- <a href="tbResList.php?qv=137&tsv=235&wNotes=on&word=p38↓">p38↓</a>, -->Pro-Inflammatory Cytokines : <a href="tbResList.php?qv=137&tsv=908&wNotes=on&word=NLRP3↓">NLRP3↓</a>, <!-- <a href="tbResList.php?qv=137&tsv=978&wNotes=on&word=IL-1β↓">IL-1β↓</a>, --> <a href="tbResList.php?qv=137&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?qv=137&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <a href="tbResList.php?qv=137&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a> <br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓ inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.--> - inhibit Growth/Metastases : <a href="tbResList.php?qv=137&tsv=604&wNotes=on">TumMeta↓</a>, <a href="tbResList.php?qv=137&tsv=323&wNotes=on">TumCG↓</a>, <a href="tbResList.php?qv=137&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=137&tsv=204&wNotes=on">MMPs↓</a>, <a href="tbResList.php?qv=137&tsv=201&wNotes=on">MMP2↓</a>, <a href="tbResList.php?qv=137&tsv=203&wNotes=on">MMP9↓</a>, <!-- <a href="tbResList.php?qv=137&tsv=308&wNotes=on">TIMP2</a>, --> <a href="tbResList.php?qv=137&tsv=415&wNotes=on">IGF-1↓</a>, <a href="tbResList.php?qv=137&tsv=428&wNotes=on">uPA↓</a>, <a href="tbResList.php?qv=137&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=137&tsv=1284&wNotes=on">ROCK1↓</a>, <a href="tbResList.php?qv=137&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?qv=137&tsv=273&wNotes=on">RhoA↓</a>, <a href="tbResList.php?qv=137&tsv=214&wNotes=on">NF-κB↓</a>, <!-- <a href="tbResList.php?qv=137&tsv=79&wNotes=on">CXCR4↓</a>, --> <!-- <a href="tbResList.php?qv=137&tsv=1247&wNotes=on">SDF1↓</a>, --> <a href="tbResList.php?qv=137&tsv=304&wNotes=on">TGF-β↓</a>, <a href="tbResList.php?qv=137&tsv=719&wNotes=on">α-SMA↓</a>, <a href="tbResList.php?qv=137&tsv=105&wNotes=on">ERK↓</a> <!-- <a href="tbResList.php?qv=137&tsv=1178&wNotes=on">MARK4↓</a> --><!-- contributing to tumor growth, invasion, and metastasis--> <br> <!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, --> - reactivate genes thereby inhibiting cancer cell growth : <a href="tbResList.php?qv=137&tsv=140&wNotes=on">HDAC↓</a>, <!-- <a href="tbResList.php?qv=137&wNotes=on&word=DNMT">DNMTs↓</a>, --> <!-- <a href="tbResList.php?qv=137&tsv=108&wNotes=on">EZH2↓</a>, --> <a href="tbResList.php?qv=137&tsv=236&wNotes=on">P53↑</a>, <!-- <a href="tbResList.php?qv=137&wNotes=on&word=HSP">HSP↓</a>, --> <!-- <a href="tbResList.php?qv=137&tsv=506&wNotes=on">Sp proteins↓</a>, --> <!-- <a href="tbResList.php?qv=137&wNotes=on&word=TET">TET↑</a> --> <br> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?qv=137&tsv=322&wNotes=on">TumCCA↑</a>, <a href="tbResList.php?qv=137&tsv=73&wNotes=on">cyclin D1↓</a>, <a href="tbResList.php?qv=137&tsv=378&wNotes=on">cyclin E↓</a>, <a href="tbResList.php?qv=137&tsv=467&wNotes=on">CDK2↓</a>, <a href="tbResList.php?qv=137&tsv=894&wNotes=on">CDK4↓</a>, <a href="tbResList.php?qv=137&tsv=895&wNotes=on">CDK6↓</a>, <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?qv=137&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?qv=137&tsv=324&wNotes=on">TumCI↓</a>, <a href="tbResList.php?qv=137&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <!-- encourages invasion, proliferation, EMT, and angiogenesis --> <a href="tbResList.php?qv=137&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?qv=137&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=137&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=137&wNotes=on&word=TOP">TOP1↓</a>, <a href="tbResList.php?qv=137&tsv=657&wNotes=on">TET1</a>, <br> <!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS --> - inhibits <a href="tbResList.php?qv=137&tsv=129&wNotes=on">glycolysis</a> /<a href="tbResList.php?qv=137&tsv=947&wNotes=on">Warburg Effect</a> and <a href="tbResList.php?qv=137&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> : <a href="tbResList.php?qv=137&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=137&tsv=772&wNotes=on">PKM2↓</a>, <a href="tbResList.php?qv=137&tsv=35&wNotes=on">cMyc↓</a>, <a href="tbResList.php?qv=137&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>, <a href="tbResList.php?qv=137&tsv=906&wNotes=on">LDH↓</a>, <a href="tbResList.php?qv=137&tsv=175&wNotes=on&word=LDH">LDHA↓</a>, <a href="tbResList.php?qv=137&tsv=773&wNotes=on">HK2↓</a>, <a href="tbResList.php?qv=137&wNotes=on&word=PFK">PFKs↓</a>, <a href="tbResList.php?qv=137&wNotes=on&word=PDK">PDKs↓</a>, <!-- <a href="tbResList.php?qv=137&tsv=847&wNotes=on">ECAR↓</a>, --> <!-- <a href="tbResList.php?qv=137&tsv=230&wNotes=on">OXPHOS↓</a>, --> <a href="tbResList.php?qv=137&tsv=356&wNotes=on">GRP78↑</a>, <!-- <a href="tbResList.php?qv=137&tsv=1278&wNotes=on">Glucose↓</a>, --> <a href="tbResList.php?qv=137&tsv=623&wNotes=on">GlucoseCon↓</a> <br> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - inhibits <a href="tbResList.php?qv=137&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=137&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=137&tsv=143&wNotes=on">HIF-1α↓</a>, <!-- <a href="tbResList.php?qv=137&wNotes=on&word=NOTCH">Notch↓</a>, --> <!-- <a href="tbResList.php?qv=137&wNotes=on&word=FGF">FGF↓</a>, --> <!-- <a href="tbResList.php?qv=137&wNotes=on&word=PDGF">PDGF↓</a>, --> <!-- <a href="tbResList.php?qv=137&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, --> <!-- <a href="tbResList.php?qv=137&&wNotes=on&word=ITG">Integrins↓</a>, --> <br> <!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, --> <!-- - inhibits Cancer Stem Cells : <a href="tbResList.php?qv=137&tsv=795&wNotes=on">CSC↓</a>, <a href="tbResList.php?qv=137&tsv=524&wNotes=on">CK2↓</a>, <a href="tbResList.php?qv=137&tsv=141&wNotes=on">Hh↓</a>, <a href="tbResList.php?qv=137&tsv=434&wNotes=on">GLi↓</a>, <a href="tbResList.php?qv=137&tsv=124&wNotes=on">GLi1↓</a>, <a href="tbResList.php?qv=137&tsv=677&wNotes=on">CD133↓</a>, <a href="tbResList.php?qv=137&tsv=655&wNotes=on">CD24↓</a>, <a href="tbResList.php?qv=137&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=137&tsv=357&wNotes=on">n-myc↓</a>, <a href="tbResList.php?qv=137&tsv=656&wNotes=on">sox2↓</a>, <a href="tbResList.php?qv=137&wNotes=on&word=NOTCH">Notch2↓</a>, <a href="tbResList.php?qv=137&tsv=1024&wNotes=on">nestin↓</a>, <a href="tbResList.php?qv=137&tsv=508&wNotes=on">OCT4↓</a>, <br> --> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=137&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=137&tsv=4&wNotes=on">AKT↓</a>, <!--<a href="tbResList.php?qv=137&wNotes=on&word=JAK">JAK↓</a>, --> <a href="tbResList.php?qv=137&wNotes=on&word=STAT">STAT↓</a>, <!--<a href="tbResList.php?qv=137&tsv=377&wNotes=on">Wnt↓</a>, --> <a href="tbResList.php?qv=137&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=137&tsv=9&wNotes=on">AMPK</a>, <!--<a href="tbResList.php?qv=137&tsv=475&wNotes=on">α↓</a>, --> <a href="tbResList.php?qv=137&tsv=105&wNotes=on">ERK↓</a>, <!--<a href="tbResList.php?qv=137&tsv=1014&wNotes=on">5↓</a>, --> <a href="tbResList.php?qv=137&tsv=168&wNotes=on">JNK</a>, <br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=137&tsv=1106&wNotes=on">chemo-sensitization</a>, <a href="tbResList.php?qv=137&tsv=1171&wNotes=on">chemoProtective</a>, <a href="tbResList.php?qv=137&tsv=1107&wNotes=on">RadioSensitizer</a>, <a href="tbResList.php?qv=137&tsv=1185&wNotes=on">RadioProtective</a>, <a href="tbResList.php?qv=137&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <a href="tbResList.php?qv=137&tsv=1105&wNotes=on">Neuroprotective</a>, <a href="tbResList.php?qv=137&tsv=557&wNotes=on">Cognitive</a>, <a href="tbResList.php?qv=137&tsv=1175&wNotes=on">Renoprotection</a>, <a href="tbResList.php?qv=137&tsv=1179&wNotes=on">Hepatoprotective</a>, <a href="tbResList.php?&qv=137&tsv=1188&wNotes=on">CardioProtective</a>, <br> <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=137&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br>
138
-
PG
Propyl gallate
NP
<b>An ester</b> formed by the condensation of gallic acid and propanol.<br> Propyl gallate (PG), chemically known as propyl-3,4,5-trihydroxybenzoate, is widely present in processed food and cosmetics, hair products, and lubricants.<br> PG alone demonstrated antioxidative and cytoprotective properties against cellular damage and gained a pro-oxidative property in combination with copper (II). It was reported that PG was one of the most active compounds capable of generating H2O2 in DMEM media<br>
139
-
PS
Pterostilbene
NP
<b>Antioxidant</b> found in blueberries, cranberries and grapes.<br> Pterostilbene (trans-3,5-dimethoxy-40-hydroxystilbene) is a naturally occurring stilbene, found mainly in blueberries and grapes. It is a dimethylated derivative of resveratrol with comparable antioxidant, anti-inflammatory and anticarcinogenic properties [26].<br>
279
-
Purp
Purpurone
NP
<b>Purpurone</b> is a natural product. Many reports indicate that it belongs to a family of naphthoquinone derivatives.<br> <br> Pathways:<br> Induction of Apoptosis (Intrinsic/Mitochondrial Pathway):<br> – affecting MMP, leading to the release of cytochrome c and activation of downstream caspases.<br> Inhibition of NF-κB Signaling:<br> Cell Cycle Arrest: (often at the G2/M phase).<br> Induction of Oxidative Stress (ROS Generation):<br> Anti-Angiogenic Effects: inhibiting angiogenesis<br> ACLY inhibitor: IC50 = 7 uM <br>
237
-
Phen
PXD, phenoxodiol
D
<b>Phenoxodiol (PXD)</b> is a synthetic compound that has been investigated as a potential therapeutic agent for the treatment of various types of cancer.<br> Phenoxodiol is an inhibitor of ENOX2 (ecto-nicotinamide adenine dinucleotide oxidase 2), also known as tNOX (tumor-associated NADH oxidase).<br>
140
-
QC
Quercetin
NP
</b>Plant pigment</b> (flavonoid) found in red wine, onions, green tea, apples and berries.<br> Quercetin is thought to contribute to anticancer effects through several mechanisms:<br> -Antioxidant Activity:<br> -Induction of Apoptosis:modify Bax:Bcl-2 ratio<br> -Anti-inflammatory Effects:<br> -Cell Cycle Arrest:<br> -Inhibition of Angiogenesis and Metastasis: (VEGF)<br> <br> Cellular Pathways:<br> -PI3K/Akt/mTOR Pathway: central to cell proliferation, survival, and metabolism.<br> -MAPK/ERK Pathway: influencing cell proliferation, differentiation, and apoptosis.<br> -NF-κB Pathway: downregulate NF-κB <br> -JAK/STAT Pathway: interfere with the activation of STAT3<br> -Apoptotic Pathways: intrinsic (mitochondrial) and extrinsic (death receptor-mediated) pathways<br> <br> Quercetin has been used at doses around 500–1000 mg per day<br> Quercetin’s bioavailability from foods or standard supplements can be low.<br> <br> -Note <a href="tbResList.php?qv=140&tsv=1109&wNotes=on&exSp=open">half-life</a> 11 to 28 hours.<br> <a href="tbResList.php?qv=140&tsv=792&wNotes=on&exSp=open">BioAv</a> low 1-10%, poor water-solubility, consuming with fat may improve bioavialability. also piperine or VitC. <br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - induce <a href="tbResList.php?qv=140&tsv=275&wNotes=on">ROS</a> production in cancer cells (higher dose). Typicallys Lowers ROS in normal cells(unless it is high dose?)or depends on Redox status?. "quercetin paradox"<br> - ROS↑ related: <a href="tbResList.php?qv=140&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?qv=140&tsv=103&wNotes=on">ER Stress↑</a>, <a href="tbResList.php?qv=140&tsv=459&wNotes=on">UPR↑</a>, <a href="tbResList.php?qv=140&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=140&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>, <a href="tbResList.php?qv=140&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?qv=140&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?qv=140&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?qv=140&tsv=239&wNotes=on">cl-PARP↑</a>, <a href="tbResList.php?qv=140&wNotes=on&word=HSP">HSP↓</a>, <a href="tbResList.php?qv=140&wNotes=on&word=Prx">Prx</a>,<!-- mitochondrial antioxidant enzyme--> <br> <!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, --> - Confusing info about Lowering AntiOxidant defense in Cancer Cells: <a href="tbResList.php?qv=140&tsv=226&wNotes=on&word=NRF2↓">NRF2↓</a>(some contrary), <a href="tbResList.php?qv=140&word=Trx&wNotes=on">TrxR↓**</a>,<!-- major antioxidant system --> <a href="tbResList.php?qv=140&tsv=298&wNotes=on&word=SOD">SOD↓</a>(contrary), <a href="tbResList.php?qv=140&tsv=137&wNotes=on&word=GSH↓">GSH↓</a> <a href="tbResList.php?qv=140&tsv=46&wNotes=on">Catalase↓</a>(contrary), <a href="tbResList.php?qv=140&tsv=597&wNotes=on">HO1↓</a>(some contrary), <a href="tbResList.php?qv=140&wNotes=on&word=GPx">GPx↓</a>(some contrary) <br> - Raises <a href="tbResList.php?qv=140&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?qv=140&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>, <a href="tbResList.php?qv=140&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?qv=140&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?qv=140&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?qv=140&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?qv=140&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?qv=140&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?qv=140&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, <a href="tbResList.php?qv=140&tsv=235&wNotes=on&word=p38↓">p38↓</a>, Pro-Inflammatory Cytokines : <a href="tbResList.php?qv=140&tsv=908&wNotes=on&word=NLRP3↓">NLRP3↓</a>, <a href="tbResList.php?qv=140&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, <a href="tbResList.php?qv=140&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?qv=140&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <a href="tbResList.php?qv=140&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a> <br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓ inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.--> - inhibit Growth/Metastases : <a href="tbResList.php?qv=140&tsv=604&wNotes=on">TumMeta↓</a>, <a href="tbResList.php?qv=140&tsv=323&wNotes=on">TumCG↓</a>, <a href="tbResList.php?qv=140&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=140&tsv=204&wNotes=on">MMPs↓</a>, <a href="tbResList.php?qv=140&tsv=201&wNotes=on">MMP2↓</a>, <a href="tbResList.php?qv=140&tsv=203&wNotes=on">MMP9↓</a>, <a href="tbResList.php?qv=140&tsv=308&wNotes=on">TIMP2</a>, <a href="tbResList.php?qv=140&tsv=415&wNotes=on">IGF-1↓</a>, <a href="tbResList.php?qv=140&tsv=428&wNotes=on">uPA↓</a>, <a href="tbResList.php?qv=140&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=140&tsv=1284&wNotes=on">ROCK1↓</a>, <a href="tbResList.php?qv=140&tsv=110&wNotes=on">FAK↓</a>, <!-- <a href="tbResList.php?qv=140&tsv=273&wNotes=on">RhoA↓</a>, --> <a href="tbResList.php?qv=140&tsv=214&wNotes=on">NF-κB↓</a>, <a href="tbResList.php?qv=140&tsv=79&wNotes=on">CXCR4↓</a>, <a href="tbResList.php?qv=140&tsv=1247&wNotes=on">SDF1↓</a>, <a href="tbResList.php?qv=140&tsv=304&wNotes=on">TGF-β↓</a>, <a href="tbResList.php?qv=140&tsv=719&wNotes=on">α-SMA↓</a>, <a href="tbResList.php?qv=140&tsv=105&wNotes=on">ERK↓</a> <!-- <a href="tbResList.php?qv=140&tsv=1178&wNotes=on">MARK4↓</a> --><!-- contributing to tumor growth, invasion, and metastasis--> <br> <!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, --> - reactivate genes thereby inhibiting cancer cell growth : <a href="tbResList.php?qv=140&tsv=140&wNotes=on">HDAC↓</a>, <a href="tbResList.php?qv=140&wNotes=on&word=DNMT">DNMTs↓</a>, <a href="tbResList.php?qv=140&tsv=108&wNotes=on">EZH2↓</a>, <a href="tbResList.php?qv=140&tsv=236&wNotes=on">P53↑</a>, <a href="tbResList.php?qv=140&wNotes=on&word=HSP">HSP↓</a>, <a href="tbResList.php?qv=140&tsv=506&wNotes=on">Sp proteins↓</a>, <a href="tbResList.php?qv=140&wNotes=on&word=TET">TET↑</a> <br> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?qv=140&tsv=322&wNotes=on">TumCCA↑</a>, <a href="tbResList.php?qv=140&tsv=73&wNotes=on">cyclin D1↓</a>, <a href="tbResList.php?qv=140&tsv=378&wNotes=on">cyclin E↓</a>, <a href="tbResList.php?qv=140&tsv=467&wNotes=on">CDK2↓</a>, <a href="tbResList.php?qv=140&tsv=894&wNotes=on">CDK4↓</a>, <a href="tbResList.php?qv=140&tsv=895&wNotes=on">CDK6↓</a>, <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?qv=140&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?qv=140&tsv=324&wNotes=on">TumCI↓</a>, <a href="tbResList.php?qv=140&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <!-- encourages invasion, proliferation, EMT, and angiogenesis --> <a href="tbResList.php?qv=140&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?qv=140&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=140&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=140&wNotes=on&word=TOP">TOP1↓</a>, <a href="tbResList.php?qv=140&tsv=657&wNotes=on">TET1</a>, <br> <!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS --> - inhibits <a href="tbResList.php?qv=140&tsv=129&wNotes=on">glycolysis</a> <!-- /<a href="tbResList.php?qv=140&tsv=947&wNotes=on">Warburg Effect</a> --> and <a href="tbResList.php?qv=140&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> : <a href="tbResList.php?qv=140&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=140&tsv=772&wNotes=on">PKM2↓</a>, <a href="tbResList.php?qv=140&tsv=35&wNotes=on">cMyc↓</a>, <a href="tbResList.php?qv=140&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>, <a href="tbResList.php?qv=140&tsv=906&wNotes=on">LDH↓</a>, <a href="tbResList.php?qv=140&tsv=175&wNotes=on&word=LDH">LDHA↓</a>, <a href="tbResList.php?qv=140&tsv=773&wNotes=on">HK2↓</a>, <a href="tbResList.php?qv=140&wNotes=on&word=PFK">PFKs↓</a>, <a href="tbResList.php?qv=140&wNotes=on&word=PDK">PDKs↓</a>, <a href="tbResList.php?qv=140&tsv=847&wNotes=on">ECAR↓</a>, <a href="tbResList.php?qv=140&tsv=230&wNotes=on">OXPHOS↓</a>, <a href="tbResList.php?qv=140&tsv=356&wNotes=on">GRP78↑</a>, <!-- <a href="tbResList.php?qv=140&tsv=1278&wNotes=on">Glucose↓</a>, --> <a href="tbResList.php?qv=140&tsv=623&wNotes=on">GlucoseCon↓</a> <br> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - inhibits <a href="tbResList.php?qv=140&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=140&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=140&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=140&wNotes=on&word=NOTCH">Notch↓</a>, <a href="tbResList.php?qv=140&wNotes=on&word=FGF">FGF↓</a>, <a href="tbResList.php?qv=140&wNotes=on&word=PDGF">PDGF↓</a>, <a href="tbResList.php?qv=140&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, <!-- <a href="tbResList.php?qv=140&&wNotes=on&word=ITG">Integrins↓</a>, --> <br> <!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, --> - some indication of inhibiting Cancer Stem Cells : <a href="tbResList.php?qv=140&tsv=795&wNotes=on">CSC↓</a>, <a href="tbResList.php?qv=140&tsv=524&wNotes=on">CK2↓</a>, <a href="tbResList.php?qv=140&tsv=141&wNotes=on">Hh↓</a>, <!-- <a href="tbResList.php?qv=140&tsv=434&wNotes=on">GLi↓</a>, --> <!-- <a href="tbResList.php?qv=140&tsv=124&wNotes=on">GLi1↓</a>, --> <!-- <a href="tbResList.php?qv=140&tsv=677&wNotes=on">CD133↓</a>, --> <a href="tbResList.php?qv=140&tsv=655&wNotes=on">CD24↓</a>, <a href="tbResList.php?qv=140&tsv=342&wNotes=on">β-catenin↓</a>, <!-- <a href="tbResList.php?qv=140&tsv=357&wNotes=on">n-myc↓</a>, --> <!-- <a href="tbResList.php?qv=140&tsv=656&wNotes=on">sox2↓</a>, --> <a href="tbResList.php?qv=140&wNotes=on&word=NOTCH">Notch2↓</a>, <!-- <a href="tbResList.php?qv=140&tsv=1024&wNotes=on">nestin↓</a>, --> <!-- <a href="tbResList.php?qv=140&tsv=508&wNotes=on">OCT4↓</a>, --> <br> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=140&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=140&tsv=4&wNotes=on">AKT↓</a>, <a href="tbResList.php?qv=140&wNotes=on&word=JAK">JAK↓</a>, <a href="tbResList.php?qv=140&wNotes=on&word=STAT">STAT↓</a>, <a href="tbResList.php?qv=140&tsv=377&wNotes=on">Wnt↓</a>, <a href="tbResList.php?qv=140&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=140&tsv=9&wNotes=on">AMPK</a>, <a href="tbResList.php?qv=140&tsv=475&wNotes=on">α↓</a>, <a href="tbResList.php?qv=140&tsv=105&wNotes=on">ERK↓</a>, <!-- <a href="tbResList.php?qv=140&tsv=1014&wNotes=on">5↓</a>, --> <a href="tbResList.php?qv=140&tsv=168&wNotes=on">JNK</a>, - <a href="tbResList.php?qv=140&wNotes=on&word=SREBP">SREBP</a> (related to cholesterol).<br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=140&tsv=1106&wNotes=on">chemo-sensitization</a>, <a href="tbResList.php?qv=140&tsv=1171&wNotes=on">chemoProtective</a>, <a href="tbResList.php?qv=140&tsv=1107&wNotes=on">RadioSensitizer</a>, <a href="tbResList.php?qv=140&tsv=1185&wNotes=on">RadioProtective</a>, <a href="tbResList.php?qv=140&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <a href="tbResList.php?qv=140&tsv=1105&wNotes=on">Neuroprotective</a>, <a href="tbResList.php?qv=140&tsv=557&wNotes=on">Cognitive</a>, <a href="tbResList.php?qv=140&tsv=1175&wNotes=on">Renoprotection</a>, <a href="tbResList.php?qv=140&tsv=1179&wNotes=on">Hepatoprotective</a>, <a href="tbResList.php?&qv=140&tsv=1188&wNotes=on">CardioProtective</a>, <br> <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=140&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br>
212
-
RF
Radio Frequency
T
<b>Typically</b> in MHz. Example 900MHz/1W<br>
201
-
Rad
Radiotherapy/Radiation
T
<b>Treatment</b> of disease with radiation, especially by selective irradiation with x-rays or other ionizing radiation and by ingestion of radioisotopes.<br> <br> Radiosensitizer<br> Atorvaqone, (mitochondria inhibitor) decrease O2 consumption making more O2 available as a radiosensitizer.<br>
188
-
Ralox
raloxifen
RD
<b>Raloxifene</b> is a type of drug called a selective oestrogen receptor modulator (SERM). Raloxifene is a medication used to treat postmenopausal osteoporosis and the risk reduction of invasive breast cancer in post-menopausal women.<br>
255
-
RAPA
Rapamycin
D
</b>Rapamycin</b> <br>
242
-
RSL3
Ras-selective lethal 3
D
ferroptosis inducer
</b>RSL3 (Ras-selective lethal 3)</b> is a small molecule that has been shown to have anti-cancer properties. It is a ferroptosis inducer, which means that it induces a type of cell death that is characterized by the accumulation of iron and the production of reactive oxygen species (ROS).<br> <br> RSL3 works by inhibiting the activity of the enzyme GPX4 (glutathione peroxidase 4), which is involved in the regulation of lipid peroxidation and the maintenance of cellular redox balance. In cancer cells, GPX4 is often overexpressed, and RSL3's inhibition of this enzyme leads to an accumulation of lipid peroxides and a disruption in cellular redox balance.<br>
208
-
RSQ
Resiquimod
RD
<b>Resiquimod</b> is a synthetic compound that acts as an immune response modifier. It is a toll-like receptor 7 and 8 (TLR7/8) agonist, which means it activates these receptors on immune cells, such as dendritic cells and macrophages.<br>
141
-
RES
Resveratrol
NP
polyphenol
<b>Found</b> in red grapes and products made with grapes.<br> Resveratrol is a polyphenol compound found in various plant species, including grapes, berries, and peanuts. <br> • Anti-inflammatory effects, Antioxidant effects:<br> - <a href="tbResList.php?qv=141&tsv=10&wNotes=on">Antiplatelet aggregation</a> for stroke prevention<br> - <a href="tbResList.php?qv=141&tsv=792&wNotes=on">BioAvialability</a> use piperine <br> - some sources may use Japanese knotweed roots (Reynoutria Japonica - root) as source which might contain Emodin (laxative)<br> -known as Nrf2 activator, both in cancer and normal cells. Which raises controversity of use in ROS↑ therapies. Interestingly there are reports of <a href="https://nestronics.ca/dbx/tbResList.php?qv=141&&tsv=226&wNotes=on&exSp=open">NRF2↑ and ROS↑</a> in cancer cells. This raises the question of if it is a chemosensitizer. However other reports indicate NRF2 droping with Res, indicating it maybe a chemosenstizer.<br> - RES is also considered to be them most effective natural <a href="tbResList.php?qv=141&tsv=634&wNotes=on&word=SIRT1↑">SIRT1↑</a> -activating compound (STACs). <br> <br> However, in the presence of certain metals, such as copper or iron, resveratrol can undergo a process called Fenton reaction, which can lead to the generation of reactive oxygen species (ROS). The pro-oxidant effects of resveratrol are often observed at high concentrations, typically above 50-100 μM, and in the presence of certain metals or other pro-oxidant agents. In contrast, the antioxidant effects of resveratrol are typically observed at lower concentrations, typically below 10-20 μM.<br> <br> Clinical trials have used doses ranging from 150 mg to 5 grams per day. Lower doses (< 1 g/day) are often well-tolerated, but higher doses might be necessary for therapeutic effects and can be associated with side effects.<br> <br> -Note <a href="tbResList.php?qv=141&tsv=1109&wNotes=on&exSp=open">half-life</a> 1-3 hrs?.<br> <a href="tbResList.php?qv=141&tsv=792&wNotes=on&exSp=open">BioAv</a> poor: min 5uM/L required for chemopreventive effects, but 25mg Oral only yeilds 20nM. co-administration of piperine <br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - usually induce <a href="tbResList.php?qv=141&tsv=275&wNotes=on">ROS</a> production in cancer cells, while reducing ROS in normal cells.<br> - ROS↑ related: <a href="tbResList.php?qv=141&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?qv=141&tsv=103&wNotes=on">ER Stress↑</a>, <a href="tbResList.php?qv=141&tsv=459&wNotes=on">UPR↑</a>, <a href="tbResList.php?qv=141&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=141&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>, <a href="tbResList.php?qv=141&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?qv=141&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?qv=141&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?qv=141&tsv=239&wNotes=on">cl-PARP↑</a>, <a href="tbResList.php?qv=141&wNotes=on&word=HSP">HSP↓</a>, <!-- <a href="tbResList.php?qv=141&wNotes=on&word=Prx">Prx</a>, --><!-- mitochondrial antioxidant enzyme--> <br> <!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, --> - Lowers AntiOxidant defense in Cancer Cells: <a href="tbResList.php?qv=141&tsv=226&wNotes=on&word=NRF2">NRF2</a>(typically increased), <a href="tbResList.php?qv=141&word=Trx&wNotes=on">TrxR↓**</a>,<!-- major antioxidant system --> <a href="tbResList.php?qv=141&wNotes=on&word=SOD">SOD↓</a>, <a href="tbResList.php?qv=141&tsv=137&wNotes=on&word=GSH↓">GSH↓</a> <a href="tbResList.php?qv=141&tsv=46&wNotes=on">Catalase↓</a> <a href="tbResList.php?qv=141&tsv=597&wNotes=on">HO1↓</a>(wrong direction), <a href="tbResList.php?qv=141&wNotes=on&word=GPx">GPx↓</a> <br> - Raises <a href="tbResList.php?qv=141&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?qv=141&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>, <a href="tbResList.php?qv=141&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?qv=141&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?qv=141&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?qv=141&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?qv=141&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?qv=141&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?qv=141&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, <a href="tbResList.php?qv=141&tsv=235&wNotes=on&word=p38↓">p38↓</a>, Pro-Inflammatory Cytokines : <a href="tbResList.php?qv=141&tsv=908&wNotes=on&word=NLRP3↓">NLRP3↓</a>, <a href="tbResList.php?qv=141&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, <a href="tbResList.php?qv=141&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?qv=141&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <a href="tbResList.php?qv=141&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a> <br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓ inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.--> - inhibit Growth/Metastases : <a href="tbResList.php?qv=141&tsv=604&wNotes=on">TumMeta↓</a>, <a href="tbResList.php?qv=141&tsv=323&wNotes=on">TumCG↓</a>, <a href="tbResList.php?qv=141&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=141&tsv=204&wNotes=on">MMPs↓</a>, <a href="tbResList.php?qv=141&tsv=201&wNotes=on">MMP2↓</a>, <a href="tbResList.php?qv=141&tsv=203&wNotes=on">MMP9↓</a>, <a href="tbResList.php?qv=141&tsv=308&wNotes=on">TIMP2</a>, <a href="tbResList.php?qv=141&tsv=415&wNotes=on">IGF-1↓</a>, <a href="tbResList.php?qv=141&tsv=428&wNotes=on">uPA↓</a>, <a href="tbResList.php?qv=141&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=141&tsv=1284&wNotes=on">ROCK1↓</a>, <a href="tbResList.php?qv=141&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?qv=141&tsv=273&wNotes=on">RhoA↓</a>, <a href="tbResList.php?qv=141&tsv=214&wNotes=on">NF-κB↓</a>, <a href="tbResList.php?qv=141&tsv=79&wNotes=on">CXCR4↓</a>, <a href="tbResList.php?qv=141&tsv=1247&wNotes=on">SDF1↓</a>, <a href="tbResList.php?qv=141&tsv=304&wNotes=on">TGF-β↓</a>, <a href="tbResList.php?qv=141&tsv=719&wNotes=on">α-SMA↓</a>, <a href="tbResList.php?qv=141&tsv=105&wNotes=on">ERK↓</a> <!-- <a href="tbResList.php?qv=141&tsv=1178&wNotes=on">MARK4↓</a> --><!-- contributing to tumor growth, invasion, and metastasis--> <br> <!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, --> - reactivate genes thereby inhibiting cancer cell growth : <a href="tbResList.php?qv=141&tsv=140&wNotes=on">HDAC↓</a>, <!-- <a href="tbResList.php?qv=141&tsv=85&wNotes=on">DNMT1↓</a>, --> <!-- <a href="tbResList.php?qv=141&tsv=86&wNotes=on">DNMT3A↓</a>, --> <a href="tbResList.php?qv=141&tsv=108&wNotes=on">EZH2↓</a>, <a href="tbResList.php?qv=141&tsv=236&wNotes=on">P53↑</a>, <a href="tbResList.php?qv=141&wNotes=on&word=HSP">HSP↓</a>, <a href="tbResList.php?qv=141&tsv=506&wNotes=on">Sp proteins↓</a>, <br> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?qv=141&tsv=322&wNotes=on">TumCCA↑</a>, <a href="tbResList.php?qv=141&tsv=73&wNotes=on">cyclin D1↓</a>, <a href="tbResList.php?qv=141&tsv=378&wNotes=on">cyclin E↓</a>, <a href="tbResList.php?qv=141&tsv=467&wNotes=on">CDK2↓</a>, <a href="tbResList.php?qv=141&tsv=894&wNotes=on">CDK4↓</a>, <a href="tbResList.php?qv=141&tsv=895&wNotes=on">CDK6↓</a>, <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?qv=141&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?qv=141&tsv=324&wNotes=on">TumCI↓</a>, <a href="tbResList.php?qv=141&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <!-- encourages invasion, proliferation, EMT, and angiogenesis --> <a href="tbResList.php?qv=141&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?qv=141&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=141&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=141&tsv=1117&wNotes=on">TOP1↓</a>, <a href="tbResList.php?qv=141&tsv=657&wNotes=on">TET1↓</a>, <br> <!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS --> - inhibits <a href="tbResList.php?qv=141&tsv=129&wNotes=on">glycolysis</a> /<a href="tbResList.php?qv=141&tsv=947&wNotes=on">Warburg Effect</a> and <a href="tbResList.php?qv=141&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> : <a href="tbResList.php?qv=141&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=141&tsv=772&wNotes=on">PKM2↓</a>, <a href="tbResList.php?qv=141&tsv=35&wNotes=on">cMyc↓</a>, <a href="tbResList.php?qv=141&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>, <a href="tbResList.php?qv=141&tsv=906&wNotes=on">LDH↓</a>, <a href="tbResList.php?qv=141&tsv=175&wNotes=on&word=LDH">LDHA↓</a>, <a href="tbResList.php?qv=141&tsv=773&wNotes=on">HK2↓</a>, <a href="tbResList.php?qv=141&wNotes=on&word=PFK">PFKs↓</a>, <a href="tbResList.php?qv=141&wNotes=on&word=PDK">PDKs↓</a>, <a href="tbResList.php?qv=141&tsv=847&wNotes=on">ECAR↓</a>, <a href="tbResList.php?qv=141&tsv=230&wNotes=on">OXPHOS↓</a>, <a href="tbResList.php?qv=141&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=141&tsv=1278&wNotes=on">Glucose↓</a>, <a href="tbResList.php?qv=141&tsv=623&wNotes=on">GlucoseCon↓</a> <br> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - inhibits <a href="tbResList.php?qv=141&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=141&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=141&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=141&wNotes=on&word=NOTCH">Notch↓</a>, <a href="tbResList.php?qv=141&wNotes=on&word=FGF">FGF↓</a>, <a href="tbResList.php?qv=141&wNotes=on&word=PDGF">PDGF↓</a>, <a href="tbResList.php?qv=141&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, <a href="tbResList.php?qv=141&&wNotes=on&word=ITG">Integrins↓</a>, <br> <!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, --> - inhibits Cancer Stem Cells : <a href="tbResList.php?qv=141&tsv=795&wNotes=on">CSC↓</a>, <a href="tbResList.php?qv=141&tsv=524&wNotes=on">CK2↓</a>, <a href="tbResList.php?qv=141&tsv=141&wNotes=on">Hh↓</a>, <!-- <a href="tbResList.php?qv=141&tsv=434&wNotes=on">GLi↓</a>, <a href="tbResList.php?qv=141&tsv=124&wNotes=on">GLi1↓</a>, --> <a href="tbResList.php?qv=141&tsv=677&wNotes=on">CD133↓</a>, <a href="tbResList.php?qv=141&tsv=655&wNotes=on">CD24↓</a>, <a href="tbResList.php?qv=141&tsv=342&wNotes=on">β-catenin↓</a>, <!-- <a href="tbResList.php?qv=141&tsv=357&wNotes=on">n-myc↓</a>, --> <a href="tbResList.php?qv=141&tsv=656&wNotes=on">sox2↓</a>, <a href="tbResList.php?qv=141&tsv=222&wNotes=on">notch2↓</a>, <a href="tbResList.php?qv=141&tsv=1024&wNotes=on">nestin↓</a>, <a href="tbResList.php?qv=141&tsv=508&wNotes=on">OCT4↓</a>, <br> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=141&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=141&tsv=4&wNotes=on">AKT↓</a>, <a href="tbResList.php?qv=141&wNotes=on&word=JAK">JAK↓</a>, <a href="tbResList.php?qv=141&wNotes=on&word=STAT">STAT↓</a>, <a href="tbResList.php?qv=141&tsv=377&wNotes=on">Wnt↓</a>, <a href="tbResList.php?qv=141&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=141&tsv=9&wNotes=on">AMPK</a>, <!-- <a href="tbResList.php?qv=141&tsv=475&wNotes=on">α↓</a>, --> <a href="tbResList.php?qv=141&tsv=105&wNotes=on">ERK↓</a>, <!-- <a href="tbResList.php?qv=141&tsv=1014&wNotes=on">5↓</a>, --> <a href="tbResList.php?qv=141&tsv=168&wNotes=on">JNK</a>, <br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=141&tsv=1106&wNotes=on">chemo-sensitization</a>, <a href="tbResList.php?qv=141&tsv=1171&wNotes=on">chemoProtective</a>, <a href="tbResList.php?qv=141&tsv=1107&wNotes=on">RadioSensitizer</a>, <a href="tbResList.php?qv=141&tsv=1185&wNotes=on">RadioProtective</a>, <a href="tbResList.php?qv=141&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <a href="tbResList.php?qv=141&tsv=1105&wNotes=on">Neuroprotective</a>, <a href="tbResList.php?qv=141&tsv=557&wNotes=on">Cognitive</a>, <a href="tbResList.php?qv=141&tsv=1175&wNotes=on">Renoprotection</a>, <a href="tbResList.php?qv=141&tsv=1179&wNotes=on">Hepatoprotective</a>, <a href="tbResList.php?&qv=141&tsv=1188&wNotes=on">CardioProtective</a>, <br> <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=141&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br>
290
-
RetA
Retinoic Acid
NP
<b>Retinoic acid</b> is a naturally occurring derivative of vitamin A (retinol).<br> <br> Retinoic acid is produced in the body from dietary vitamin A. Vitamin A can be ingested in two primary forms:<br> • Preformed vitamin A (retinol and its esters) found in animal products like liver, dairy, and fish.<br> • Provitamin A carotenoids (such as beta-carotene) found in colorful fruits and vegetables. Once ingested, these compounds are converted into retinol, which can then be oxidized to retinal and further oxidized to retinoic acid.<br> <br> All-trans retinoic acid (ATRA) is a key component in the treatment of acute promyelocytic leukemia (APL). In APL, ATRA induces the differentiation of malignant promyelocytes into mature granulocytes, leading to clinical remission.<br> <br> -Retinoic acid can have antioxidant properties<br> -High levels of retinoic acid have been associated with increased ROS production and oxidative stress<br> -The potential prooxidant action may contribute to its anti-cancer effects by inducing oxidative damage in cancer cells, thereby enhancing apoptosis.<br>
142
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RosA
Rosmarinic acid
NP
polyphenol
<b>Polyphenol</b> of many herbs - rosemary, perilla, sage mint and basil. Rosmarinic acid (RA) is predominantly found in a variety of medicinal and culinary herbs, especially those belonging to the Lamiaceae family, including rosemary (Rosmarinus officinalis), basil (Ocimum basilicum), sage (Salvia officinalis), thyme (Thymus vulgaris), and mints (Mentha spp.). In addition to the Lamiaceae family, RA is also present in plants from other families, such as Boraginaceae and Apiaceae.<br> -Rosmarinic acid is one of the hydroxycinnamic acids, and was initially isolated and purified from the extract of rosemary, a member of mint family (Lamiaceae)<br> -Its chemical structure allows it to act as a free radical scavenger by donating hydrogen atoms to stabilize ROS and free radicals. <br> RA’s dual nature as both a phenolic acid and a flavonoid-related compound enables it to chelate metal ions and prevent the formation of free radicals, thus interrupting oxidative chain reactions. It can modulate the activity of enzymes involved in OS, such as catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx), underscoring its potential role in preventing oxidative damage at the cellular level.<br> -divided as rosemary extract, carnosic acid, rosmarinic acid?<br> <br> Summary:<br> -Capacity to chelate transition metal ions, particularly <a href="tbResList.php?qv=142&tsv=835&wNotes=on">ironChelator</a> (Fe2+) and copper (Cu2+)<br> -RA plus Cu(II)-induced oxidative DNA damage, which causes ROS<br> -rosmarinic acid (RA) as a potential inhibitor of <a href="tbResList.php?qv=142&tsv=1178&wNotes=on">MARK4↓</a> (inhibiting to tumor growth, invasion, and metastasis) activity (IC50 = 6.204 µM)<br> <br> -Note <a href="tbResList.php?qv=142&tsv=1109&wNotes=on&exSp=open">half-life</a> 1.5–2 hours.<br> <a href="tbResList.php?qv=142&tsv=792&wNotes=on&exSp=open">BioAv</a> water-soluble, rapid absorbtion <br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - varying results of <a href="tbResList.php?qv=142&tsv=275&wNotes=on">ROS</a> up or down in cancer cells. Plus a <a href="https://nestronics.ca/dbx/tbResEdit.php?rid=3017">report</a> of lowering ROS and no effect on Tumor cell viability.<br> However always seems to lower <a href="tbResList.php?qv=142&tsv=275&wNotes=on&word=ROS↓">ROS↓</a> in normal cells.<br> - ROS↑ related: <a href="tbResList.php?qv=142&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?qv=142&tsv=103&wNotes=on">ER Stress↑</a>, <a href="tbResList.php?qv=142&tsv=459&wNotes=on">UPR↑</a>, <!-- <a href="tbResList.php?qv=142&tsv=356&wNotes=on">GRP78↑</a>, --> <!-- <a href="tbResList.php?qv=142&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>, --> <a href="tbResList.php?qv=142&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?qv=142&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?qv=142&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?qv=142&tsv=239&wNotes=on">cl-PARP↑</a>, <a href="tbResList.php?qv=142&wNotes=on&word=HSP">HSP↓</a>, <!--<a href="tbResList.php?qv=142&wNotes=on&word=Prx">Prx</a>, mitochondrial antioxidant enzyme--> <br> <!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, --> - No indication of Lowering AntiOxidant defense in Cancer Cells: <!--<a href="tbResList.php?qv=142&tsv=226&wNotes=on&word=NRF2↓">NRF2↓</a>, <a href="tbResList.php?qv=142&word=Trx&wNotes=on">TrxR↓**</a>, <a href="tbResList.php?qv=142&tsv=298&wNotes=on&word=SOD↓">SOD↓</a>, <a href="tbResList.php?qv=142&tsv=137&wNotes=on&word=GSH↓">GSH↓</a> <a href="tbResList.php?qv=142&tsv=46&wNotes=on">Catalase↓</a> <a href="tbResList.php?qv=142&tsv=597&wNotes=on">HO1↓</a> <a href="tbResList.php?qv=142&wNotes=on&word=GPx">GPx↓</a> --> <br> - Raises <a href="tbResList.php?qv=142&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells:(and perhaps even in cancer cells) <a href="tbResList.php?qv=142&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>, <a href="tbResList.php?qv=142&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>***, <a href="tbResList.php?qv=142&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?qv=142&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?qv=142&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?qv=142&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?qv=142&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?qv=142&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, <a href="tbResList.php?qv=142&tsv=235&wNotes=on&word=p38↓">p38↓</a>, Pro-Inflammatory Cytokines : <a href="tbResList.php?qv=142&tsv=908&wNotes=on&word=NLRP3↓">NLRP3↓</a>, <a href="tbResList.php?qv=142&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, <a href="tbResList.php?qv=142&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?qv=142&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <a href="tbResList.php?qv=142&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a> <br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓ inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.--> - inhibit Growth/Metastases : <a href="tbResList.php?qv=142&tsv=604&wNotes=on">TumMeta↓</a>, <a href="tbResList.php?qv=142&tsv=323&wNotes=on">TumCG↓</a>, <a href="tbResList.php?qv=142&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=142&tsv=204&wNotes=on">MMPs↓</a>, <a href="tbResList.php?qv=142&tsv=201&wNotes=on">MMP2↓</a>, <a href="tbResList.php?qv=142&tsv=203&wNotes=on">MMP9↓</a>, <!-- <a href="tbResList.php?qv=142&tsv=308&wNotes=on">TIMP2</a>, --> <!-- <a href="tbResList.php?qv=142&tsv=415&wNotes=on">IGF-1↓</a>, --> <!-- <a href="tbResList.php?qv=142&tsv=428&wNotes=on">uPA↓</a>, --> <a href="tbResList.php?qv=142&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=142&tsv=1284&wNotes=on">ROCK1↓</a>, <!-- <a href="tbResList.php?qv=142&tsv=110&wNotes=on">FAK↓</a>, --> <a href="tbResList.php?qv=142&tsv=273&wNotes=on">RhoA↓</a>, <a href="tbResList.php?qv=142&tsv=214&wNotes=on">NF-κB↓</a>, <!-- <a href="tbResList.php?qv=142&tsv=79&wNotes=on">CXCR4↓</a>, --> <!-- <a href="tbResList.php?qv=142&tsv=1247&wNotes=on">SDF1↓</a>, --> <!-- <a href="tbResList.php?qv=142&tsv=304&wNotes=on">TGF-β↓</a>, --> <!-- <a href="tbResList.php?qv=142&tsv=719&wNotes=on">α-SMA↓</a>, --> <a href="tbResList.php?qv=142&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=142&tsv=1178&wNotes=on">MARK4↓</a> <!-- contributing to tumor growth, invasion, and metastasis--> <br> <!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, --> - reactivate genes thereby inhibiting cancer cell growth(weak) : <a href="tbResList.php?qv=142&tsv=984&wNotes=on">HDAC2↓</a>, <a href="tbResList.php?qv=142&tsv=469&wNotes=on">DNMTs↓weak</a>, <!--<a href="tbResList.php?qv=142&tsv=86&wNotes=on">DNMT3A↓</a>, --> <!--<a href="tbResList.php?qv=142&tsv=108&wNotes=on">EZH2↓</a>, --> <a href="tbResList.php?qv=142&tsv=236&wNotes=on">P53↑</a>, <a href="tbResList.php?qv=142&wNotes=on&word=HSP">HSP↓</a>, <!--<a href="tbResList.php?qv=142&tsv=506&wNotes=on">Sp proteins↓</a>, --> <br> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?qv=142&tsv=322&wNotes=on">TumCCA↑</a>, <a href="tbResList.php?qv=142&tsv=73&wNotes=on">cyclin D1↓</a>, <a href="tbResList.php?qv=142&tsv=378&wNotes=on">cyclin E↓</a>, <a href="tbResList.php?qv=142&tsv=467&wNotes=on">CDK2↓</a>, <a href="tbResList.php?qv=142&tsv=894&wNotes=on">CDK4↓</a>, <!--<a href="tbResList.php?qv=142&tsv=895&wNotes=on">CDK6↓</a>,--> <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?qv=142&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?qv=142&tsv=324&wNotes=on">TumCI↓</a>, <!--<a href="tbResList.php?qv=142&tsv=110&wNotes=on">FAK↓</a>, --> <a href="tbResList.php?qv=142&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=142&tsv=96&wNotes=on">EMT↓</a>, <!--<a href="tbResList.php?qv=142&tsv=1117&wNotes=on">TOP1↓</a>, --> <!--<a href="tbResList.php?qv=142&tsv=657&wNotes=on">TET1↓</a>, --> <br> <!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS --> - inhibits <a href="tbResList.php?qv=142&tsv=129&wNotes=on">glycolysis</a> /<a href="tbResList.php?qv=142&tsv=947&wNotes=on">Warburg Effect</a> and <a href="tbResList.php?qv=142&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> : <a href="tbResList.php?qv=142&tsv=143&wNotes=on">HIF-1α↓??</a>, <!--<a href="tbResList.php?qv=142&tsv=772&wNotes=on">PKM2↓</a>, --> <!--<a href="tbResList.php?qv=142&tsv=35&wNotes=on">cMyc↓</a>, --> <!--<a href="tbResList.php?qv=142&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>, --> <!--<a href="tbResList.php?qv=142&tsv=906&wNotes=on">LDH↓</a>, --> <a href="tbResList.php?qv=142&tsv=175&wNotes=on&word=LDH">LDHA↓</a>, <!--<a href="tbResList.php?qv=142&tsv=773&wNotes=on">HK2↓</a>, --> <a href="tbResList.php?qv=142&wNotes=on&word=PFK">PFKs↓</a>, <!--<a href="tbResList.php?qv=142&wNotes=on&word=PDK">PDKs↓</a>, --> <!--<a href="tbResList.php?qv=142&tsv=847&wNotes=on">ECAR↓</a>, --> <!--<a href="tbResList.php?qv=142&tsv=230&wNotes=on">OXPHOS↓</a>, --> <a href="tbResList.php?qv=142&tsv=356&wNotes=on">GRP78↑</a>, <!--<a href="tbResList.php?qv=142&tsv=1278&wNotes=on">Glucose↓</a>, --> <a href="tbResList.php?qv=142&tsv=623&wNotes=on">GlucoseCon↓</a> <br> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - inhibits <a href="tbResList.php?qv=142&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=142&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=142&tsv=143&wNotes=on">HIF-1α↓</a>, <!-- <a href="tbResList.php?qv=142&wNotes=on&word=NOTCH">Notch↓</a>, --> <!-- <a href="tbResList.php?qv=142&wNotes=on&word=FGF">FGF↓</a>, --> <!-- <a href="tbResList.php?qv=142&tsv=361&wNotes=on">PDGF↓</a>, --> <a href="tbResList.php?qv=142&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, <!-- <a href="tbResList.php?qv=142&&wNotes=on&word=ITG">Integrins↓</a>, --> <br> <!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, --> - inhibits Cancer Stem Cells (few references) : <a href="tbResList.php?qv=142&tsv=795&wNotes=on">CSC↓</a>, <!-- <a href="tbResList.php?qv=142&tsv=524&wNotes=on">CK2↓</a>, --> <a href="tbResList.php?qv=142&tsv=141&wNotes=on">Hh↓</a>, <!-- <a href="tbResList.php?qv=142&tsv=434&wNotes=on">GLi↓</a>, --> <a href="tbResList.php?qv=142&tsv=124&wNotes=on">GLi1↓</a>, <!-- <a href="tbResList.php?qv=142&tsv=677&wNotes=on">CD133↓</a>, --> <!-- <a href="tbResList.php?qv=142&tsv=655&wNotes=on">CD24↓</a>, --> <!-- <a href="tbResList.php?qv=142&tsv=342&wNotes=on">β-catenin↓</a>, --> <!-- <a href="tbResList.php?qv=142&tsv=357&wNotes=on">n-myc↓</a>, --> <!-- <a href="tbResList.php?qv=142&tsv=656&wNotes=on">sox2↓</a>, --> <!-- <a href="tbResList.php?qv=142&tsv=222&wNotes=on">notch2↓</a>, --> <!-- <a href="tbResList.php?qv=142&tsv=1024&wNotes=on">nestin↓</a>, --> <!-- <a href="tbResList.php?qv=142&tsv=508&wNotes=on">OCT4↓</a>, --> <br> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=142&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=142&tsv=4&wNotes=on">AKT↓</a>, <!-- <a href="tbResList.php?qv=142&wNotes=on&word=JAK">JAK↓</a>, --> <a href="tbResList.php?qv=142&wNotes=on&word=STAT">STAT↓</a>, <!-- <a href="tbResList.php?qv=142&tsv=377&wNotes=on">Wnt↓</a>, --> <!-- <a href="tbResList.php?qv=142&tsv=342&wNotes=on">β-catenin↓</a>, --> <a href="tbResList.php?qv=142&tsv=9&wNotes=on">AMPK</a>, <!-- <a href="tbResList.php?qv=142&tsv=475&wNotes=on">α↓</a>, --> <a href="tbResList.php?qv=142&tsv=105&wNotes=on">ERK↓</a>, <!-- <a href="tbResList.php?qv=142&tsv=1014&wNotes=on">5↓</a>, --> <a href="tbResList.php?qv=142&tsv=168&wNotes=on">JNK</a>, <br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=142&tsv=1106&wNotes=on">chemo-sensitization</a>, <a href="tbResList.php?qv=142&tsv=1171&wNotes=on">chemoProtective</a>, <a href="tbResList.php?qv=142&tsv=1107&wNotes=on">RadioSensitizer</a>, <a href="tbResList.php?qv=142&tsv=1185&wNotes=on">RadioProtective</a>, <a href="tbResList.php?qv=142&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <a href="tbResList.php?qv=142&tsv=1105&wNotes=on">Neuroprotective</a>, <a href="tbResList.php?qv=142&tsv=557&wNotes=on">Cognitive</a>, <a href="tbResList.php?qv=142&tsv=1175&wNotes=on">Renoprotection</a>, <a href="tbResList.php?qv=142&tsv=1179&wNotes=on">Hepatoprotective</a>, <a href="tbResList.php?&qv=142&tsv=1188&wNotes=on">CardioProtective</a>, <br> <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=142&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br>
143
-
RT
Rutin
NP
<b>Rutin</b>, a Quercetin Glycoside<br>
144
-
SB
Saccharomyces boulardii
NP
probiotic yeast
<b>Saccharomyces boulardii</b> <br>
145
-
SS
Saikosaponin B1 and D
NP
<b>Saikosaponin</b> B1 (SSB1) and Saikosaponin D (SSD), two bioactive constituents of Radix Bupleuri<br>
203
-
Sal
salinomycin
NP
<b>Salinomycin</b> is a polyether ionophore antibiotic that is produced by the bacterium Streptomyces albus. It was first isolated in 1979 and has been found to have a range of biological activities, including antibacterial, antifungal, and anticancer properties.<br> It has been shown to induce apoptosis (programmed cell death) in a range of cancer cell lines, including breast, lung, and colon cancer cells. Salinomycin has also been found to inhibit the growth of cancer stem cells.<br>
146
-
SM
Salvia miltiorrhiza
NP
<b>Red sage</b>, redroot sage, Chinese sage or danshen.<br> Salvianolic Acid A (SAA) is predominantly isolated from Salvia miltiorrhiza, commonly known as Danshen.<br> Tanshinone IIA is the main effective component of Salvia miltiorrhiza known as 'Danshen' <br> <br> Salvianolic Acid A, primarily derived from Salvia miltiorrhiza (Danshen), shows promise in cancer research due to its ability to inhibit cell proliferation, induce apoptosis, reduce angiogenesis, and impact multiple signaling pathways involved in tumor progression.<br> <br> Salvianolic Acid A may impact several intracellular signaling pathways involved in cancer progression:<br> NF-κB Pathway: SAA might inhibit the NF-κB pathway, reducing inflammation and cell proliferation signals.<br> MAPK Pathways (ERK, JNK, p38): By modulating these pathways, SAA can influence cell survival, differentiation, and apoptosis.<br> PI3K/Akt Pathway: Inhibition of this pathway is another mechanism through which SAA can reduce cancer cell survival and proliferation.<br> Oxidative Stress Reduction: SAA’s antioxidant properties may help in reducing oxidative stress, which is implicated in cancer progression and chemoresistance.<br> Synergistic Effects with Conventional Therapies:<br> Preliminary studies suggest that Salvianolic Acid A might enhance the effectiveness of various chemotherapeutic agents.<br> <br> Some studies have observed anti-proliferative effects at concentrations around 10–50 µM. rodent models have been reported in the range of 10–100 mg/kg<br>
147
-
SANG
Sanguinarine
NP
<b>Extracted</b> from bloodroot plant from whose scientific name, Sanguinaria canadensis, its name is derived; the Mexican prickly poppy; Chelidonium majus; and Macleaya cordata.<br>
247
-
Sco
Scoulerine
NP
<b>Scoulerine</b> is an isoquinoline alkaloid found in various plants (such as members of the Menispermaceae family and in certain Corydalis species) that has attracted interest due to its potential pharmacological activities.<br> Both scoulerine and berberine belong to the broad family of isoquinoline alkaloids, meaning they share a similar biosynthetic origin and core chemical framework.<br> – Scoulerine is less commonly encountered in typical dietary sources and is mostly identified in certain herbal extracts from plants in families such as Menispermaceae or Corydalis.<br>
262
-
Selenate
Selenate
NP
<b>Selenate</b> shares similarity with sulfate and enters cells via sulfate transporters; however, it is less readily reduced and often considered less potent in rapid cytotoxicity effects.<br> <br> Selenate tends to exhibit higher IC50 values (often in the 10–100 µM range), indicating reduced potency compared to selenite in directly inducing cancer cell death.<br> <br> Less Direct ROS Generation than Selenite.<br> – Selenate’s toxicity is generally less acute because it is a more inert species until metabolically reduced.<br> – It may exert its anticancer effects once it is converted into reduced selenium species that eventually can contribute to ROS production.<br>
148
-
Sel
Selenite
NP
<b>Gypsum</b> - a calcium sulfate mineral<br>
149
-
Se
Selenium
NP
micronutrient
<b>Naturally</b> occurring element
240
-
SeMet
selenomethionine
NP
<b>Selenomethionine</b> is a naturally occurring amino acid that contains selenium, a trace element essential for human health. Selenium plays a crucial role in various bodily functions, including antioxidant defenses, immune system function, and cancer prevention.<br> Elevated SeMet expression is correlated with better overall survival and reduced risk of metastasis.<br>
282
-
sericin
sericin
NP
<b>Sericin</b> is a silk protein primarily obtained from the silkworm Bombyx mori and has attracted interest for its various biological properties. Some studies have investigated the potential anticancer properties of sericin.<br> <br> -Sericin exhibits antioxidant properties, which may help protect cells against oxidative stress. Oxidative stress is known to contribute to the development and progression of cancer, so antioxidants are often considered beneficial in preventive strategies.<br> -Sericin’s anti-inflammatory effects might help reduce inflammation-related damage and potentially slow down processes that can lead to carcinogenesis.<br>
150
-
SK
Shikonin
NP
<b>The (R)-enantiomer of alkannin</b> is known as shikonin, and the racemic mixture of the two is known as shikalkin.<br> Shikonin is a naphthoquinone derivative primarily isolated from the roots of plants in the Boraginaceae family (e.g., Lithospermum erythrorhizon). <br> Shikonin is the main active component of a Chinese medicinal plant 'Zi Cao'<br> -Shikonin is a major component of zicao (purple gromwell, the dried root of Lithospermum erythrorhizon), a Chinese herbal medicine with anti-inflammatory properties<br> -Quinone methides (QMs) are highly reactive intermediates formed from natural compounds like shikonin<br> -ic50 cancer cells 1-10uM, normal cells >10uM<br> <br> -known as Glycolysis inhibitor: ( inhibit pyruvate kinase M2 (PKM2*******), a key enzyme in the glycolytic pathway)<br> <br> Available from <a href="https://www.mcsformulas.com/" > mcsformulas.com </a> Shikonin Pro Liposomal, 30 mg<br> Also In Glycolysis Inhibithree(100 mg PHLORIZIN,10 mg TANSHINONE IIA, 8 mg Shikonin)<br> <br> -Note <a href="tbResList.php?qv=150&tsv=1109&wNotes=on&exSp=open">half-life</a>15-30mins or 8hr?.<br> <a href="tbResList.php?qv=150&tsv=792&wNotes=on&exSp=open">BioAv</a> low, poor water solubility <br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - usually induce <a href="tbResList.php?qv=150&tsv=275&wNotes=on">ROS</a> production in cancer cells, and reduce ROS in normal cells.<br> - ROS↑ related: <a href="tbResList.php?qv=150&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?qv=150&tsv=103&wNotes=on">ER Stress↑</a>, <!--<a href="tbResList.php?qv=150&tsv=459&wNotes=on">UPR↑</a>, --> <a href="tbResList.php?qv=150&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=150&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>, <a href="tbResList.php?qv=150&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?qv=150&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?qv=150&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?qv=150&tsv=239&wNotes=on">cl-PARP↑</a>, <a href="tbResList.php?qv=150&wNotes=on&word=HSP">HSP↓</a>, <!--<a href="tbResList.php?qv=150&wNotes=on&word=Prx">Prx</a>, --><!-- mitochondrial antioxidant enzyme--> <br> <!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, --> - Lowers AntiOxidant defense in Cancer Cells: <a href="tbResList.php?qv=150&tsv=226&wNotes=on&word=NRF2↓">NRF2↓</a>, <a href="tbResList.php?qv=150&word=Trx&wNotes=on">TrxR↓**</a>,<!-- major antioxidant system --> <a href="tbResList.php?qv=150&tsv=298&wNotes=on&word=SOD↓">SOD↓</a>, <a href="tbResList.php?qv=150&tsv=137&wNotes=on&word=GSH↓">GSH↓</a> <a href="tbResList.php?qv=150&tsv=46&wNotes=on">Catalase↓</a> <!-- <a href="tbResList.php?qv=150&tsv=597&wNotes=on">HO1↓</a> --> <a href="tbResList.php?qv=150&wNotes=on&word=GPx">GPx4↓</a> <br> - Raises <a href="tbResList.php?qv=150&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?qv=150&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>, <a href="tbResList.php?qv=150&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?qv=150&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?qv=150&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?qv=150&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?qv=150&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?qv=150&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?qv=150&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, <a href="tbResList.php?qv=150&tsv=235&wNotes=on&word=p38↓">p38↓</a>, Pro-Inflammatory Cytokines : <a href="tbResList.php?qv=150&tsv=908&wNotes=on&word=NLRP3↓">NLRP3↓</a>, <a href="tbResList.php?qv=150&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, <a href="tbResList.php?qv=150&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?qv=150&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <a href="tbResList.php?qv=150&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a> <br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓ inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.--> - inhibit Growth/Metastases : <a href="tbResList.php?qv=150&tsv=604&wNotes=on">TumMeta↓</a>, <a href="tbResList.php?qv=150&tsv=323&wNotes=on">TumCG↓</a>, <a href="tbResList.php?qv=150&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=150&tsv=204&wNotes=on">MMPs↓</a>, <a href="tbResList.php?qv=150&tsv=201&wNotes=on">MMP2↓</a>, <a href="tbResList.php?qv=150&tsv=203&wNotes=on">MMP9↓</a>, <!-- <a href="tbResList.php?qv=150&tsv=308&wNotes=on">TIMP2</a>, --> <a href="tbResList.php?qv=150&tsv=415&wNotes=on">IGF-1↓</a>, <a href="tbResList.php?qv=150&tsv=428&wNotes=on">uPA↓</a>, <a href="tbResList.php?qv=150&tsv=334&wNotes=on">VEGF↓</a>, <!-- <a href="tbResList.php?qv=150&tsv=1284&wNotes=on">ROCK1↓</a>, --> <a href="tbResList.php?qv=150&tsv=110&wNotes=on">FAK↓</a>, <!-- <a href="tbResList.php?qv=150&tsv=273&wNotes=on">RhoA↓</a>, --> <a href="tbResList.php?qv=150&tsv=214&wNotes=on">NF-κB↓</a>, <!-- <a href="tbResList.php?qv=150&tsv=79&wNotes=on">CXCR4↓</a>, --> <!-- <a href="tbResList.php?qv=150&tsv=1247&wNotes=on">SDF1↓</a>, --> <a href="tbResList.php?qv=150&tsv=304&wNotes=on">TGF-β↓</a>, <!-- <a href="tbResList.php?qv=150&tsv=719&wNotes=on">α-SMA↓</a>, --> <a href="tbResList.php?qv=150&tsv=105&wNotes=on">ERK↓</a> <!-- <a href="tbResList.php?qv=150&tsv=1178&wNotes=on">MARK4↓</a> --> <!-- contributing to tumor growth, invasion, and metastasis--> <br> <!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, --> <!-- - reactivate genes thereby inhibiting cancer cell growth : <a href="tbResList.php?qv=150&tsv=140&wNotes=on">HDAC↓</a>, <a href="tbResList.php?qv=150&tsv=85&wNotes=on">DNMT1↓</a>, <a href="tbResList.php?qv=150&tsv=86&wNotes=on">DNMT3A↓</a>, <a href="tbResList.php?qv=150&tsv=108&wNotes=on">EZH2↓</a>, <a href="tbResList.php?qv=150&tsv=236&wNotes=on">P53↑</a>, <a href="tbResList.php?qv=150&wNotes=on&word=HSP">HSP↓</a>, <a href="tbResList.php?qv=150&tsv=506&wNotes=on">Sp proteins↓</a>, <br> --> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?qv=150&tsv=322&wNotes=on">TumCCA↑</a>, <a href="tbResList.php?qv=150&tsv=73&wNotes=on">cyclin D1↓</a>, <a href="tbResList.php?qv=150&tsv=378&wNotes=on">cyclin E↓</a>, <a href="tbResList.php?qv=150&tsv=467&wNotes=on">CDK2↓</a>, <a href="tbResList.php?qv=150&tsv=894&wNotes=on">CDK4↓</a>, <!-- <a href="tbResList.php?qv=150&tsv=895&wNotes=on">CDK6↓</a>, --> <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?qv=150&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?qv=150&tsv=324&wNotes=on">TumCI↓</a>, <a href="tbResList.php?qv=150&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?qv=150&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=150&tsv=96&wNotes=on">EMT↓</a>, <!-- <a href="tbResList.php?qv=150&tsv=1117&wNotes=on">TOP1↓</a>, --> <!-- <a href="tbResList.php?qv=150&tsv=657&wNotes=on">TET1↓</a>, --> <br> <!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS --> - inhibits <a href="tbResList.php?qv=150&tsv=129&wNotes=on">glycolysis</a> /<a href="tbResList.php?qv=150&tsv=947&wNotes=on">Warburg Effect</a> and <a href="tbResList.php?qv=150&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> : <a href="tbResList.php?qv=150&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=150&tsv=772&wNotes=on">PKM2↓</a>, <a href="tbResList.php?qv=150&tsv=35&wNotes=on">cMyc↓</a>, <a href="tbResList.php?qv=150&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>, <a href="tbResList.php?qv=150&tsv=906&wNotes=on">LDH↓</a>, <a href="tbResList.php?qv=150&tsv=175&wNotes=on&word=LDH">LDHA↓</a>, <a href="tbResList.php?qv=150&tsv=773&wNotes=on">HK2↓</a>, <a href="tbResList.php?qv=150&wNotes=on&word=PFK">PFKs↓</a>, <a href="tbResList.php?qv=150&wNotes=on&word=PDK">PDKs↓</a>, <a href="tbResList.php?qv=150&tsv=847&wNotes=on">ECAR↓</a>, <a href="tbResList.php?qv=150&tsv=230&wNotes=on">OXPHOS↓</a>, <a href="tbResList.php?qv=150&tsv=356&wNotes=on">GRP78↑</a>, <!-- <a href="tbResList.php?qv=150&tsv=1278&wNotes=on">Glucose↓</a>, --> <a href="tbResList.php?qv=150&tsv=623&wNotes=on">GlucoseCon↓</a> <br> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - inhibits <a href="tbResList.php?qv=150&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=150&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=150&tsv=143&wNotes=on">HIF-1α↓</a>, <!-- <a href="tbResList.php?qv=150&wNotes=on&word=NOTCH">Notch↓</a>, --> <!-- <a href="tbResList.php?qv=150&wNotes=on&word=FGF">FGF↓</a>, --> <!-- <a href="tbResList.php?qv=150&tsv=361&wNotes=on">PDGF↓</a>, --> <a href="tbResList.php?qv=150&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, <a href="tbResList.php?qv=150&&wNotes=on&word=ITG">Integrins↓</a>, <br> <!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, --> <!-- - inhibits Cancer Stem Cells : <a href="tbResList.php?qv=150&tsv=795&wNotes=on">CSC↓</a>, <a href="tbResList.php?qv=150&tsv=524&wNotes=on">CK2↓</a>, <a href="tbResList.php?qv=150&tsv=141&wNotes=on">Hh↓</a>, <a href="tbResList.php?qv=150&tsv=434&wNotes=on">GLi↓</a>, <a href="tbResList.php?qv=150&tsv=124&wNotes=on">GLi1↓</a>, <a href="tbResList.php?qv=150&tsv=677&wNotes=on">CD133↓</a>, <a href="tbResList.php?qv=150&tsv=655&wNotes=on">CD24↓</a>, <a href="tbResList.php?qv=150&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=150&tsv=357&wNotes=on">n-myc↓</a>, <a href="tbResList.php?qv=150&tsv=656&wNotes=on">sox2↓</a>, <a href="tbResList.php?qv=150&tsv=222&wNotes=on">notch2↓</a>, <a href="tbResList.php?qv=150&tsv=1024&wNotes=on">nestin↓</a>, <a href="tbResList.php?qv=150&tsv=508&wNotes=on">OCT4↓</a>, <br> --> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=150&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=150&tsv=4&wNotes=on">AKT↓</a>, <a href="tbResList.php?qv=150&wNotes=on&word=JAK">JAK↓</a>, <a href="tbResList.php?qv=150&wNotes=on&word=STAT">STAT↓</a>, <!--<a href="tbResList.php?qv=150&tsv=377&wNotes=on">Wnt↓</a>, --> <a href="tbResList.php?qv=150&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=150&tsv=9&wNotes=on">AMPK</a>, <!--<a href="tbResList.php?qv=150&tsv=475&wNotes=on">α↓</a>, --> <a href="tbResList.php?qv=150&tsv=105&wNotes=on">ERK↓</a>, <!--<a href="tbResList.php?qv=150&tsv=1014&wNotes=on">5↓</a>, --> <a href="tbResList.php?qv=150&tsv=168&wNotes=on">JNK</a>, <a href="tbResList.php?qv=150&tsv=236&wNotes=on">P53↑</a>, <br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=150&tsv=1106&wNotes=on">chemo-sensitization</a>, <a href="tbResList.php?qv=150&tsv=1171&wNotes=on">chemoProtective</a>, <a href="tbResList.php?qv=150&tsv=1107&wNotes=on">RadioSensitizer</a>, <!-- <a href="tbResList.php?qv=150&tsv=1185&wNotes=on">RadioProtective</a>, --> <a href="tbResList.php?qv=150&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <a href="tbResList.php?qv=150&tsv=1105&wNotes=on">Neuroprotective</a>, <a href="tbResList.php?qv=150&tsv=557&wNotes=on">Cognitive</a>, <a href="tbResList.php?qv=150&tsv=1175&wNotes=on">Renoprotection</a>, <a href="tbResList.php?qv=150&tsv=1179&wNotes=on">Hepatoprotective</a>, <a href="tbResList.php?&qv=150&tsv=1188&wNotes=on">CardioProtective</a>, <br> <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=150&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br>
226
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STF
Short Term Fasting
NP
<b>Short-term fasting (STF)</b> 48 to 72 h before chemotherapy appears to be more effective than intermittent fasting. Preliminary data show that STF is safe but challenging in cancer patients receiving chemotherapy.<br>
151
-
GSL
Siegesbeckia glabrescens
NP
<b>Germacranolide sesquiterpene lactone (GSL)</b> was isolated from Siegesbeckia glabrescens as an inhibitor of Gli. <br>
153
-
SNP
Silver-NanoParticles
NP
<b>Silver NanoParticles</b><br> Summary: <br> 1. Smaller sizes desirable due to greater surface area, and cell penetration (enhanced permeability and retention (EPR) effect)<br> 2. Two main types: AgNP and silver ions (big debate on uses: Ag+ turning to AgCl in stomach but AgCl also effective. Take sodium-bicarbonate?<br> 3. Dose example 80kg person: 1.12-2mg/day, which can be calculated based on ppm and volume taken (see below) target < 10ppm and 120mL per day (30ppm and 1L per day caused argyria 30mg/day ) (Case Report: 9‐15 ppm@120mL, i.e. 1.1mg/L to 1.8mg/L per day)<br> Likely 10ppm --> 10mg/L, hence if take 100mL, then 1mg/day? (for Cancer)<br> The current Rfd for oral silver exposure is 5 ug/kg/d with a critical dose estimated at 14 ug/kg/d for the average person.<br> Seems like the Cancer target range is 14ug/kg/day to 25ug/kg/day. 80Kg example: 1.12mg to 2mg <a href="https://www.cancertreatmentsresearch.com/a-silver-bullet-to-kill-cancer/" > “1.4µg/kg body weight. If I would have 70kg, I would want to use 100µg/day. However, for fighting active disease, I would tend to explore higher daily dose, as I think this may be too low.” </a> <br> 4. AntiOxidants/NAC can counter act the effect of Silver NanoParticles from producing reactive oxygen species (ROS) and mitochondrial damage . NAC is a supplement form of cysteine, an amino acid that helps make glutathione, a powerful antioxidant. <br> 5. In vitro most reports indicate AgNPs increase ROS in both cancer and normal cell (but in vivo improved antioxidant system of normal may create selectivity)<br> 6. Pathways/mechanisms of action/:<br> -” intracellular ROS was increased...reduction in levels of glutathione (GSH)”<br> -”AgNPs affect the function of the vascular endothelial growth factor (VEGF)” (likely reducing levels)<br> -”expression of BAX and BCL2 genes was increased” <br> -”upregulation of proapoptotic genes (p53, p21, Bax, and caspases) and downregulation of antiapoptotic genes (Bcl-2)”<br> -” upregulation of AMPK and downregulation of mTOR, MMP-9, BCL-2, and α-SMA”<br> -”p53 is a key player...proapoptotic genes p53 and Bax were significantly increased... noticeable reduction in Bcl-2 transcript levels”<br> -” p53 participates directly in the intrinsic apoptosis pathway by regulating the mitochondrial outer membrane permeabilization”<br> - “Proapoptotic markers (BAX/BCL-XL, cleaved poly(ADP-ribose) polymerase, p53, p21, and caspases 3, 8 and 9) increased.”<br> -”The antiapoptotic markers, AKT and NF-kB, decreased in AgNP-treated cells.”<br> <br> Silver NanoParticles and Magnetic Fields<br> Summary:<br> 1. “exposure to PMF increased the ability of AgNPs uptake”<br> 2. 6x improvement from AgNPs alone<br> <br> could <a href="https://nestronics.ca/dbx/tbResList.php?qv=335&qv2=153&wNotes=on&">glucose </a> capping of SilverNPs work as trojan horse?<br>
154
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SIL
Silymarin (Milk Thistle) silibinin
NP
<b>Silymarin (Milk Thistle)</b> Flowering herb related to daisy and ragweed family.<br> Silibinin (INN), also known as silybin is the major active constituent of silymarin, a standardized extract of the milk thistle seeds. <br> -a flavonoid combination of 65–80% of seven flavolignans; the most important of these include silybin, isosilybin, silychristin, isosilychristin, and silydianin. Silybin is the most abundant compound in around 50–70% in isoforms silybin A and silybin B<br> <br> -Note <a href="tbResList.php?qv=154&tsv=1109&wNotes=on&exSp=open">half-life</a> 6hrs?.<br> <a href="tbResList.php?qv=154&tsv=792&wNotes=on&exSp=open">BioAv</a> not soluble in water, low bioA (1%). 240mg yielded only 0.34ug/ml plasma level. oral administration of SM (equivalent to 120 mg silibinin), total (unconjugated + conjugated) silibinin concentration in plasma was 1.1–1.3 μg/mL, so can on acheive levels used in most in-vitro studies. <br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - results for both inducing and reducing <a href="tbResList.php?qv=154&tsv=275&wNotes=on">ROS</a> in cancer cells. In normal cell seems to consistently lower ROS. Given low bioavailability seems unlikely one could acheieve levels in vivo to raise ROS(except level in GUT could be much higher (800uM).<br> - ROS↑ related: <a href="tbResList.php?qv=154&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <!-- <a href="tbResList.php?qv=154&tsv=103&wNotes=on">ER Stress↑</a>, --> <!-- <a href="tbResList.php?qv=154&tsv=459&wNotes=on">UPR↑</a>, --> <!-- <a href="tbResList.php?qv=154&tsv=356&wNotes=on">GRP78↑</a>, --> <a href="tbResList.php?qv=154&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>, <a href="tbResList.php?qv=154&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?qv=154&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?qv=154&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?qv=154&tsv=239&wNotes=on">cl-PARP↑</a>, <!-- <a href="tbResList.php?qv=154&wNotes=on&word=HSP">HSP↓</a>, --> <!-- <a href="tbResList.php?qv=154&wNotes=on&word=Prx">Prx</a>, --><!-- mitochondrial antioxidant enzyme--> <br> <!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, --> <!-- - Lowers AntiOxidant defense in Cancer Cells: <a href="tbResList.php?qv=154&tsv=226&wNotes=on&word=NRF2↓">NRF2↓</a>, <a href="tbResList.php?qv=154&word=Trx&wNotes=on">TrxR↓**</a>, <a href="tbResList.php?qv=154&tsv=298&wNotes=on&word=SOD↓">SOD↓</a>, <a href="tbResList.php?qv=154&tsv=137&wNotes=on&word=GSH↓">GSH↓</a> <a href="tbResList.php?qv=154&tsv=46&wNotes=on">Catalase↓</a> <a href="tbResList.php?qv=154&tsv=597&wNotes=on">HO1↓</a> <a href="tbResList.php?qv=154&wNotes=on&word=GPx">GPx↓</a> <br> --> - Raises <a href="tbResList.php?qv=154&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?qv=154&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>, <a href="tbResList.php?qv=154&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?qv=154&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?qv=154&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?qv=154&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?qv=154&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?qv=154&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?qv=154&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, <a href="tbResList.php?qv=154&tsv=235&wNotes=on&word=p38↓">p38↓</a>, Pro-Inflammatory Cytokines : <a href="tbResList.php?qv=154&tsv=908&wNotes=on&word=NLRP3↓">NLRP3↓</a>, <a href="tbResList.php?qv=154&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, <a href="tbResList.php?qv=154&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?qv=154&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <a href="tbResList.php?qv=154&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a> <br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓ inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.--> - inhibit Growth/Metastases : <a href="tbResList.php?qv=154&tsv=604&wNotes=on">TumMeta↓</a>, <a href="tbResList.php?qv=154&tsv=323&wNotes=on">TumCG↓</a>, <a href="tbResList.php?qv=154&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=154&tsv=204&wNotes=on">MMPs↓</a>, <a href="tbResList.php?qv=154&tsv=201&wNotes=on">MMP2↓</a>, <a href="tbResList.php?qv=154&tsv=203&wNotes=on">MMP9↓</a>, <a href="tbResList.php?qv=154&tsv=308&wNotes=on">TIMP2</a>, <!-- <a href="tbResList.php?qv=154&tsv=415&wNotes=on">IGF-1↓</a>, --> <a href="tbResList.php?qv=154&tsv=428&wNotes=on">uPA↓</a>, <a href="tbResList.php?qv=154&tsv=334&wNotes=on">VEGF↓</a>, <!-- <a href="tbResList.php?qv=154&tsv=1284&wNotes=on">ROCK1↓</a>, --> <a href="tbResList.php?qv=154&tsv=110&wNotes=on">FAK↓</a>, <!-- <a href="tbResList.php?qv=154&tsv=273&wNotes=on">RhoA↓</a>, --> <a href="tbResList.php?qv=154&tsv=214&wNotes=on">NF-κB↓</a>, <a href="tbResList.php?qv=154&tsv=79&wNotes=on">CXCR4↓</a>, <!-- <a href="tbResList.php?qv=154&tsv=1247&wNotes=on">SDF1↓</a>, --> <a href="tbResList.php?qv=154&tsv=304&wNotes=on">TGF-β↓</a>, <a href="tbResList.php?qv=154&tsv=719&wNotes=on">α-SMA↓</a>, <a href="tbResList.php?qv=154&tsv=105&wNotes=on">ERK↓</a> <!-- <a href="tbResList.php?qv=154&tsv=1178&wNotes=on">MARK4↓</a> --><!-- contributing to tumor growth, invasion, and metastasis--> <br> <!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, --> - reactivate genes thereby inhibiting cancer cell growth : <a href="tbResList.php?qv=154&tsv=140&wNotes=on">HDAC↓</a>, <a href="tbResList.php?qv=154&wNotes=on&word=DNMT">DNMTs↓</a>, <!-- <a href="tbResList.php?qv=154&tsv=108&wNotes=on">EZH2↓</a>, --> <a href="tbResList.php?qv=154&tsv=236&wNotes=on">P53↑</a>, <a href="tbResList.php?qv=154&wNotes=on&word=HSP">HSP↓</a>, <!-- <a href="tbResList.php?qv=154&tsv=506&wNotes=on">Sp proteins↓</a>, --> <!-- <a href="tbResList.php?qv=154&wNotes=on&word=TET">TET↑</a> --> <br> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?qv=154&tsv=322&wNotes=on">TumCCA↑</a>, <a href="tbResList.php?qv=154&tsv=73&wNotes=on">cyclin D1↓</a>, <a href="tbResList.php?qv=154&tsv=378&wNotes=on">cyclin E↓</a>, <a href="tbResList.php?qv=154&tsv=467&wNotes=on">CDK2↓</a>, <a href="tbResList.php?qv=154&tsv=894&wNotes=on">CDK4↓</a>, <!-- <a href="tbResList.php?qv=154&tsv=895&wNotes=on">CDK6↓</a>, --> <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?qv=154&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?qv=154&tsv=324&wNotes=on">TumCI↓</a>, <a href="tbResList.php?qv=154&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <!-- encourages invasion, proliferation, EMT, and angiogenesis --> <a href="tbResList.php?qv=154&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?qv=154&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=154&tsv=96&wNotes=on">EMT↓</a>, <!-- <a href="tbResList.php?qv=154&wNotes=on&word=TOP">TOP1↓</a>, --> <!-- <a href="tbResList.php?qv=154&tsv=657&wNotes=on">TET1</a>, --> <br> <!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS --> - inhibits <a href="tbResList.php?qv=154&tsv=129&wNotes=on">glycolysis</a> <!-- /<a href="tbResList.php?qv=154&tsv=947&wNotes=on">Warburg Effect</a> --> and <a href="tbResList.php?qv=154&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> : <a href="tbResList.php?qv=154&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=154&tsv=772&wNotes=on">PKM2↓</a>, <a href="tbResList.php?qv=154&tsv=35&wNotes=on">cMyc↓</a>, <a href="tbResList.php?qv=154&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>, <a href="tbResList.php?qv=154&tsv=906&wNotes=on">LDH↓</a>, <a href="tbResList.php?qv=154&tsv=175&wNotes=on&word=LDH">LDHA↓</a>, <a href="tbResList.php?qv=154&tsv=773&wNotes=on">HK2↓</a>, <a href="tbResList.php?qv=154&wNotes=on&word=PFK">PFKs↓</a>, <!-- <a href="tbResList.php?qv=154&wNotes=on&word=PDK">PDKs↓</a>, --> <!-- <a href="tbResList.php?qv=154&tsv=847&wNotes=on">ECAR↓</a>, --> <a href="tbResList.php?qv=154&tsv=230&wNotes=on">OXPHOS↓</a>, <a href="tbResList.php?qv=154&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=154&tsv=1278&wNotes=on">Glucose↓</a>, <a href="tbResList.php?qv=154&tsv=623&wNotes=on">GlucoseCon↓</a> <br> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - inhibits <a href="tbResList.php?qv=154&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=154&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=154&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=154&wNotes=on&word=NOTCH">Notch↓</a>, <!-- <a href="tbResList.php?qv=154&wNotes=on&word=FGF">FGF↓</a>, --> <a href="tbResList.php?qv=154&wNotes=on&word=PDGF">PDGF↓</a>, <a href="tbResList.php?qv=154&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, <!-- <a href="tbResList.php?qv=154&&wNotes=on&word=ITG">Integrins↓</a>, --> <br> <!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, --> - inhibits Cancer Stem Cells : <a href="tbResList.php?qv=154&tsv=795&wNotes=on">CSC↓</a>, <!-- <a href="tbResList.php?qv=154&tsv=524&wNotes=on">CK2↓</a>, --> <a href="tbResList.php?qv=154&tsv=141&wNotes=on">Hh↓</a>, <!-- <a href="tbResList.php?qv=154&tsv=434&wNotes=on">GLi↓</a>, --> <a href="tbResList.php?qv=154&tsv=124&wNotes=on">GLi1↓</a>, <!-- <a href="tbResList.php?qv=154&tsv=677&wNotes=on">CD133↓</a>, --> <!-- <a href="tbResList.php?qv=154&tsv=655&wNotes=on">CD24↓</a>, --> <a href="tbResList.php?qv=154&tsv=342&wNotes=on">β-catenin↓</a>, <!-- <a href="tbResList.php?qv=154&tsv=357&wNotes=on">n-myc↓</a>, --> <!-- <a href="tbResList.php?qv=154&tsv=656&wNotes=on">sox2↓</a>, --> <a href="tbResList.php?qv=154&wNotes=on&word=NOTCH">Notch2↓</a>, <!-- <a href="tbResList.php?qv=154&tsv=1024&wNotes=on">nestin↓</a>, --> <a href="tbResList.php?qv=154&tsv=508&wNotes=on">OCT4↓</a>, <br> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=154&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=154&tsv=4&wNotes=on">AKT↓</a>, <a href="tbResList.php?qv=154&wNotes=on&word=JAK">JAK↓</a>, <a href="tbResList.php?qv=154&wNotes=on&word=STAT">STAT↓</a>, <a href="tbResList.php?qv=154&tsv=377&wNotes=on">Wnt↓</a>, <a href="tbResList.php?qv=154&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=154&tsv=9&wNotes=on">AMPK</a>, <!-- <a href="tbResList.php?qv=154&tsv=475&wNotes=on">α↓</a>, --> <a href="tbResList.php?qv=154&tsv=105&wNotes=on">ERK↓</a>, <!-- <a href="tbResList.php?qv=154&tsv=1014&wNotes=on">5↓</a>, --> <a href="tbResList.php?qv=154&tsv=168&wNotes=on">JNK</a>, - <a href="tbResList.php?qv=154&wNotes=on&word=SREBP">SREBP</a> (related to cholesterol).<br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=154&tsv=1106&wNotes=on">chemo-sensitization</a>, <a href="tbResList.php?qv=154&tsv=1171&wNotes=on">chemoProtective</a>, <a href="tbResList.php?qv=154&tsv=1107&wNotes=on">RadioSensitizer</a>, <a href="tbResList.php?qv=154&tsv=1185&wNotes=on">RadioProtective</a>, <a href="tbResList.php?qv=154&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <a href="tbResList.php?qv=154&tsv=1105&wNotes=on">Neuroprotective</a>, <a href="tbResList.php?qv=154&tsv=557&wNotes=on">Cognitive</a>, <a href="tbResList.php?qv=154&tsv=1175&wNotes=on">Renoprotection</a>, <a href="tbResList.php?qv=154&tsv=1179&wNotes=on">Hepatoprotective</a>, <a href="tbResList.php?&qv=154&tsv=1188&wNotes=on">CardioProtective</a>, <br> <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=154&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br>
155
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SIM
Simvastatin
NP
Statin
<b>Brand name Zocor (drug)</b><br>
267
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SDT
SonoDynamic Therapy UltraSound
T
<b>Sonodynamic therapy (SDT)</b> is an emerging, non-invasive treatment modality that employs ultrasound energy in conjunction with sonosensitizers to induce cytotoxicity in target tissues. A key mechanism by which SDT exerts its therapeutic effects is through the generation of reactive oxygen species (ROS). <br> Also known as high-intensity focused ultrasound (HIFU)<br> <br> SDT relies on the ultrasound-triggered activation of sonosensitizers (similar in concept to photosensitizers used in photodynamic therapy). When activated by ultrasound, these compounds undergo energy transitions that lead to the production of ROS, such as singlet oxygen and free radicals.<br> <br> -Advantages of SDT include its non-invasive nature, deep tissue penetration of ultrasound, and the ability to target localized areas with high precision.<br> -Challenges remain in precisely controlling ROS production and ensuring that the resulting oxidative stress is sufficient to induce cell death in tumor cells without overwhelming damage to surrounding normal tissues.<br> <br> Sonosensitizers:<br> – Hematoporphyrin Derivative (HPD) and Photofrin<br> – Protoporphyrin IX (PpIX)<br> – Chlorin e6 (Ce6)<br> – Phthalocyanine compounds<br> – Titanium Dioxide (TiO2) Nanoparticles<br> – Other metallic or semiconductor nanoparticles, sometimes functionalized or loaded with traditional sensitizer molecules (e.g., gold nanoparticles, copper-cysteamine), have been explored to enhance ROS production and improve tumor targeting.<br> – Curcumin, derived from turmeric, has been shown in several studies to exhibit sonosensitizing properties.<br> – Under ultrasound activation, quercetin may act as a sonosensitizer, increasing ROS generation and contributing to cancer cell apoptosis.<br> <br> US frequency range of 150 kHz–3 MHz, irradiation dose of 2–3 W cm−2, and the actuation duration range of 1–20 min are used for SDT research<br> <br> <a href="https://can-amhifu.com/" > https://can-amhifu.com/ </a> <br> <br> https://canadaclinicsupply.com/product/soundcare-plus-professional-dual-ultrasound-device-by-roscoe/ <br> https://physiostore.ca/product-category/therapeutic-modalities/therapeutic-ultrasound/clinical-ultrasound-systems/ <br> https://physiostore.ca/richmar-home-ultrasound-2000-2nd-edition/ <br>
16
-
SRF
Sorafenib (brand name Nexavar)
D
kinase inhibitor drug
<b>Inhibitors</b> of vascular endothelial growth factor receptor (VEGFR); used to treat kidney, liver and thyroid cancers.<br>
276
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Squ
Squalene
NP
<b>Squalene</b>, a natural triterpene found in olive oil, shark liver oil, and other sources, has been investigated for its potential anticancer effects. Although squalene is best known as an intermediate in cholesterol biosynthesis, its antioxidant and membrane‐protective properties may contribute to anticancer activity through several mechanisms and pathways.<br> <br> Antioxidant Activity and Lipid Protection<br> -Squalene can quench free radicals and protect cell membranes from lipid peroxidation. This antioxidant property may reduce DNA damage and mutagenesis that contribute to cancer initiation.<br> <br> Modulation of the Mevalonate Pathway<br> -Squalene is a precursor in the cholesterol biosynthesis pathway (the mevalonate pathway). Alterations in this pathway are implicated in cancer cell proliferation and survival. By influencing this pathway, squalene might indirectly affect the synthesis of isoprenoids, which are involved in the post-translational modification of proteins (e.g., RAS, RHO), critical for cell growth and differentiation.<br>
18
-
statins
statins
NP
<b>Statins</b>, inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, which act downstream of ACL in the cholesterol synthesis pathway, can dramatically enhance the anti-tumor effects of ACL inhibition.<br>
286
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Sulfas
Sulfasalazine
RD
<b>Sulfasalazine</b> is primarily known as an anti-inflammatory and disease‐modifying antirheumatic drug (DMARD), used for conditions such as rheumatoid arthritis and inflammatory bowel diseases (e.g., ulcerative colitis). <br> <br> -Inhibit the nuclear factor kappa B (NF-κB) pathway.<br> -Sulfasalazine has been noted to interfere with the cystine/glutamate antiporter (system x_c⁻), which can reduce glutathione levels in cancer cells, potentially making them more susceptible to oxidative stress.<br> <br> -Ability to inhibit anti-oxidant production (for ProOxidant effect).<br>
156
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SFN
Sulforaphane (mainly Broccoli)
NP
<b>Sulforaphane</b> is an isothiocyanate derived from glucoraphanin, a compound found predominantly in cruciferous vegetables such as broccoli, Brussels sprouts, and cabbage. It is well known for its potent antioxidant and detoxification properties and has gained significant attention for its potential chemopreventive and anticancer effects.<br> <br> Summary<br> 1.primarily attenuates both DNMTs and HDACs, individually suppressing DNA hypermethylation and histones deacetylation, ultimately upregulating NRF2 (best known for NRF2↑)<br> 2.Antioxidant Activity:<br> • Nrf2 activation leads to the upregulation of a host of antioxidant and detoxification enzymes (e.g., glutathione S-transferase, NAD(P)H:quinone oxidoreductase 1, heme oxygenase-1), which in turn decrease oxidative stress and lower ROS levels.<br> 3.Pro-oxidant Effects in Cancer Cells and Under High-Dose Conditions (>=10uM?)<br> • In certain cancer cell types or at higher concentrations, sulforaphane can paradoxically lead to an increase in ROS levels.<br> • The elevated ROS may overwhelm the cancer cells’ antioxidant defenses, leading to oxidative stress–mediated cell death (apoptosis).<br> • This context-dependent pro-oxidant effect has been explored for its potential in selectively targeting cancer cells while leaving normal cells less affected. <br> <br> - Might not be a good candidate for pro-oxidant strategy depending on concentration >10uM?.<br> - Strong Activation of Nrf2 (best known for) at low to moderate concentrations, hence reduces oxidative stress in both cancer and normal cells.<br> - AMPK signaling activated by SFN, high concentrations of ROS are produced<br> - ROS generation also results in depletion of GSH levels<br> - HIF-1α and VEGF inhibitor<br> - Might be effective against cancer stem cells<br> - <a href="https://www.cancertreatmentsresearch.com">But I would not combine that with radiation, </a> as Sulforaphane activates the anti-oxidant master regulator of cells.<br> - <a href="https://www.cancertreatmentsresearch.com">“I very much agree: </a> Sulforaphane is a very good addition, even more when the choice is an anti-oxidant therapy” <br> - well known as HDAC inhibitor (typically 5-10um concentrations)<br> -<a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC4394840/">A transient decrease </a>in HDAC activity has also been observed in healthy humans 3 h after providing a daily 200 µM SFN dose, resulting in a plasma concentration of SFN metabolites of 0.1–0.2 µM.<br> <br> <br> Dose/Bioavailabilty information:<br> SFN at a daily dose of 2.2 µM/kg body weight, with a mean plasma level of 0.13 µM <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC4394840/#F2">Sprout 127.6 grams = 205uM±19.9 </a>content yields SFN 0.5 to 2uM in plasma. <br> However, it is important to consider that at lower doses, specifically 2.5 μM, SFN resulted in a slight increase in cell proliferation by 5.18–11.84% within a 6 to 48 h treatment window.<br> -A therapeutic dose starts at approx 60 grams of the sprouts.<br> -100 g of Broccoli sprouts contain about 15–20 mg of sulforaphane<br> –Organic Broccoli Sprout Powder (Health Ranger) – Avmacol® – NanoPSA (a blend of NanoStilbene™ and Broccoli Sprout Extract). <br> -<a href="https://www.mcsformulas.com/vitamins-supplements/broccoli-ultra-sulforaphane/"> -750 mg Sulforaphane Glucosinolate in Daily One Serving (2 capsules) (30mg Sulforaphane)</a> <br> <br> Total sulforaphane metabolite concentration in plasma was the highest (>2 μM) at 3 h in human subjects who consumed fresh broccoli sprouts (40g) <br> -human studies with broccoli sprouts or extracts report plasma sulforaphane levels in the low micromolar range (typically 1–2 µM) after ingesting realistic, food-based quantities of sprouts (often in the range of 30–50 g of sprouts or a concentrated extract).<br> <br> BroccoSprouts are young broccoli sprouts that have garnered attention because they contain high amounts of glucoraphanin—a precursor molecule to sulforaphane. Studies have shown that broccoli sprouts can have sulforaphane precursor levels (i.e., glucoraphanin levels) that are 10 to 100 times higher than those found in mature broccoli heads. Glucoraphanin content in broccoli sprouts can range anywhere from about 30 to over 100 mg per 100 grams of fresh sprouts. Once activated (e.g., during consumption when myrosinase acts on glucoraphanin), these levels translate into a significant sulforaphane yield, meaning that even a small amount of broccoli sprouts can deliver a potent dose of this bioactive compound.<br> <br> Importantly, glucoraphanin itself is not bioactive. Rather, enzymatic hydrolysis by myrosinase, present in the plant tissue or in the mammalian microbiome, is necessary to form the active component, SFN.<br> - GFN (glucoraphanin) is hydrolyzed in vivo to SFN via the myrosinase, which is present in gut bacteria as well as the plant itself (also in Radish)<br> - Do not cook the vegetables, or if you do add myrosinase back in by adding radish.<br> - <a href="tbResEdit.php?rid=1729">mild heat</a> of broccoli (60–70 °C) inactivated ESP and preserved myrosinase and increased SF yield 3–7-fold<br> - <a href="tbResEdit.php?rid=2556">chewing </a> of fresh broccoli sprouts increases the interaction of glucosinolates with myrosinase and consequently, increases the bioavailability of SFN in the body<br> <br> -Note <a href="tbResList.php?qv=156&tsv=1109&wNotes=on&exSp=open">half-life</a> 2-3 hrs.<br> <a href="tbResList.php?qv=156&tsv=792&wNotes=on&exSp=open">BioAv</a> is good (15-80%) but requires myrosinase <br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - induce <a href="tbResList.php?qv=156&tsv=275&wNotes=on">ROS</a> production<br> - ROS↑ related: <a href="tbResList.php?qv=156&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?qv=156&tsv=103&wNotes=on">ER Stress↑</a>, <a href="tbResList.php?qv=156&tsv=459&wNotes=on">UPR↑</a>, <a href="tbResList.php?qv=156&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=156&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>, <a href="tbResList.php?qv=156&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?qv=156&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?qv=156&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?qv=156&tsv=239&wNotes=on">cl-PARP↑</a>, <a href="tbResList.php?qv=156&wNotes=on&word=HSP">HSP↓</a>, <a href="tbResList.php?qv=156&wNotes=on&word=Prx">Prx</a>,<!-- mitochondrial antioxidant enzyme--> <br> <!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, --> - Lowers AntiOxidant defense in Cancer Cells: <a href="tbResList.php?qv=156&tsv=226&wNotes=on&word=NRF2">NRF2↓</a>(contrary, actually most raises NRF2), <a href="tbResList.php?qv=156&word=Trx&wNotes=on">TrxR↓**</a>,<!-- major antioxidant system --> <!-- <a href="tbResList.php?qv=156&tsv=298&wNotes=on&word=SOD↓">SOD↓</a>, --> <a href="tbResList.php?qv=156&tsv=137&wNotes=on&word=GSH↓">GSH↓</a>, <a href="tbResList.php?qv=156&tsv=46&wNotes=on">Catalase↓</a>(contrary), <a href="tbResList.php?qv=156&tsv=597&wNotes=on">HO1↓</a>(contrary), <a href="tbResList.php?qv=156&wNotes=on&word=GPx">GPx↓</a> <br> - Raises <a href="tbResList.php?qv=156&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?qv=156&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>, <a href="tbResList.php?qv=156&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?qv=156&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?qv=156&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?qv=156&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?qv=156&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?qv=156&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?qv=156&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, <a href="tbResList.php?qv=156&tsv=235&wNotes=on&word=p38↓">p38↓</a>, Pro-Inflammatory Cytokines : <a href="tbResList.php?qv=156&tsv=908&wNotes=on&word=NLRP3↓">NLRP3↓</a>, <a href="tbResList.php?qv=156&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, <a href="tbResList.php?qv=156&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?qv=156&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <a href="tbResList.php?qv=156&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a> <br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓ inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.--> - inhibit Growth/Metastases : <a href="tbResList.php?qv=156&tsv=604&wNotes=on">TumMeta↓</a>, <a href="tbResList.php?qv=156&tsv=323&wNotes=on">TumCG↓</a>, <a href="tbResList.php?qv=156&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=156&tsv=204&wNotes=on">MMPs↓</a>, <a href="tbResList.php?qv=156&tsv=201&wNotes=on">MMP2↓</a>, <a href="tbResList.php?qv=156&tsv=203&wNotes=on">MMP9↓</a>, <!-- <a href="tbResList.php?qv=156&tsv=308&wNotes=on">TIMP2</a>, --> <a href="tbResList.php?qv=156&tsv=415&wNotes=on">IGF-1↓</a>, <!-- <a href="tbResList.php?qv=156&tsv=428&wNotes=on">uPA↓</a>, --> <a href="tbResList.php?qv=156&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=156&tsv=1284&wNotes=on">ROCK1↓</a>, <a href="tbResList.php?qv=156&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?qv=156&tsv=273&wNotes=on">RhoA↓</a>, <a href="tbResList.php?qv=156&tsv=214&wNotes=on">NF-κB↓</a>, <a href="tbResList.php?qv=156&tsv=79&wNotes=on">CXCR4↓</a>, <!-- <a href="tbResList.php?qv=156&tsv=1247&wNotes=on">SDF1↓</a>, --> <!-- <a href="tbResList.php?qv=156&tsv=304&wNotes=on">TGF-β↓</a>, --> <a href="tbResList.php?qv=156&tsv=719&wNotes=on">α-SMA↓</a>, <a href="tbResList.php?qv=156&tsv=105&wNotes=on">ERK↓</a> <!-- <a href="tbResList.php?qv=156&tsv=1178&wNotes=on">MARK4↓</a> --> <!-- contributing to tumor growth, invasion, and metastasis--> <br> <!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, --> - reactivate genes thereby inhibiting cancer cell growth : <a href="tbResList.php?qv=156&tsv=140&wNotes=on">HDAC↓</a>, <a href="tbResList.php?qv=156&wNotes=on&word=DNMT">DNMTs↓</a>, <a href="tbResList.php?qv=156&tsv=108&wNotes=on">EZH2↓</a>, <a href="tbResList.php?qv=156&tsv=236&wNotes=on">P53↑</a>, <a href="tbResList.php?qv=156&wNotes=on&word=HSP">HSP↓</a>, <a href="tbResList.php?qv=156&tsv=506&wNotes=on">Sp proteins↓</a>, <!-- <a href="tbResList.php?qv=156&wNotes=on&word=TET">TET↑</a> --> <br> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?qv=156&tsv=322&wNotes=on">TumCCA↑</a>, <a href="tbResList.php?qv=156&tsv=73&wNotes=on">cyclin D1↓</a>, <a href="tbResList.php?qv=156&tsv=378&wNotes=on">cyclin E↓</a>, <a href="tbResList.php?qv=156&tsv=467&wNotes=on">CDK2↓</a>, <a href="tbResList.php?qv=156&tsv=894&wNotes=on">CDK4↓</a>, <a href="tbResList.php?qv=156&tsv=895&wNotes=on">CDK6↓</a>, <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?qv=156&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?qv=156&tsv=324&wNotes=on">TumCI↓</a>, <a href="tbResList.php?qv=156&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <!-- encourages invasion, proliferation, EMT, and angiogenesis --> <a href="tbResList.php?qv=156&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?qv=156&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=156&tsv=96&wNotes=on">EMT↓</a>, <!-- <a href="tbResList.php?qv=156&tsv=1117&wNotes=on">TOP1↓</a>, --> <!-- <a href="tbResList.php?qv=156&tsv=657&wNotes=on">TET1↓</a>, --> <br> <!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS --> - inhibits <a href="tbResList.php?qv=156&tsv=129&wNotes=on">glycolysis</a> /<a href="tbResList.php?qv=156&tsv=947&wNotes=on">Warburg Effect</a> and <a href="tbResList.php?qv=156&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> : <a href="tbResList.php?qv=156&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=156&tsv=772&wNotes=on">PKM2↓</a>, <a href="tbResList.php?qv=156&tsv=35&wNotes=on">cMyc↓</a>, <a href="tbResList.php?qv=156&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>, <a href="tbResList.php?qv=156&tsv=906&wNotes=on">LDH↓</a>, <a href="tbResList.php?qv=156&tsv=175&wNotes=on&word=LDH">LDHA↓</a>, <a href="tbResList.php?qv=156&tsv=773&wNotes=on">HK2↓</a>, <!-- <a href="tbResList.php?qv=156&wNotes=on&word=PFK">PFKs↓</a>, --> <!-- <a href="tbResList.php?qv=156&wNotes=on&word=PDK">PDKs↓</a>, --> <a href="tbResList.php?qv=156&tsv=847&wNotes=on">ECAR↓</a>, <a href="tbResList.php?qv=156&tsv=230&wNotes=on">OXPHOS↓</a>, <a href="tbResList.php?qv=156&tsv=356&wNotes=on">GRP78↑</a>, <!-- <a href="tbResList.php?qv=156&tsv=1278&wNotes=on">Glucose↓</a>, --> <a href="tbResList.php?qv=156&tsv=623&wNotes=on">GlucoseCon↓</a> <br> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - inhibits <a href="tbResList.php?qv=156&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=156&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=156&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=156&wNotes=on&word=NOTCH">Notch↓</a>, <!-- <a href="tbResList.php?qv=156&wNotes=on&word=FGF">FGF↓</a>, --> <a href="tbResList.php?qv=156&wNotes=on&word=PDGF">PDGF↓</a>, <a href="tbResList.php?qv=156&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, <a href="tbResList.php?qv=156&&wNotes=on&word=ITG">Integrins↓</a>, <br> <!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, --> - inhibits Cancer Stem Cells : <a href="tbResList.php?qv=156&tsv=795&wNotes=on">CSC↓</a>, <!-- <a href="tbResList.php?qv=156&tsv=524&wNotes=on">CK2↓</a>, --> <a href="tbResList.php?qv=156&tsv=141&wNotes=on">Hh↓</a>, <a href="tbResList.php?qv=156&tsv=434&wNotes=on">GLi↓</a>, <a href="tbResList.php?qv=156&tsv=124&wNotes=on">GLi1↓</a>, <a href="tbResList.php?qv=156&tsv=677&wNotes=on">CD133↓</a>, <!-- <a href="tbResList.php?qv=156&tsv=655&wNotes=on">CD24↓</a>, --> <a href="tbResList.php?qv=156&tsv=342&wNotes=on">β-catenin↓</a>, <!-- <a href="tbResList.php?qv=156&tsv=357&wNotes=on">n-myc↓</a>, --> <a href="tbResList.php?qv=156&tsv=656&wNotes=on">sox2↓</a>, <a href="tbResList.php?qv=156&wNotes=on&word=NOTCH">notch2↓</a>, <a href="tbResList.php?qv=156&tsv=1024&wNotes=on">nestin↓</a>, <a href="tbResList.php?qv=156&tsv=508&wNotes=on">OCT4↓</a>, <br> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=156&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=156&tsv=4&wNotes=on">AKT↓</a>, <a href="tbResList.php?qv=156&wNotes=on&word=JAK">JAK↓</a>, <a href="tbResList.php?qv=156&wNotes=on&word=STAT">STAT↓</a>, <a href="tbResList.php?qv=156&tsv=377&wNotes=on">Wnt↓</a>, <a href="tbResList.php?qv=156&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=156&tsv=9&wNotes=on">AMPK</a>, <!-- <a href="tbResList.php?qv=156&tsv=475&wNotes=on">α↓</a>, --> <a href="tbResList.php?qv=156&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=156&tsv=1014&wNotes=on">5↓</a>, <!-- <a href="tbResList.php?qv=156&tsv=168&wNotes=on">JNK</a>, --> - <a href="tbResList.php?qv=156&wNotes=on&word=SREBP">SREBP</a> (related to cholesterol).<br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=156&tsv=1106&wNotes=on">chemo-sensitization</a>, <a href="tbResList.php?qv=156&tsv=1171&wNotes=on">chemoProtective</a>, <a href="tbResList.php?qv=156&tsv=1107&wNotes=on">RadioSensitizer</a>, <a href="tbResList.php?qv=156&tsv=1185&wNotes=on">RadioProtective</a>, <a href="tbResList.php?qv=156&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <a href="tbResList.php?qv=156&tsv=1105&wNotes=on">Neuroprotective</a>, <a href="tbResList.php?qv=156&tsv=557&wNotes=on">Cognitive</a>, <a href="tbResList.php?qv=156&tsv=1175&wNotes=on">Renoprotection</a>, <a href="tbResList.php?qv=156&tsv=1179&wNotes=on">Hepatoprotective</a>, <a href="tbResList.php?&qv=156&tsv=1188&wNotes=on">CardioProtective</a>, <br> <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=156&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br>
17
-
SNT
sunitinib
D
<b>Inhibitors</b> of vascular endothelial growth factor receptor (VEGFR) <br>
157
-
SuD
Sutherlandioside D
NP
<b>Extract of Sutherlandia frutescens</b> is a medicinal plant. S. frutescens commonly known as the “cancer bush” by South African healers.<br>
189
-
Tam
tamoxifen
D
<b>Tamoxifen</b> is an endocrine anti-hormone drug used to treat breast cancer and other tumours. Tamoxifen is a hormone therapy that treats or prevents hormone receptor-positive breast cancer.<br>
158
-
Tau
Taurine
NP
<b>Amino acid</b> that benefits the heart, brain and immune system.<br> <br> Taurine, an organic compound containing sulfur in its chemical structure, possesses anti-inflammatory, anti-oxidant, and various physiological functions within the cardiovascular, kidney, endocrine, and immune systems.<br> Also an LDH inhibitor<br>
224
-
TMZ
temozolomide
D
<b>Temozolomide</b> is a chemotherapeutic agent used to treat: GBM<br> Temozolomide works by interfering with DNA replication: temozolomide is a alkylating agent that adds an alkyl group to the DNA molecule, which interferes with the replication of DNA and ultimately leads to cell death.<br>
159
-
TF
Theaflavin
NP
<b>Chemical</b> in black tea formed from fermentation of green tea.<br>
160
-
Tb
Theobromine
NP
<b>Theobromine</b>, also known as xantheose, is the principal alkaloid of Theobroma cacao (cacao plant).<br>
161
-
TV
Thymol-Thymus vulgaris
NP
<b>Thyme</b>
162
-
TQ
Thymoquinone
NP
Anti-oxidant, anti-tumor
<b>Thymoquinone</b> is a bioactive compound found in the seeds of Nigella sativa, commonly known as black seed or black cumin. <br> Pathways:<br> -Cell cycle arrest, apoptosis induction, ROS generation in cancer cells<br> -inhibit the activation of NF-κB, Suppress the PI3K/Akt signaling cascade<br> -Inhibit angiogenic factors such as VEGF, MMPs<br> -Inhibit HDACs, UHRF1, and DNMTs<br> <br> -Note <a href="tbResList.php?qv=162&tsv=1109&wNotes=on&exSp=open">half-life</a> 3-6hrs.<br> <a href="tbResList.php?qv=162&tsv=792&wNotes=on&exSp=open">BioAv</a> low oral bioavailability due to its lipophilic nature. Note refridgeration of Black seed oil improves the stability of TQ.<br> DIY: ~1 part lecithin : 2–3 parts black seed oil : 4–5 parts warm water. (chat ai)<br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - usually induce <a href="tbResList.php?qv=162&tsv=275&wNotes=on">ROS</a> production in Cancer cells, and lowers ROS in normal cells<br> - ROS↑ related: <a href="tbResList.php?qv=162&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?qv=162&tsv=103&wNotes=on">ER Stress↑</a>, <!-- <a href="tbResList.php?qv=162&tsv=459&wNotes=on">UPR↑</a>, --> <a href="tbResList.php?qv=162&tsv=356&wNotes=on">GRP78↑</a>, <!-- <a href="tbResList.php?qv=162&tsv=38&wNotes=onon&word=Ca+2↑">Ca+2↑</a>, --> <a href="tbResList.php?qv=162&tsv=77&wNotes=on">Cyt‑c↑</a>, <a href="tbResList.php?qv=162&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?qv=162&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?qv=162&tsv=239&wNotes=on">cl-PARP↑</a>, <a href="tbResList.php?qv=162&wNotes=on&word=HSP">HSP↓</a>, <a href="tbResList.php?qv=162&wNotes=on&word=Prx">Prx</a>,<!-- mitochondrial antioxidant enzyme--> <br> <!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, --> - May Low AntiOxidant defense in Cancer Cells: <a href="tbResList.php?qv=162&tsv=226&wNotes=on&word=NRF2↓">NRF2↓</a>(usually contrary), <!-- <a href="tbResList.php?qv=162&word=Trx&wNotes=on">TrxR↓**</a>, --><!-- major antioxidant system --> <!-- <a href="tbResList.php?qv=162&tsv=298&wNotes=on&word=SOD↓">SOD↓</a>, --> <a href="tbResList.php?qv=162&tsv=137&wNotes=on&word=GSH↓">GSH↓</a> <!-- <a href="tbResList.php?qv=162&tsv=46&wNotes=on">Catalase↓</a> --> <a href="tbResList.php?qv=162&tsv=597&wNotes=on">HO1↓</a>(contrary), <a href="tbResList.php?qv=162&wNotes=on&word=GPx">GPx↓</a> <br> - Raises <a href="tbResList.php?qv=162&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?qv=162&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>, <a href="tbResList.php?qv=162&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?qv=162&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?qv=162&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?qv=162&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?qv=162&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?qv=162&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?qv=162&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, <a href="tbResList.php?qv=162&tsv=235&wNotes=on&word=p38↓">p38↓</a>, Pro-Inflammatory Cytokines : <a href="tbResList.php?qv=162&tsv=908&wNotes=on&word=NLRP3↓">NLRP3↓</a>, <a href="tbResList.php?qv=162&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, <a href="tbResList.php?qv=162&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?qv=162&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <a href="tbResList.php?qv=162&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a> <br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓ inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-?B and u-PA, MMP-1 and MMP-13.--> - inhibit Growth/Metastases : <a href="tbResList.php?qv=162&tsv=604&wNotes=on">TumMeta↓</a>, <a href="tbResList.php?qv=162&tsv=323&wNotes=on">TumCG↓</a>, <a href="tbResList.php?qv=162&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=162&tsv=204&wNotes=on">MMPs↓</a>, <a href="tbResList.php?qv=162&tsv=201&wNotes=on">MMP2↓</a>, <a href="tbResList.php?qv=162&tsv=203&wNotes=on">MMP9↓</a>, <!-- <a href="tbResList.php?qv=162&tsv=308&wNotes=on">TIMP2</a>, --> <!-- <a href="tbResList.php?qv=162&tsv=415&wNotes=on">IGF-1↓</a>, --> <!-- <a href="tbResList.php?qv=162&tsv=428&wNotes=on">uPA↓</a>, --> <a href="tbResList.php?qv=162&tsv=334&wNotes=on">VEGF↓</a>, <!-- <a href="tbResList.php?qv=162&tsv=1284&wNotes=on">ROCK1↓</a>, --> <a href="tbResList.php?qv=162&tsv=110&wNotes=on">FAK↓</a>, <!-- <a href="tbResList.php?qv=162&tsv=273&wNotes=on">RhoA↓</a>, --> <a href="tbResList.php?qv=162&tsv=214&wNotes=on">NF-κB↓</a>, <a href="tbResList.php?qv=162&tsv=79&wNotes=on">CXCR4↓</a>, <!-- <a href="tbResList.php?qv=162&tsv=1247&wNotes=on">SDF1↓</a>, --> <a href="tbResList.php?qv=162&tsv=304&wNotes=on">TGF-β↓</a>, <!-- <a href="tbResList.php?qv=162&tsv=719&wNotes=on">α-SMA↓</a>, --> <a href="tbResList.php?qv=162&tsv=105&wNotes=on">ERK↓</a> <!-- <a href="tbResList.php?qv=162&tsv=1178&wNotes=on">MARK4↓</a> --> <!-- contributing to tumor growth, invasion, and metastasis--> <br> <!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, --> - reactivate genes thereby inhibiting cancer cell growth : <a href="tbResList.php?qv=162&tsv=140&wNotes=on">HDAC↓</a>, <a href="tbResList.php?qv=162&wNotes=on&word=DNMT">DNMTs↓</a>, <a href="tbResList.php?qv=162&tsv=108&wNotes=on">EZH2↓</a>, <a href="tbResList.php?qv=162&tsv=236&wNotes=on">P53↑</a>, <a href="tbResList.php?qv=162&wNotes=on&word=HSP">HSP↓</a>, <a href="tbResList.php?qv=162&tsv=506&wNotes=on">Sp proteins↓</a>, <a href="tbResList.php?qv=162&wNotes=on&word=TET">TET↑</a> <br> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?qv=162&tsv=322&wNotes=on">TumCCA↑</a>, <a href="tbResList.php?qv=162&tsv=73&wNotes=on">cyclin D1↓</a>, <a href="tbResList.php?qv=162&tsv=378&wNotes=on">cyclin E↓</a>, <a href="tbResList.php?qv=162&tsv=467&wNotes=on">CDK2↓</a>, <a href="tbResList.php?qv=162&tsv=894&wNotes=on">CDK4↓</a>, <a href="tbResList.php?qv=162&tsv=895&wNotes=on">CDK6↓</a>, <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?qv=162&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?qv=162&tsv=324&wNotes=on">TumCI↓</a>, <a href="tbResList.php?qv=162&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <!-- encourages invasion, proliferation, EMT, and angiogenesis --> <a href="tbResList.php?qv=162&tsv=110&wNotes=on">FAK↓</a>, <a href="tbResList.php?qv=162&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=162&tsv=96&wNotes=on">EMT↓</a>, <!-- <a href="tbResList.php?qv=162&wNotes=on&word=TOP">TOP1↓</a>, --> <!-- <a href="tbResList.php?qv=162&tsv=657&wNotes=on">TET1</a>, --> <br> <!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS --> - inhibits <a href="tbResList.php?qv=162&tsv=129&wNotes=on">glycolysis</a> /<a href="tbResList.php?qv=162&tsv=947&wNotes=on">Warburg Effect</a> and <a href="tbResList.php?qv=162&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> : <a href="tbResList.php?qv=162&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=162&tsv=772&wNotes=on">PKM2↓</a>, <a href="tbResList.php?qv=162&tsv=35&wNotes=on">cMyc↓</a>, <a href="tbResList.php?qv=162&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>, <a href="tbResList.php?qv=162&tsv=906&wNotes=on">LDH↓</a>, <a href="tbResList.php?qv=162&tsv=175&wNotes=on&word=LDH">LDHA↓</a>, <a href="tbResList.php?qv=162&tsv=773&wNotes=on">HK2↓</a>, <!-- <a href="tbResList.php?qv=162&wNotes=on&word=PFK">PFKs↓</a>, --> <a href="tbResList.php?qv=162&wNotes=on&word=PDK">PDKs↓</a>, <!-- <a href="tbResList.php?qv=162&tsv=847&wNotes=on">ECAR↓</a>, --> <!-- <a href="tbResList.php?qv=162&tsv=230&wNotes=on">OXPHOS↓</a>, --> <a href="tbResList.php?qv=162&tsv=356&wNotes=on">GRP78↑</a>, <!-- <a href="tbResList.php?qv=162&tsv=1278&wNotes=on">Glucose↓</a>, --> <a href="tbResList.php?qv=162&tsv=623&wNotes=on">GlucoseCon↓</a> <br> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - inhibits <a href="tbResList.php?qv=162&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=162&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=162&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=162&wNotes=on&word=NOTCH">Notch↓</a>, <!-- <a href="tbResList.php?qv=162&wNotes=on&word=FGF">FGF↓</a>, --> <!-- <a href="tbResList.php?qv=162&wNotes=on&word=PDGF">PDGF↓</a>, --> <a href="tbResList.php?qv=162&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, <a href="tbResList.php?qv=162&&wNotes=on&word=ITG">Integrins↓</a>, <br> <!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, --> <!-- - inhibits Cancer Stem Cells : <a href="tbResList.php?qv=162&tsv=795&wNotes=on">CSC↓</a>, <a href="tbResList.php?qv=162&tsv=524&wNotes=on">CK2↓</a>, <a href="tbResList.php?qv=162&tsv=141&wNotes=on">Hh↓</a>, <a href="tbResList.php?qv=162&tsv=434&wNotes=on">GLi↓</a>, <a href="tbResList.php?qv=162&tsv=124&wNotes=on">GLi1↓</a>, <a href="tbResList.php?qv=162&tsv=677&wNotes=on">CD133↓</a>, <a href="tbResList.php?qv=162&tsv=655&wNotes=on">CD24↓</a>, <a href="tbResList.php?qv=162&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=162&tsv=357&wNotes=on">n-myc↓</a>, <a href="tbResList.php?qv=162&tsv=656&wNotes=on">sox2↓</a>, <a href="tbResList.php?qv=162&wNotes=on&word=NOTCH">Notch2↓</a>, <a href="tbResList.php?qv=162&tsv=1024&wNotes=on">nestin↓</a>, <a href="tbResList.php?qv=162&tsv=508&wNotes=on">OCT4↓</a>, <br> --> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=162&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=162&tsv=4&wNotes=on">AKT↓</a>, <a href="tbResList.php?qv=162&wNotes=on&word=JAK">JAK↓</a>, <a href="tbResList.php?qv=162&wNotes=on&word=STAT">STAT↓</a>, <a href="tbResList.php?qv=162&tsv=377&wNotes=on">Wnt↓</a>, <a href="tbResList.php?qv=162&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=162&tsv=9&wNotes=on">AMPK</a>, <a href="tbResList.php?qv=162&tsv=475&wNotes=on">α↓</a>, <a href="tbResList.php?qv=162&tsv=105&wNotes=on">ERK↓</a>, <!-- <a href="tbResList.php?qv=162&tsv=1014&wNotes=on">5↓</a>, --> <a href="tbResList.php?qv=162&tsv=168&wNotes=on">JNK</a>, <!-- - <a href="tbResList.php?qv=162&wNotes=on&word=SREBP">SREBP</a> (related to cholesterol). --><br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=162&tsv=1106&wNotes=on">chemo-sensitization</a>, <a href="tbResList.php?qv=162&tsv=1171&wNotes=on">chemoProtective</a>, <a href="tbResList.php?qv=162&tsv=1107&wNotes=on">RadioSensitizer</a>, <a href="tbResList.php?qv=162&tsv=1185&wNotes=on">RadioProtective</a>, <a href="tbResList.php?qv=162&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <a href="tbResList.php?qv=162&tsv=1105&wNotes=on">Neuroprotective</a>, <a href="tbResList.php?qv=162&tsv=557&wNotes=on">Cognitive</a>, <a href="tbResList.php?qv=162&tsv=1175&wNotes=on">Renoprotection</a>, <a href="tbResList.php?qv=162&tsv=1179&wNotes=on">Hepatoprotective</a>, <a href="tbResList.php?&qv=162&tsv=1188&wNotes=on">CardioProtective</a>, <br> <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=162&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br>
287
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TC
Tinospora Cordifolia
NP
<b>Tinospora cordifolia (also known as Guduchi)</b><br> <br> 1. Immunomodulatory Pathways :Enhance the activity of macrophages, natural killer (NK) cells, and T-lymphocytes.<br> 2. NF-κB Signaling Pathway: may inhibit the activation of NF-κB.<br> 3. PI3K/Akt/mTOR Pathway<br> 4. MAPK Pathways (ERK, JNK, and p38 MAPK)<br> 5. Apoptotic Pathways (Intrinsic and Extrinsic)<br> 6. Oxidative Stress and Reactive Oxygen Species (ROS) Modulation<br> - May act as an antioxidant in normal cells while paradoxically enhancing ROS production in cancer cells.<br> Elevated ROS in tumor cells can lead to oxidative damage and apoptosis, serving as an anticancer mechanism.<br>
232
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TiO2
Titanium Dioxide
NP
<b>Titanium dioxide (titanium(IV) oxide, titania, TiO2)</b> is an inorganic compound that owes its recent rise in scientific interest to photoactivity. After the illumination in aqueous media with UV light, TiO2 produces an array of reactive oxygen species (ROS). The capability to produce ROS and thus induce cell death has found application in the photodynamic therapy (PDT) for the treatment of a wide range of maladies, from psoriasis to cancer. <br> Also used as food additive<br>
185
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Tomatine
Tomatine
NA
<b>α-Tomatineis</b> a glycoalkaloid, found in the stems and leaves of tomato plants, and in the fruits at much lower concentrations.<br>
326
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TACE
Transarterial Chemoembolization
T
<b>TACE</b>, which stands for Transarterial Chemoembolization—a treatment primarily used for certain types of cancer, most notably liver cancer (hepatocellular carcinoma).<br> <br> TACE is a minimally invasive procedure that involves delivering chemotherapy directly into the artery that supplies blood to a tumor (most commonly in the liver) and then injecting substances to block (embolize) the artery. This dual action attacks the tumor by:<br> -Concentrating chemotherapy at the site of the tumor.<br> -Restricting the tumor’s blood supply, which helps to starve the cancer cells of oxygen and nutrients.<br> <br> How It Works:<br> -Catheter Insertion: A catheter is inserted through a small incision, usually in the groin, and navigated into the arterial system to reach the hepatic artery (if treating liver cancer).<br> -Chemotherapy Delivery: A concentrated dose of chemotherapy is delivered directly into the blood vessels feeding the tumor.<br> -Embolization: Embolic agents (such as gelatin sponge particles, microspheres, or other embolic materials) are then injected to block the artery, thereby limiting the tumor’s blood flow.<br>
260
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Tras
Trastuzumab
D
<b>Trastuzumab</b> is a targeted therapy used in the treatment of certain types of cancer, most notably HER2-positive breast cancer. <br> <br> It specifically targets the human epidermal growth factor receptor 2 (HER2), a protein that is overexpressed in some types of breast cancer and other cancers.<br> -Is a Her2 inhibitor used in breast cancer. <br> <br> Trastuzumab has revolutionized the treatment of HER2-positive breast cancer, significantly improving both response rates and overall survival.<br>
205
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TSA
Trichostatin A
NP
<b>Trichostatin A (TSA)</b> is a naturally occurring compound that belongs to the class of histone deacetylase inhibitors (HDACis). <br> TSA has been shown to induce apoptosis (programmed cell death) in various cancer cell lines, including leukemia, breast, and lung cancer cells.<br>
324
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Trip
triptolide
NP
<b>Triptolide</b> is a diterpenoid triepoxide primarily isolated from the traditional Chinese medicinal plant Tripterygium wilfordii Hook F (commonly known as Thunder God Vine).<br> <br> Pathways:<br> -Activation of caspases (key executioners of apoptosis)<br> -Disruption of mitochondrial membrane potential<br> -Cell Cycle Arrest<br> -Suppresses expression of c-myc and mitochondrial hexokinase II (HK-II) in cancer cells<br>
163
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Tu
Tulsi
NP
<b>Holy basil</b> or Ocimum sanctum
319
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TTT
Tumor Treating Fields
T
<b>Tumor Treating Fields (TTFields)</b> are a physical, noninvasive treatment modality that uses alternating electric fields in the intermediate frequency range (typically around 100–300 kHz) and low intensity to disrupt cancer cell division. Unlike conventional therapies that target specific molecular pathways with drugs, TTFields work by exerting physical forces on charged and polarizable cellular structures. Nevertheless, several downstream biological effects and pathways have been observed when tumor cells are exposed to TTFields.<br>
313
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Ukrain
Ukrain
NP
<b>Ukrain</b> is often said to be based on extracts from the greater celandine plant (Chelidonium majus), which has been used in traditional medicine.<br> -Although its active components are derived from a natural source, the final product is processed and standardized in a pharmaceutical setting. This means Ukrain is more accurately described as a semi-synthetic or phytochemical-based drug rather than a crude natural remedy.<br> -Celandine sap is used to treat warts and skin cancer (98% alkaloids)<br> -Chelidonine (80% of alkaloids) is most important<br> <br> -Claimed to affect cancer cells and not normal cells<br> <br> Pathways:<br> -Ukrain may induce apoptosis, MMP depolarization, cyt-c release, caspase activation.<br> -Ukrain might increase the production of reactive oxygen species in cancer cells.<br> -Cell Cycle Arrest<br> -p53 pathway<br> -(MAPK) pathways<br> -NF-κB) signaling<br> -Inhibit angiogenesis<br> <br> The researchers suggest there might be a probable relationship between liver injury and consumption of Chelidonium majus.<br> <a href="https://www.ukrain.ua/" >https://www.ukrain.ua/ </a> <br> <a href="https://www.researchgate.net/scientific-contributions/A-Liepins-40092131"> Dr. Andrejs Liepins</a><br> Memorial University of Newfoundland<br> Faculty of Medicine<br> St John's Newfoundland<br> Canada A1B 3V6<br>
304
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urea
urea
NP
<b>Urea</b> is a small, organic molecule (chemical formula: CO(NH₂)₂) that is the primary nitrogen-containing waste product in mammals. It is produced in the liver through the urea cycle, a metabolic pathway that converts toxic ammonia (a byproduct of protein metabolism) into urea, which is then excreted in urine by the kidneys.<br> <br> -Urea can act as a solubilizing agent for certain drugs, especially those that might benefit from improved solubility in aqueous environments. <br> -Presence of urea (as a carrier) increased the aqueous solubility of capsaicin by 3.6-fold compared to pure capsaicin<br> -Urea disrupts the hydrogen bonding within the water molecules which allows hydrophobic solutes to become solvated in water<br> <br> -In dermatology, urea is commonly present in creams, lotions, and ointments not only for its moisturizing effects but also for its ability to enhance the absorption of other therapeutic agents.<br>
164
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UA
Ursolic acid
NP
<b>Natural compound</b> found in apples and rosemary.<br>
303
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Vem
verapamil
D
<b>Verapamil</b> belongs to the phenylalkylamine class of compounds and is a fully synthetic molecule originally developed for its potent calcium channel–blocking properties.<br> <br> Pathways:<br> -P-glycoprotein Inhibition (MDR1). -P-gp is overexpressed in many cancer cells<br> -Inhibition of P-gp by verapamil can enhance the intracellular concentration of chemotherapeutic agents, potentially restoring drug sensitivity.<br> -As a calcium channel blocker, verapamil inhibits L-type calcium channels.<br>
165
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VitB12
Vitamin B12
NP
<b>Helps</b> make red blood cells, metabolize food and prevent nerve damage.<br>
166
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VitC
Vitamin C (Ascorbic Acid)
NP
<b>High-dose vitamin C:</b> Some studies have suggested that high-dose vitamin C may be effective in treating certain types of cancer, such as ovarian cancer and pancreatic cancer.<br> Symptoms of vitamin C deficiency include fatigue, weakness, poor wound healing, ecchymoses, xerosis, lower extremity edema, and musculoskeletal pain—most of them are often observed in end-stage cancer patients. -Vitamin C is an essential nutrient involved in the repair of tissue, the formation of collagen, and the enzymatic production of certain neurotransmitters. It is required for the functioning of several enzymes and is important for immune system function.<br> -Ascorbic Acid, Different levels in different Organs<br> Homeostasis ranging from about 0.2 mM in the muscle and heart, and up to 10 mM in the brain and adrenal gland. -(Note the Oncomagnetic success in the brain also was then under conditions of high Vitamin C)<br> <br> -Ascorbic acid is an electron donor<br> Ascorbic Acid, can be a Pro-oxidant<br> "The pro-oxidative activity of ascorbic acid (Figure 2) is associated with the interaction with transition metal ions (especially iron and copper). Under conditions of high, millimolar ascorbate concentration, vitamin C catalyzes the reduction of free transition metal ions, which causes the formation of oxygen radicals."<br> Ascorbic Acid, formation of H2O2 (Hydrogen Peroxide)<br> Many studies indicate the toxicity of ascorbate to cancer cells. Much evidence indicates that the underlying phenomenon is the pro-oxidative activity of ascorbate, which induces the formation of H2O2 and oxidative stress.<br> "ascorbate at concentrations achieved only by i.v. administration may be a pro-drug for formation of H(2)O(2)"<br> -High dose VitC therapy may not be for those with kidney problems<br> -Oral supplement up to 10g/day?<br> -Direct regulator of <a href="tbResList.php?qv=166&wNotes=on&word=TET">TET↑</a><br> -caution for (G6PD-) deficient patients receiving vitamin C infusions <br> <br> -Note plasma <a href="tbResList.php?qv=166&tsv=1109&wNotes=on&exSp=open">half-life</a> 30mins to 1hr, 1.5-2hr elimination half-life.<br> oral <a href="tbResList.php?qv=166&tsv=792&wNotes=on&exSp=open">BioAv</a> water soluble, but has limitiations as 100mg yeilds 60uM/L in plasma, but 1000mg only yeilds 85uM/L. mM concentration are required for effectiveness on cancer cells. Hence why IV administration is common. Boosting <a href="https://nestronics.ca/dbx/tbResEdit.php?rid=3138">HIF</a> increases the intracellular uptake of oxidized VitC <br> Pathways:<br> <!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑--> - high dose induces <a href="tbResList.php?qv=166&tsv=275&wNotes=on">ROS</a> production in cancer cells. Otherwise well known antioxidant in normal cells.<br> - ROS↑ related: <a href="tbResList.php?qv=166&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm), <a href="tbResList.php?qv=166&tsv=103&wNotes=on">ER Stress↑</a>, <!-- <a href="tbResList.php?qv=166&tsv=459&wNotes=on">UPR↑</a>, --> <!-- <a href="tbResList.php?qv=166&tsv=356&wNotes=on">GRP78↑</a>, --> <!-- <a href="tbResList.php?qv=166&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>, --> <!-- <a href="tbResList.php?qv=166&tsv=77&wNotes=on">Cyt‑c↑</a>, --> <a href="tbResList.php?qv=166&wNotes=on&word=Casp">Caspases↑</a>, <a href="tbResList.php?qv=166&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>, <a href="tbResList.php?qv=166&tsv=239&wNotes=on">cl-PARP↑</a>, <!-- <a href="tbResList.php?qv=166&wNotes=on&word=HSP">HSP↓</a>, --> <!-- <a href="tbResList.php?qv=166&wNotes=on&word=Prx">Prx</a>, --><!-- mitochondrial antioxidant enzyme--> <br> <!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, --> - Lowers AntiOxidant defense in Cancer Cells: <a href="tbResList.php?qv=166&tsv=226&wNotes=on&word=NRF2↓">NRF2↓</a>, <a href="tbResList.php?qv=166&word=Trx&wNotes=on">TrxR↓**</a>,<!-- major antioxidant system --> <a href="tbResList.php?qv=166&tsv=298&wNotes=on&word=SOD↓">SOD↓</a>, <a href="tbResList.php?qv=166&tsv=137&wNotes=on&word=GSH↓">GSH↓</a> <a href="tbResList.php?qv=166&tsv=46&wNotes=on">Catalase↓</a> <a href="tbResList.php?qv=166&tsv=597&wNotes=on">HO1↓</a> <a href="tbResList.php?qv=166&wNotes=on&word=GPx">GPx↓</a> <br> - Raises <a href="tbResList.php?qv=166&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a> defense in Normal Cells: <a href="tbResList.php?qv=166&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>, <a href="tbResList.php?qv=166&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>, <a href="tbResList.php?qv=166&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>, <a href="tbResList.php?qv=166&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>, <a href="tbResList.php?qv=166&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>, <br> <!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, --> - lowers <a href="tbResList.php?qv=166&tsv=953&wNotes=on&word=Inflam">Inflammation</a> : <a href="tbResList.php?qv=166&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>, <a href="tbResList.php?qv=166&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>, <a href="tbResList.php?qv=166&tsv=235&wNotes=on&word=p38↓">p38↓</a>, Pro-Inflammatory Cytokines : <a href="tbResList.php?qv=166&tsv=908&wNotes=on&word=NLRP3↓">NLRP3↓</a>, <a href="tbResList.php?qv=166&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, <a href="tbResList.php?qv=166&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <a href="tbResList.php?qv=166&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>, <a href="tbResList.php?qv=166&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a> <br> <!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓ inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.--> - inhibit Growth/Metastases : <a href="tbResList.php?qv=166&tsv=604&wNotes=on">TumMeta↓</a>, <a href="tbResList.php?qv=166&tsv=323&wNotes=on">TumCG↓</a>, <a href="tbResList.php?qv=166&tsv=96&wNotes=on">EMT↓</a>, <a href="tbResList.php?qv=166&tsv=204&wNotes=on">MMPs↓</a>, <a href="tbResList.php?qv=166&tsv=201&wNotes=on">MMP2↓</a>, <a href="tbResList.php?qv=166&tsv=203&wNotes=on">MMP9↓</a>, <a href="tbResList.php?qv=166&tsv=308&wNotes=on">TIMP2</a>, <a href="tbResList.php?qv=166&tsv=415&wNotes=on">IGF-1↓</a>, <!-- <a href="tbResList.php?qv=166&tsv=428&wNotes=on">uPA↓</a>, --> <a href="tbResList.php?qv=166&tsv=334&wNotes=on">VEGF↓</a>, <!-- <a href="tbResList.php?qv=166&tsv=1284&wNotes=on">ROCK1↓</a>, --> <!-- <a href="tbResList.php?qv=166&tsv=110&wNotes=on">FAK↓</a>, --> <!-- <a href="tbResList.php?qv=166&tsv=273&wNotes=on">RhoA↓</a>, --> <a href="tbResList.php?qv=166&tsv=214&wNotes=on">NF-κB↓</a>, <!-- <a href="tbResList.php?qv=166&tsv=79&wNotes=on">CXCR4↓</a>, --> <!-- <a href="tbResList.php?qv=166&tsv=1247&wNotes=on">SDF1↓</a>, --> <!-- <a href="tbResList.php?qv=166&tsv=304&wNotes=on">TGF-β↓</a>, --> <!-- <a href="tbResList.php?qv=166&tsv=719&wNotes=on">α-SMA↓</a>, --> <!-- <a href="tbResList.php?qv=166&tsv=105&wNotes=on">ERK↓</a> --> <!-- <a href="tbResList.php?qv=166&tsv=1178&wNotes=on">MARK4↓</a> --> <!-- contributing to tumor growth, invasion, and metastasis--> <br> <!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, --> - reactivate genes thereby inhibiting cancer cell growth : <!-- <a href="tbResList.php?qv=166&tsv=140&wNotes=on">HDAC↓</a>, --> <!-- <a href="tbResList.php?qv=166&tsv=85&wNotes=on">DNMT1↓</a>, --> <!-- <a href="tbResList.php?qv=166&tsv=86&wNotes=on">DNMT3A↓</a>, --> <!-- <a href="tbResList.php?qv=166&tsv=108&wNotes=on">EZH2↓</a>, --> <a href="tbResList.php?qv=166&tsv=236&wNotes=on">P53↑</a>, <!-- <a href="tbResList.php?qv=166&wNotes=on&word=HSP">HSP↓</a>, --> <!-- <a href="tbResList.php?qv=166&tsv=506&wNotes=on">Sp proteins↓</a>, --> <a href="tbResList.php?qv=166&wNotes=on&word=TET">TET↑</a> <br> <!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ --> - cause Cell cycle arrest : <a href="tbResList.php?qv=166&tsv=322&wNotes=on">TumCCA↑</a>, <a href="tbResList.php?qv=166&tsv=73&wNotes=on">cyclin D1↓</a>, <!-- <a href="tbResList.php?qv=166&tsv=378&wNotes=on">cyclin E↓</a>, --> <a href="tbResList.php?qv=166&tsv=467&wNotes=on">CDK2↓</a>, <!-- <a href="tbResList.php?qv=166&tsv=894&wNotes=on">CDK4↓</a>, --> <!-- <a href="tbResList.php?qv=166&tsv=895&wNotes=on">CDK6↓</a>, --> <br> <!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, --> - inhibits Migration/Invasion : <a href="tbResList.php?qv=166&tsv=326&wNotes=on">TumCMig↓</a>, <a href="tbResList.php?qv=166&tsv=324&wNotes=on">TumCI↓</a>, <a href="tbResList.php?qv=166&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <!-- encourages invasion, proliferation, EMT, and angiogenesis --> <!-- <a href="tbResList.php?qv=166&tsv=110&wNotes=on">FAK↓</a>, --> <a href="tbResList.php?qv=166&tsv=105&wNotes=on">ERK↓</a>, <a href="tbResList.php?qv=166&tsv=96&wNotes=on">EMT↓</a>, <!-- <a href="tbResList.php?qv=166&tsv=1117&wNotes=on">TOP1↓</a>, --> <a href="tbResList.php?qv=166&tsv=657&wNotes=on">TET1↓</a>, <br> <!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS --> - inhibits <a href="tbResList.php?qv=166&tsv=129&wNotes=on">glycolysis</a> /<a href="tbResList.php?qv=166&tsv=947&wNotes=on">Warburg Effect</a> and <a href="tbResList.php?qv=166&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> : <a href="tbResList.php?qv=166&tsv=143&wNotes=on">HIF-1α↓</a>, <a href="tbResList.php?qv=166&tsv=772&wNotes=on">PKM2↓</a>, <a href="tbResList.php?qv=166&tsv=35&wNotes=on">cMyc↓</a>, <a href="tbResList.php?qv=166&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>, <a href="tbResList.php?qv=166&tsv=906&wNotes=on">LDH↓</a>, <a href="tbResList.php?qv=166&tsv=175&wNotes=on&word=LDH">LDHA↓</a>, <a href="tbResList.php?qv=166&tsv=773&wNotes=on">HK2↓</a>, <a href="tbResList.php?qv=166&wNotes=on&word=PFK">PFKs↓</a>, <a href="tbResList.php?qv=166&wNotes=on&word=PDK">PDKs↓</a>, <a href="tbResList.php?qv=166&tsv=847&wNotes=on">ECAR↓</a>, <!-- <a href="tbResList.php?qv=166&tsv=230&wNotes=on">OXPHOS↓</a>, --> <a href="tbResList.php?qv=166&tsv=356&wNotes=on">GRP78↑</a>, <a href="tbResList.php?qv=166&tsv=1278&wNotes=on">Glucose↓</a>, <a href="tbResList.php?qv=166&tsv=623&wNotes=on">GlucoseCon↓</a> <br> <!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)--> - inhibits <a href="tbResList.php?qv=166&tsv=447&wNotes=on">angiogenesis↓</a> : <a href="tbResList.php?qv=166&tsv=334&wNotes=on">VEGF↓</a>, <a href="tbResList.php?qv=166&tsv=143&wNotes=on">HIF-1α↓</a>, <!-- <a href="tbResList.php?qv=166&wNotes=on&word=NOTCH">Notch↓</a>, --> <!-- <a href="tbResList.php?qv=166&wNotes=on&word=FGF">FGF↓</a>, --> <!-- <a href="tbResList.php?qv=166&wNotes=on&word=PDGF">PDGF↓</a>, --> <!-- <a href="tbResList.php?qv=166&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>, --> <!-- <a href="tbResList.php?qv=166&&wNotes=on&word=ITG">Integrins↓</a>, --> <br> <!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, --> <!-- - inhibits Cancer Stem Cells : <a href="tbResList.php?qv=166&tsv=795&wNotes=on">CSC↓</a>, <a href="tbResList.php?qv=166&tsv=524&wNotes=on">CK2↓</a>, <a href="tbResList.php?qv=166&tsv=141&wNotes=on">Hh↓</a>, <a href="tbResList.php?qv=166&tsv=434&wNotes=on">GLi↓</a>, <a href="tbResList.php?qv=166&tsv=124&wNotes=on">GLi1↓</a>, <a href="tbResList.php?qv=166&tsv=677&wNotes=on">CD133↓</a>, <a href="tbResList.php?qv=166&tsv=655&wNotes=on">CD24↓</a>, <a href="tbResList.php?qv=166&tsv=342&wNotes=on">β-catenin↓</a>, <a href="tbResList.php?qv=166&tsv=357&wNotes=on">n-myc↓</a>, <a href="tbResList.php?qv=166&tsv=656&wNotes=on">sox2↓</a>, <a href="tbResList.php?qv=166&tsv=222&wNotes=on">notch2↓</a>, <a href="tbResList.php?qv=166&tsv=1024&wNotes=on">nestin↓</a>, <a href="tbResList.php?qv=166&tsv=508&wNotes=on">OCT4↓</a>, <br> --> <!-- OTHERS : --> - Others: <a href="tbResList.php?qv=166&tsv=252&wNotes=on">PI3K↓</a>, <a href="tbResList.php?qv=166&tsv=4&wNotes=on">AKT↓</a>, <!-- <a href="tbResList.php?qv=166&wNotes=on&word=JAK">JAK↓</a>, --> <a href="tbResList.php?qv=166&wNotes=on&word=STAT">STAT↓</a>, <!-- <a href="tbResList.php?qv=166&tsv=377&wNotes=on">Wnt↓</a>, --> <!-- <a href="tbResList.php?qv=166&tsv=342&wNotes=on">β-catenin↓</a>, --> <a href="tbResList.php?qv=166&tsv=9&wNotes=on">AMPK</a>, <!-- <a href="tbResList.php?qv=166&tsv=475&wNotes=on">α↓</a>, --> <a href="tbResList.php?qv=166&tsv=105&wNotes=on">ERK↓</a>, <!-- <a href="tbResList.php?qv=166&tsv=1014&wNotes=on">5↓</a>, --> <a href="tbResList.php?qv=166&tsv=168&wNotes=on">JNK</a>, <br> <!-- SYNERGIES : --> - Synergies: <a href="tbResList.php?qv=166&tsv=1106&wNotes=on">chemo-sensitization</a>, <a href="tbResList.php?qv=166&tsv=1171&wNotes=on">chemoProtective</a>, <a href="tbResList.php?qv=166&tsv=1107&wNotes=on">RadioSensitizer</a>, <a href="tbResList.php?qv=166&tsv=1185&wNotes=on">RadioProtective</a>, <a href="tbResList.php?qv=166&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>, <a href="tbResList.php?qv=166&tsv=1105&wNotes=on">Neuroprotective</a>, <a href="tbResList.php?qv=166&tsv=557&wNotes=on">Cognitive</a>, <!-- <a href="tbResList.php?qv=166&tsv=1175&wNotes=on">Renoprotection</a>, --> <a href="tbResList.php?qv=166&tsv=1179&wNotes=on">Hepatoprotective</a>, <!-- <a href="tbResList.php?&qv=166&tsv=1188&wNotes=on">CardioProtective</a>, --> <br> <br> <!-- SELECTIVE: --> - Selectivity: <a href="tbResList.php?qv=166&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a> <br>
167
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VitD3
Vitamin D3
NP
Promote calcium and phosphorus absorption
<b>- Major VITAL study</b> stated Vit D did not reduce invasive cancer, but Secondary Analysis stated reduces the incidence of metastatic cancer at diagnosis.<br> - Amount needed may depend on your BMI.<br> - Vitamin D deficiency, as determined by serum 25(OH)D concentrations of less than 30 ng/mL,<br> - Target achieving 80 ng/mL<br> - Reduces oxidative stress (ROS)<br> - Nrf2 plays a key role in protecting cells against oxidative stress; this is modulated by vitamin D<br> - Vit D supplementation may not be compatible with pro-oxidant therapy?<br> <br> The minimal level is considered to be 30 ng/mL (50 nmol/L).<br> - One recommendation is to get your level up to around 125 ng/ml<br> - Chemo depletes Vitamin D levels so 10,000 IUs daily? – ask your doctor first.<br> <br> After correction of vitamin D deficiency through loading doses of oral vitamin D (or safe sun exposure), adequate maintenance doses of vitamin D3 are needed. This can be achieved in approximately 90% of the adult population <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC6627346/" >with vitamin D supplementation between 1000 to 4000 IU/day,</a> 10,000 IU twice a week, or 50,000 IU twice a month [10,125]. On a population basis, such doses would allow approximately 97% of people to maintain their serum 25(OH)D concentrations above 30 ng/mL [19,126]. Others, such as persons with obesity, those with gastrointestinal disorders, and during pregnancy and lactation, are likely to require doses of 6,000 IU/day.<br> <br> Vitamin D, particularly its active form 1,25-dihydroxyvitamin D (calcitriol), exerts multiple biological effects that may influence cancer development and progression. <br> Calcitriol has been reported to induce cell cycle arrest (often at the G0/G1 phase) and promote pro-apoptotic mechanisms in various cancer cell types.<br> <br> Inhibition of Angiogenesis:<br> Some studies indicate that vitamin D can reduce the expression of pro-angiogenic factors, thereby potentially limiting the blood supply to tumors, which is necessary for tumor growth and metastasis.<br> <br> Effects on the Wnt/β-catenin Pathway:<br> The Wnt/β-catenin signaling pathway, often dysregulated in several cancers (for example, colorectal cancer), may be modulated by vitamin D.<br> Calcitriol has been shown in some models to inhibit β-catenin signaling, which is associated with decreased cell proliferation and tumor progression.<br> Vitamin D may interact with other signaling pathways, including the PI3K/AKT/mTOR pathway, which is involved in cell survival and proliferation.<br>
307
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VitE
Vitamin E
NP
<b>Vitamin E</b> is a fat‐soluble antioxidant<br> It primarily comprises two families:<br> Tocopherols<br> α-Tocopherol (most active and abundant form found in human tissues)<br> β-Tocopherol<br> γ-Tocopherol <br> δ-Tocopherol<br> Tocotrienols<br> α-Tocotrienol<br> β-Tocotrienol<br> <a href="tbResList.php?qv=321&exTr=open">γ-Tocotrienol</a> <br> δ-Tocotrienol<br> <br> <br> -Vitamin E can neutralize free radicals, which are reactive molecules that may damage cells and potentially contribute to cancer development. This antioxidant property has led researchers to explore whether vitamin E could help protect cells from damage during cancer treatment.<br> -Cancer Prevention: Some epidemiological studies suggested that higher intake of vitamin E (usually through diet rather than supplements) might be associated with a lower risk of certain cancers. <br>
168
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VitK2
Vitamin K2
NP
<b>Vitamin K2 (menaquinone) </b><br> Menaquinone-4 (MK-4), a subtype of vitamin K2 Helps blood clot, calcium metabolise and heart health.<br> Bone health: Vitamin K2 helps to regulate calcium levels in the body, which can help to prevent conditions such as osteoporosis and fractures.<br> Vitamin K2 has been studied for its potential role in cancer prevention and treatment. Some of the key findings include:<br> -Shown to inhibit the growth of cancer cells, including those found in leukemia, lung cancer, and prostate cancer.<br> -Shown to induce apoptosis (cell death) in cancer cells, which can help to prevent the spread of cancer.<br> -Shown to have anti-angiogenic effects, which means it can help to prevent the formation of new blood vessels that feed cancer cells.<br> -Synergistic effects with other nutrients, such as vitamin D and calcium, to enhance its anti-cancer effects.<br> <br> Vitamin K2 exists in several forms known as menaquinones, with MK-4 and MK-7 being the most studied. MK-4 is often used in Japan for therapeutic purposes, whereas MK-7 (derived from bacterial fermentation) is widely available as a supplement in Western countries.<br> For bone and cardiovascular health—and by extension, exploring potential anticancer benefits—doses for MK-7 commonly range from 90 to 200 micrograms per day.<br> <!-- <a href="tbProdEdit.php?pid=168">VitK2 link</a><br> -->
264
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VitB1/Thiamine
VitB1/Thiamine
NP
<b>VitB1/Thiamine</b><br>
230
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VitK3
VitK3,menadione
D
<b>Menadione</b> (2-methyl-1,4-naphthoquinone, also termed vitamin K3)<br> Menadione-induced ROS generation is concentration-dependent and high concentrations trigger cell death.<br> Clinical trials conducted on patients with prostate cancer showed that ascorbic acid-menadione produced an immediate drop in tumor cell numbers through a mechanism named autoschizis.<br>
305
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SAHA
Vorinostat
D
<b>Suberoylanilide hydroxamic acid (SAHA)</b> (Vorinostat) is a synthetic compound. It was designed and developed as a small-molecule inhibitor targeting HDAC enzymes.<br> <br> -Anticancer effects primarily through the inhibition of histone deacetylases (HDACs).<br> -Reactivation of tumor suppressor genes.<br> -Cell cycle arrest via upregulation of inhibitors like p21.<br>
176
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WBV
Whole Body Vibration
T
Therapy
<b>Whole Body Vibration</b><br>
314
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Wog
Wogonin
NP
<b>Wogonin</b> is a naturally occurring flavonoid typically isolated from Scutellaria baicalensis and has been the focus of cancer research due to its potential anticancer properties. <br> <br> Pathways:<br> -PI3K/Akt Pathway Inhibition<br> -NF-κB Pathway Suppression<br> -MAPK Pathway Modulation (ERK, JNK, and p38)<br> -STAT3 Signaling Inhibition:<br> -Reactive Oxygen Species (ROS) Generation<br> -Decreases in HKII, PDK1, and LDHA expression<br> -Suppression of lactate generation, and reduced glucose uptake<br>
318
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Wor
Worenine
NP
<b>Worenine</b> - Coptis Chinensis (Huanglian in Chinese), a famous traditional herbal medicine used for clearing heat and detoxification.<br> Worenine is classified as a plant-derived alkaloid.<br> <br> -Worenine may exert anti-inflammatory and antioxidant effects.<br> -Production of lactic acid and the uptake and consumption of glucose is significantly inhibited.<br> -The protein and mRNA levels of GLUT3, HK2, PFK-L, PKM2, and LDHA in HCT116 cells are reduced.<br>
202
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wortm
wortmannin
NP
<b>Wortmannin</b> is a naturally occurring compound that is known for its inhibitory effects on certain enzymes, particularly phosphatidylinositol 3-kinase (PI3K). It is a fungal metabolite that was first isolated from the fungus Penicillium wortmanni.<br> Widely used in research as a tool to study the PI3K signaling pathway.<br> -known as AKT inhibitor<br> <br> Wortmannin is a potent, naturally derived compound best known for its role as an inhibitor of phosphoinositide 3-kinases (PI3Ks). Unlike vitamins such as vitamin D or vitamin K2, wortmannin is not used as a nutritional supplement or therapeutic agent in the typical clinical setting.<br> <br> - In cell culture studies, wortmannin is commonly used at concentrations in the low nanomolar range (e.g., 10–100 nM) to inhibit PI3K activity.<br> <br> - In animal models, the dosing regimen can vary widely depending on the species, route of administration, and study design. Typical experimental doses may range from 0.1 to 1.0 mg/kg, but these studies are primarily investigative and not directed toward therapeutic dosing in humans.<br>
298
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Xyl
Xylitol
NP
<b>Xylitol</b> is a naturally occurring sugar alcohol commonly found in many fruits and vegetables and is often used as a low-calorie sweetener. While xylitol is best known for its dental health benefits and as a sugar substitute, there is emerging interest in its potential roles in cancer-related research.<br> <br> -Xylitol may exert antioxidant effects that help reduce oxidative stress.<br> -Xylitol is well known for its effects on oral bacteria. Since the microbiome can play a role in modulating systemic inflammation and even cancer risk, xylitol’s ability to alter microbial composition might have indirect implications for cancer risk or progression.<br>
169
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Zeo
Zeolite
NP
<b>Zeolite</b> is a mineral that can detox heavy metals, bacteria, and other toxins from the body.<br> <br> Manufacturers sometimes recommend amounts in the range of 500 mg to 2 g per day, but these are not based on standardized clinical trials for cancer treatment or prevention.<br> <br> Zeolites have been used for their absorptive properties or as carriers in drug delivery systems; however, there is no established “therapeutic dose” for cancer.<br> <br> Zeolites have a porous structure that can adsorb various molecules, including toxins, heavy metals, and possibly some free radicals.<br> <br> It has been hypothesized that by binding and removing potential carcinogens or inflammatory mediators from the gastrointestinal tract, zeolite may reduce systemic inflammation or oxidative stress that contribute to cancer development.<br> <br> There are suggestions that zeolite, by absorbing reactive oxygen species or metal ions that catalyze oxidative stress, could indirectly contribute to reduced cellular damage—a factor in cancer initiation and progression.<br>
170
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Z
Zinc
NP
<b>Zinc</b> is an essential mineral that supports immune function, wound healing, skin health, and more.<br> <br> Zinc is an essential cofactor for many enzymes, including superoxide dismutase (SOD), which scavenges free radicals and limits oxidative stress—a known contributor to DNA damage and cancer initiation.<br> <br> Maintaining adequate zinc status (typically, serum concentrations within a normal reference range of roughly 70–120 µg/dL) is important for overall health, while both deficiency and excessive intake may have implications for cancer risk.<br> <br> Some zinc-dependent enzymes, such as histone deacetylases (HDACs) or components of chromatin remodeling complexes, rely on zinc for their function.<br> <br> Zinc can modulate several intracellular signaling cascades. For example, zinc ions may affect the activity of protein kinases and phosphatases.<br> <br> Evidence suggests that alterations in zinc levels can impact growth factor signaling pathways, which are vital in controlling cell growth and survival and are often dysregulated in cancer.<br> <br> Zinc is involved in the regulation of cell cycle progression and apoptosis (programmed cell death). It can modulate the activity of several transcription factors (e.g., p53) that regulate growth arrest and apoptosis in response to cellular stress.<br>
231
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ZO
Zinc Oxide
NP
<b>Zinc oxide</b> nanoparticles have become one of the most popular metal oxide nanoparticles and recently emerged as a promising potential candidate in the fields of optical, electrical, food packaging, and biomedical applications due to their biocompatibility, low toxicity, and low cost. They have a role in cell apoptosis, as they trigger excessive reactive oxygen species (ROS) formation and release zinc ions (Zn2+) that induce cell death.<br> <br> ZnO nanoparticles have been shown to generate reactive oxygen species (ROS) in certain settings. Elevated ROS levels can induce oxidative stress, leading to cellular damage and apoptosis. Experimental data suggest that exposure to ZnO nanoparticles can trigger apoptosis (programmed cell death) via mitochondrial pathways or caspase activation in some cancer cell lines.<br> <br> Additional reports indicate that ZnO may cause cell cycle arrest in specific phases, contributing to its antiproliferative effects.<br> Studies have shown that ZnO nanoparticles can modulate various signaling pathways related to cellular stress and survival, including MAPK, NF-κB, and PI3K/AKT pathways.<br>
320
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β‐Ele
β‐Elemene
NP
<b>β‐Elemene</b> is a naturally occurring sesquiterpene that has garnered interest for its potential anticancer properties. It is primarily isolated from plants in the Curcuma genus (such as Curcuma wenyujin), which are traditionally used in Chinese medicine.<br>
321
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γ-Toc
γ-Tocotrienol
NP
<b>γ‐Tocotrienol</b> is one of the tocotrienol isomers in the vitamin E family.<br> γ‐Tocotrienol is naturally found in certain plant oils.<br> <br> – Notable sources include palm oil, rice bran oil, barley, and annatto.<br> – Among these, annatto oil is often highlighted as a particularly rich source of tocotrienols (with γ‐tocotrienol being one of the major components).<br> <br> • Relationship within the Vitamin E Family<br> – Tocotrienols, including the γ isomer, are one of the two classes of vitamin E compounds (the other being tocopherols).<br> <br> Pathways:<br> -Inhibition of NF‑κB Signaling<br> -downregulate the PI3K/Akt signaling cascade<br> -inhibit STAT3 activation<br> -Cell Cycle Arrest<br> -Antioxidant and Anti‑Inflammatory Effects(reduce reactive oxygen species (ROS) levels)<br> -may reduce angiogenic factors such as vascular endothelial growth factor (VEGF)<br> <br> <a href="https://nowfoods.ca/product/gamma-e-complex-tocopherols-tocotrienols/">Gamma E Complex (Tocopherols/Tocotrienols) example source</a><br> <br>
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