Half-Life Cancer Research Results
Half-Life, Half-Life: Click to Expand ⟱
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For many drugs, the half-life is the time it takes for half of the drug’s active substance to be eliminated from the bloodstream.
In medicine, knowing a drug’s half-life helps in designing treatment regimens that reduce adverse effects.
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Scientific Papers found: Click to Expand⟱
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*cardioP↑, Epidemiological studies associate regular, moderate intake of blueberries and/or anthocyanins with reduced risk of cardiovascular disease, death, and type 2 diabetes, and with improved weight maintenance and neuroprotection.
*neuroP↑,
*Inflam↓, Among the more important healthful aspects of blueberries are their anti-inflammatory and antioxidant actions and their beneficial effects on vascular and glucoregulatory function
*antiOx↓,
*GutMicro↑, Blueberry phytochemicals may affect gastrointestinal microflora and contribute to host health
*Half-Life↑, However, >50% of the 13C still remained in the body after 48 h
*LDL↓, controlled study of 58 diabetic patients, blueberry intake led to a decline in LDL cholesterol, triglycerides, and adiponectin and an increase in HDL cholesterol
*adiP↓,
*HDL↑,
*CRP↓, reduction was documented in inflammatory markers, including serum high-sensitivity C-reactive protein, soluble vascular adhesion molecule-1, and plasma IL-1β
*IL1β↓,
*Risk↓, lower Parkinson disease risk was associated with the highest quintile of anthocyanin (RR: 0.76) and berry (RR: 0.77) intake
*Risk↓, Nurse's Health Study, greater intake of blueberries and strawberries was associated with slower rates of cognitive decline in older adults, with an estimated delay in decline of about 2.5 y
*cognitive↑, Cognitive performance in elderly adults improved after 12 wk of daily intake of blueberry (94) or Concord grape (95) juice.
*memory↑, Better task switching and reduced interference in memory was found in healthy older adults after 90 d of blueberry supplementation
*other↑, After 12 wk of blueberry consumption, greater brain activity was detected using magnetic resonance imaging in healthy older adults during a cognitive challenge.
*BOLD↑, Similarly, during a memory test, regional blood oxygen level-dependent activity detected by MRI (99) was enhanced in the subjects taking blueberry, but not in those taking placebo.
*NO↓, 50–200 mg/d bilberry showed a dose-dependent decrease in neurotoxic NO and malondialdehyde, combined with an increase in neuroprotective antioxidant capacity due to glutathione, vitamin C, superoxide dismutase, and glutathione peroxidase
*MDA↓,
*GSH↑,
*VitC↑,
*SOD↑,
*GPx↑,
*eff↓, The percentage loss of blueberry anthocyanins during −18°C storage was 12% after 10 mo of storage
*eff↓, Freeze-dried blueberry powder loses anthocyanins in a temperature-dependent manner with a half-life of 139, 39, and 12 d when stored at 25, 42, and 60°C, respectively
*eff↓, Blueberries are low in ascorbic acid and high in anthocyanins (187), and notably anthocyanins are readily degraded by ascorbic acid
*eff↝, Shelf-stable blueberry products like jam (196), juice (197), and extracts (198) can lose polyphenolic compounds when stored at ambient temperature whereas refrigeration mitigates losses.
*Risk↓, It can be safely stated that daily moderate intake (50 mg anthocyanins, one-third cup of blueberries) can mitigate the risk of diseases and conditions of major socioeconomic importance in the Western world.
eff↑, Synergistic effect of pantethine on auranofin
Half-Life↑, The gold ions can be maintained for a relatively long period in the blood (plasma half-lives of auranofin gold of 1.8 days in rats, 19.5 days in dogs, and 17 days in humans)37,71,72.
*BioAv↝, intramuscularly administered gold is greater than 95% bioavailable, whereas only 20 to 30% of an orally administered dose of auranofin is absorbed.
*Dose↝, 50mg intramuscular injection of GST, serum gold concentrations rise sharply, peaking between 4 and 8 mg/L in approximately 2 hours and declining to an average of 3 mg/L by 7 days.
*Half-Life↑, Both compounds are retained within the body for prolonged periods.
*BioAv↝, In human subjects, parenterally administered gold is widely distributed among bodily tissues, showing a predilection for tissues of the reticuloendothelial system as well as the kidney and adrenal cortex.
*other↝, auranofin but animal studies have shown comparatively less affinity for the liver, kidney and spleen.
TrxR↓, mechanism of action of auranofin was correlated with thioredoxin reductase inhibition,
other↝, but other modes of action such as interference with mitochondrial protein import and NADH kinase were also described and discussed
IL6↑, Conversely, auranofin stimulated IL-6 and IL-8 secretion in monocytes,
IL8↑,
NK cell⇅, NK activation was only observed at low doses of auranofin, while high doses inhibited NK activity
COX2↓, suppression of pro-inflammatory factors such as COX-2 (cyclooxygenase-2), NOS (nitric oxide synthase), NF-κB (nuclear factor-κB), and TrxR, as well as on the activation of peroxyredoxin-1 and Nrf2 (nuclear factor erythroid 2-related factor 2) [19].
NOS2↓,
NRF2↑,
Prx↑,
Half-Life↑, plasma half-lives of 15–25 days [24]
Dose↝, To avoid frequently occurring diarrhea, oral doses of 3–6 mg per day, or below, should also be considered when repurposing auranofin for the treatment of other human diseases.
ROS↑, Imbalances in this system lead to the accumulation of cytotoxic ROS.
NF-kB↓, Auranofin can bind to IKK, which ultimately leads to NF-κB inhibition
BioAv↓, BA is greatly hindered by its poor water solubility, low bioavailability, and off-target toxicity
toxicity↝,
BioAv↑, nanoparticles, liposomes, micelles, and nanofibers, aiming to improve its solubility and bioavailability, prolong plasma half-life, and enhance targeting ability, thereby augmenting its anti-cancer efficacy
Half-Life↑,
BioAv↓, Despite the pharmacological activity of BA, it has been associated with some drawbacks, such as poor aqueous solubility and short half-life in vivo, which limit therapeutic application.
Half-Life↓,
BioAv↑, enhancing BA's aqueous solubility, half-life, and efficacy by using nanoscale drug delivery systems.
Half-Life↑,
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Dose↝, Bevacizumab is a clear, colorless solution administered i.v. [2, 3] in combination with chemotherapy in doses of 5, 7.5, 10, or 15 mg/kg
other↑, promising results are being achieved in patients with chronic diffuse diabetic macular edema and age-related macular degeneration (AMD), for which bevacizumab is being injected intravitreally at a dose of 1.25 mg [
VEGF↓, Bevacizumab acts by selectively binding circulating VEGF, thereby inhibiting the binding of VEGF to its cell surface receptors.
eff↑, These effects also lower tissue interstitial pressure, increase vascular permeability, may increase delivery of chemotherapeutic agents, and favor apoptosis of tumor endothelial cells
Half-Life↑, estimated half-life was 19.9 days (range, 11–50 days) and the predicted time to reach steady-state was approximately 100 days
Dose↝, Bicalutamide is a nonsteroidal pure antiandrogen given at a dosage of 150 mg once daily as monotherapy for the treatment of early (localised or locally advanced) nonmetastatic prostate cancer.
BioAv↑, Bicalutamide is slowly and saturably absorbed, but absorption is unaffected by food.
Half-Life↑, It has a long plasma elimination half-life (1 week) and accumulates about 10-fold in plasma during daily administration.
CYP3A4↓, In vitro data suggest that (R)-bicalutamide has the potential to inhibit CYP3A4 and, to a lesser extent, CYP2C9, 2C19 and 2D6.
PSA↓, Bicalutamide produces a dose-related decrease in prostate-specific antigen (PSA) at dosages < or = 150 mg/day.
*Half-Life↑, half-life of circulating boron after dietary intake is about 21 h [7]
*VitD↑, hypothesized that boron supplementation increases the biological half-live and bioavailability of vitamin D [4].
*cardioP↑, cardio-metabolic correlates of plasma boron concentrations, these cardio-protective benefits might be (at least partially) mediated by boron.
*RenoP↓, higher concentrations of boron within the body in individuals with slightly reduced kidney function, than pointing towards a direct detrimental effect of boron on renal function.
*Half-Life↑, The half-life of boric acid in humans is on the order of 1 day. They also infused 600 mg of
boric acid into seven human subjects and calculated a mean half-life of 21 hr.
*other↑, Bone contained the highest level of boron of any tissue. After only 1 day on the
diet, the boron content of bone increased
20-fold.
NP/CIPN↓, For example, the 8% patch is currently used in the treatment of localized neuropathic conditions, such as postherpetic neuralgia (PHN).
BioAv↑, Because capsaicin is not water-soluble, alcohols and other organic solvents are used to solubilize capsaicin in topical preparations and sprays.
Half-Life↑, Capsaicin levels declined very rapidly, with a mean population elimination half-life of 1.64 h.
TRPV1↑, Rapid desensitization first involves capsaicin binding of TRPV1
Pain↓, hese studies suggest that a high-dose patch of capsaicin has tolerable efficacy in patients with a localized pain as a result of nerve injury
TRPV1↑, agents acting on TRPV1 receptors, as well as capsaicin itself,
eff↑, Combining cetuximab with immunotherapy and other targeted agents further expands the therapeutic landscape, offering renewed hope for mCRC patients who face the development of resistance to conventional therapies.
Half-Life↑, Pharmacokinetic differences include cetuximab’s non-linear clearance and longer half-life, while panitumumab exhibits both linear and non-linear clearance mechanisms and a shorter half-life [23].
Half-Life↑, These studies revealed that clearance from the bloodstream was relatively slow, with a median half-life of 7 days
EGFR↓, Cetuximab also aids in downregulating EGFR-dependent signaling by promoting the internalization of EGFR
OS↑, Cetuximab improved OS and PFS compared with best supportive care (BSC), while maintaining quality of life [
QoL↑,
eff↑, The BEACON trial illustrated that the combination of BRAF inhibition and anti-EGFR therapy using cetuximab yielded better results compared with irinotecan-based chemotherapy in refractory BRAF V600E mCRC patients.
KRAS↓, nhibition of KRAS G12C and Cetuximab
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TumVol↓, chitosan-based nanoparticles reduced tumors (doxorubicin (DOX) + survivin siRNA and curcumin + siRNA).
toxicity↓, Their initial studies reveal low toxicity and long-term medication delivery.
Half-Life↑,
eff↑, that allows drug release in reductive cellular environments (especially cancer cells with elevated glutathione levels),
selectivity↑, This clever nanocarrier reacts to intracellular cues and delivers its therapeutic payload mostly to cancer cells while protecting healthy tissues
Dose↝, These co-delivery systems take advantage of chitosan's mucoadhesive properties and protection against enzymatic degradation, enabling oral or nasal administration routes that traditionally pose challenges for peptide delivery
*BDNF↑, Chitosan nanoparticles delivering a combination of brain-derived neurotrophic factor (BDNF) protein and Nrf2 plasmid DNA have been shown to support synaptic plasticity, inhibit oxidative stress, and slow neurodegeneration.
*NRF2↑,
*ROS↓,
*neuroP↑,
*memory↑, In preclinical trials, such strategies improved memory retention, cognitive performance, and neuronal survival in rodent models
*cognitive↑,
*Obesity↓, obese non-human primates illustrated how chitosan-based codelivery of metformin and fibroblast growth factor 21 (FGF21) plasmid DNA targeted adipose tissue to achieve a 40 % reduction in visceral fat
DDS↑, This paper focuses on the strategies implemented using chitin and chitosan biopolymers in drug delivery for cancer treatment.
antiOx↑, it has intrinsic material properties such as antioxidant, antibacterial, and antitumor
Bacteria↓,
AntiTum↑,
Half-Life↑, They are the perfect choice for use in drug delivery systems that call for a sustained drug release over a long timeframe because of this attribute
BioAv↑, These polysaccharides have demonstrated favorable properties, including biodegradability, biocompatibility, and low toxicity, making them ideal candidates for use as drug carriers.
toxicity↓,
*other↝, CS typically exhibits molecular weights ranging from 300 to 1000 kDa, influenced by its degree of acetylation.
*BioAv↓, Generally, CS is insoluble in water at neutral pH
eff↑, This pH-responsive solubility can be advantageous in drug delivery to specific regions of the body with varying pH levels
toxicity↓, It is non-toxic, biodegradable, and biocompatible.
eff↑, Owing to the favourable attributes of CS, it is widely used in the nanoencapsulation of EOs.
TumCD↑, CS nanoparticles have shown potent cytotoxic effects against human breast cancer MCF-7 cells with an IC50 ranging from 3.72 to 17.81 μg/mL after a 72 h incubation period.
Half-Life↑, It was reported that EO-loaded CS nanoparticles are able to circulate in the bloodstream for a relatively long time and accumulate at the cancer cell site
selectivity↑,
EPR↑, This can be achieved through the enhanced permeability and retention (EPR) effect.
ROS↑, Z. multiflora EO-loaded CS nanoparticles triggered the production of intracellular reactive oxygen species (ROS) in the mitochondria, which leads to apoptosis.
Apoptosis↑,
eff↑, CS-nanoencapsulated Citrus EOs exhibited improved cytotoxic properties against cancerous MDA-MB-468 cells.
eff↑, Promising due to interaction between negatively charged nucleic acids and positively charged chitosan
DDS↑, CHITOSAN IN DRUG DELIVERY SYSTEMS
Chitosan-based nanoparticles (CS-NPs) are able to overcome mucosal barriers and release drugs in a delayed manner
Half-Life↑,
eff↑, Enhancement of antitumor properties of gene delivery by co-delivery with drug
eff↑, Oral administration shows low efficacy and significant side effects, however, promising results with CS-NPs
angioG↓, Both chitosan and its various derivatives have been reported to selectively permeate through the cancer cell membranes and show anticancer activity through the cellular enzymatic, antiangiogenic, immunoenhancing, antioxidant defense mechanism, and ap
*Imm↑,
*antiOx↑,
selectivity↑, They get sequestered from noncancer cells and provide their enhanced bioavailability in cancer cells in a sustained release manner.
other↝, The degree of deacetylation (DDA) of chitin ranges from 60 to 100 % and molecular weight of commercially obtained chitosan ranges from 3800 to 20,000 Daltons.
toxicity↓, The degree of deacetylation (DDA) of chitin ranges from 60 to 100 % and molecular weight of commercially obtained chitosan ranges from 3800 to 20,000 Daltons.
BioAv↑,
eff↝, exert anticancer activity with minimal toxicity on noncancer cells [13] and such activity against different cancer cell lines significantly depends upon molecular weight and DDA [
Half-Life↑, Sustained Release Mechanism
MPT↑, Chitosan MDA-MB-231 Permeation enhancement, lowering of MMP9 activity
MMP9↓,
lipid-P↑, induction of lipid peroxidation, enhanced permeation and retention (EPR) effect
EPR↑,
NK cell↑, Immunoenhancement through increase in activity of NK cells, T cells, killer lymphocytes and cytokins.
Casp3↑, Cellular apoptosis, activation of caspase-3 and caspase-8,
Casp8↑,
TumCCA↑, Cytokine signaling cell cycle arrest, ROS activation
ROS↑,
DDS↑, CMCS has been prepared as a carrier of anticancer drug such as 5- fluorouracil, curcumin, and doxorubicin
VEGF↓, decrease in VEGF level and increase in TIMP1 level after 14-day treatment of mouse serum with CMCS in vivo.
TIMP1↑,
ChemoSen↑, The paclitaxel loaded modified glycol chitosan nanoparticles in the size of 400 nm has been found to show sustained release of paclitaxel to bring about the inhibition of MCF-7 tumor growth due to EPR effect in vitro
eff↑, Chitosan-curcumin nanoformulation has been found to show anticancer activity following the apoptotic pathways associated with DNA damage, cell-cycle blockage, and elevation of ROS levels in vivo
DDS↑, attained promising recognition from researchers for improving the pharmacokinetics and pharmacodynamics of chemotherapeutics.
eff↓, CS-NPs for target-specific delivery of chemotherapeutics have also been considered.
*Bacteria↓, Owing to their inherent antimicrobial, antioxidant, wound healing, analgesic, anti-rheumatic, immunomodulatory, mucoadhesive, antiproliferative, and antimetastatic properties, CS and CS-NPs have been extensively investigated
*antiOx↑,
*Wound Healing↑,
*Imm↑,
TumCP↓,
TumMeta↓,
angioG↓, anticancer potential of CS and CS-NPs was attributed to their antiangiogenic, antioxidant, immunoenhancing, and apoptotic effects
Apoptosis↑,
ROS↑, apoptotic effect of CS-NPs is due to the generation of reactive oxygen species (ROS), which induce apoptosis and cause severe stress to the mitochondria and endoplasmic reticulum.
ER Stress↑,
BioAv↑, CS-NPs improve the rate and extent of absorption of chemotherapeutics from the site of administration owing to their prolonged residence time.
Half-Life↑,
eff↑, interesting approach employing high-intensity ultrasound was proposed by Choi et al35 to improve the penetration of CS-NPs into tumor tissues.
EPR↑, permeated CS-NPs were retained in tumor tissues for longer periods. This phenomenon is called “Enhanced Permeation and Retention (EPR)” effect.
ChemoSen↑, In addition to monodelivery, CS-NPs have shown tremendous potential for combined delivery of chemotherapeutics.
eff↑, CS-NPs have been conjugated with a variety of targeting ligands (eg, folic acid, hyaluronic acid, transferrin, antibodies, peptides, and aptamers) to enable selective intracellular delivery.
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*toxicity↓, Unlike what happens in other mammals -pets- included, theobromine is safe for humans and has fewer unwanted effects than caffeine
*eff↑, Theobromine, which is found in higher amounts than caffeine, seems to be behind several effects attributed to cocoa intake.
*Half-Life↑, Half-life of theobromine is higher than caffeine even in rodents, which have a faster hepatic metabolism. The mean half-life in plasma from healthy volunteers is approximately 10 h
*eff↑, Theobromine is useful in asthma and in other respiratory tract problems such as cough for which no definitive drug has been developed.
*Inflam↓, Benefits of the theobromine on cough seem to be related with its anti-inflammatory potential as well as with modulation of airway reactivity
*HDL↑, The results of the clinical trial NCT01481389 (clinicaltrials.org) suggest that theobromine but not flavonoids is the responsible for the increase in HDL levels in individuals taking cocoa products
*Obesity↓, theobromine has been considered useful for weight loss and it is supplemented to herbal tea preparations
TumCP↓, inhibits proliferation, migration, and invasion of malignant tumor cells.
TumCMig↓,
TumCI↓,
eff↑, divalent copper ions can enhance the antitumor effects of DSF
Imm↑, immunomodulatory properties of DSF
ROS↑, Elevated production of reactive oxygen species (ROS) and suppression of the ROS/NF-κB signaling pathway
NF-kB↓,
chemoP↑, DSF has been shown to effectively inhibit NF-κB pathway activity and augment the apoptotic impact of 5-fluorouracil (5-FU) on colorectal cancer cells when administered in conjunction with 5-FU
JNK↑, Activate the JNK signaling pathway
FOXO↑, In acute myeloid leukemia, DSF/Cu2+ enhances the expression of the oncogene FOXO and inhibits the expression of the oncogene MYC, inducing G0/G1 cell cycle arrest and tumor cell apoptosis
Myc↑,
TumCCA↑,
Apoptosis↑,
RadioS↑, DSF/Cu2+ enhances the efficacy of conventional chemotherapy and chemoradiation, while remaining cost-effective
PD-L1↑, DSF can upregulate PD-L1 expression by promoting DNMT1-mediated hypomethylation of IRF7
eff↑, DSF was found to markedly enhance the efficacy of anti-PD-1 antibody treatment
CSCs↓, Inhibition of cancer stem cells
Dose↝, DSF's oral dosage form is ineffective for cancer treatment due to its instability in the gastric environment and rapid degradation in the body
Half-Life↑, DSF encapsulated PEG-PLGA NPs have been shown to improve tumor site delivery and prolong systemic circulation half-life.
*AChE↓, effects of this alkaloid have been attributed to its ability to inhibit the cholinergic enzyme acetylcholinesterase (AChE), acting as an acetylcholinesterase inhibitor (AChEI).
*neuroP↑, summarize the neuroprotective effects of HupA on AD,
*BBB↑, HupA is an unsaturated sesquiterpene alkaloid compound that effectively crosses the blood-brain barrier (BBB), acting as a mixed-competitive, reversible, and selective AChE inhibitor
*Half-Life↑, with a half-life of 5 h in the bloodstream, reaching a peak concentration at approximately 60 min in humans
*cognitive↑, hows evidence of improved cognition
*Dose↝, significant cognitive enhancement in patients receiving 0.4 mg of HupA twice a day.
*BACE↓, while downregulating the membrane translocation of BACE1
*IronCh↑, HupA might act directly as an Fe2+ chelator, reducing the capacity of IRP-1 to induce APP translation
*TfR1/CD71↓, HupA also downregulates TFR1 expression in mice in vivo, which reduces the uptake of transferrin-bound iron (TBI) in neurons
*ROS↓, HupA indirectly reduces ROS
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*antiOx↑, the antioxidant effect of lycopene
*ROS↓, Lycopene has the ability to reduce reactive oxygen species (ROS) and eliminate singlet oxygen, nitrogen dioxide, hydroxyl radicals, and hydrogen peroxide
*BioAv↝, human body cannot synthesize lycopene. It must be supplied with the diet
*Half-Life↑, half-life of lycopene in human plasma is 12–33 days
*BioAv↓, bioavailability decreases with age and in the case of certain diseases
*BioAv↑, heat treatment process of food increases the bioavailability of lycopene
*cardioP↑, positive effect on cardiovascular diseases, including the regulation of blood lipid levels
*neuroP↑, beneficial effects in nervous system disorders, including neurodegenerative diseases such as Parkinson′s disease and Alzheimer′s disease
*H2O2↓, Lycopene has the ability to reduce reactive oxygen species (ROS) and eliminate singlet oxygen, nitrogen dioxide, hydroxyl radicals, and hydrogen peroxide
*VitC↑, ability to regenerate non-enzymatic antioxidants such as vitamin C and E.
*VitE↑,
*GPx↑, increase in cardiac GSH-Px activity and an increase in cardiac GSH levels
*GSH↑,
*MPO↓, also a decrease in the level of cardiac myeloperoxidase (MPO), cardiac H2O2, and a decrease in cardiac glutathione S transferase (GSH-ST) activity.
*GSTs↓,
*SOD↑, increasing the activity of GSH-Px and SOD in the liver
*NF-kB↓, reducing the expression of NF-κB mRNA in the heart
*IL1β↓, decreased the level of IL-1β and IL-6 and increased the level of anti-inflammatory IL-10 in the heart
*IL6↓,
*IL10↑,
*MAPK↓, inhibited the activation of the ROS-dependent pro-hypertrophic mitogen-activated protein kinase (MAPK) and protein kinase B (Akt) signaling pathways.
*Akt↓,
*COX2↓, decrease in the levels of pro-inflammatory mediators in heart: COX-2, TNF-α, IL-6, and IL-1β and an increase in the anti-inflammatory cardiac TGF-β1.
*TNF-α↓,
*TGF-β1↑,
*NO↓, reduced NO levels in heart and cardiac NOS activity
*GSR↑, increase in the level of cardiac and hepatic SOD, CAT, GSH, GPx, and glutathione reductase (GR)
*NRF2↑, It also activated nuclear factor-erythroid 2 related factor 2 (Nrf2). This affected the downstream expression of HO-1 [97].
*HO-1↑,
*TAC↑, Researchers observed an increase in the liver in TAC and GSH levels and an increase in GSH-Px and SOD activity
*Inflam↓, study showed that lycopene was anti-inflammatory
*BBB↑, Lycopene is a lipophilic compound, which makes it easier to penetrate the blood–brain barrier.
*neuroP↑, Lycopene had also a neuroprotective effect by restoring the balance of the NF-κB/Nrf2 pathway.
*memory↑, lycopene on LPS-induced neuroinflammation and oxidative stress in C57BL/6J mice. The tested carotenoid prevented memory loss
antiOx↓, Lycopene is a potent antioxidant that fights ROS and, subsequently, complications.
ROS↓,
BP↓, It reduces blood pressure via inhibiting the angiotensin-converting enzyme and regulating nitrous oxide bioavailability.
LDL↓, important role in lowering of LDL (low-density lipoproteins) and improving HDL (high-density lipoproteins) levels to minimize atherosclerosis
*toxicity∅, Lycopene is a natural substance that may be used in high doses as a dietary supplement without causing harm to human health or physiology
eff↑, Thermal food processing, particularly in the presence of cooking oils, causes lycopene to micellize and enhance its intestinal absorption rate by a factor of ten
ROS↑, As a pro-oxidant, lycopene may have both good and negative impacts in biological systems, as well as influence the course of human illnesses.
*Half-Life↑, Plasma lycopene has a half-life of 12–33 days in the human body
*BioAv↓, Tomato lycopene is not easily absorbed since it is integrated into the nutritional matrix.
*BioAv↑, Clinical research demonstrates that heat-processed tomato products absorb lycopene more quickly than raw sources, and that adding oil increases absorption
*antiOx↑, Lycopene’s ability to protect against oxidative stress has been established
*HDAC↓, BA appears to function as a histone deacetylase (HDAC) inhibitor while PBA acts as a chemical chaperone and/or a HDAC inhibitor.
*Half-Life↑, In humans, the plasma concentration of BA decreased quickly with a half-life of approximately 5 min once the infusion had ended
*Half-Life↑, The mean half-lives of PBA, PAA and PAGN in blood plasma were 0.7, 1.2 and 1.7 h, respectively, after an intravenous infusion of sodium phenylbutyrate to human subjects and 1, 1.8 and 2.8 h in serum, respectively, after an oral PB 9 to 45 g/day
*lipoGen↓, in vivo studies have shown that PBA ameliorated fructose-induced hepatosteatosis by inhibiting lipogenesis.
*ER Stress↓, PBA blocked fructose-driven expression of SREBP1c and its target genes by attenuating ER stres
*FAO↑, BA and PBA promote fatty acid β-oxidation
*ROS↓, Moreover, PBA prevented palmitate-induced autophagy-dependent reactive oxygen species (ROS) formation further supporting the protective role of PBA against lipotoxicity.
*BioAv↑, The absolute bioavailability of PBA averaged 78% in human subjects following the oral administrations of 9-45 g/day
*Half-Life↑, pharmacokinetic properties of PL-BSA-NPs were shown that PL-BSA-NPs could maintain
a certain level of blood drug concentration for a long time, thus demonstrating the sustained release and increased
bioavailability of PL.
*BioAv↑,
eff↑, antitumor activity of the PL-BSA-NPs and found that PL can significantly inhibit HepG2 cell proliferation, and that PL-BSA-NPs enhanced the inhibitory effect of PL on this
proliferative effect.
ROS↑, t PL can destroy liver cancer cells by increasing ROS levels.
*toxicity↓, Pterostilbene is generally safe for use in humans up to 250 mg/day.
*Half-Life↑, Pterostilbene has a longer half-life (105 minutes versus 14 minutes)
*BioAv↑, and higher oral bioavailability (80% versus 20%) compared to resveratrol
*BioAv↑, 80% bioavailability versus 20% for resveratrol
*Half-Life↑, half-life of pterostilbene? 105 minutes. Compare that to resveratrol, which is just 14 minutes
*BBB↑, Just like alpha lipoic acid, pterostilbene has been found to cross the blood brain barrier, which means it might offer protective assistance for neurodegenerative diseases like Alzheimer’s disease and cognitive decline from other oxidative stress con
*BP↓, May reduce blood pressure
*cognitive↑, May slow age-related cognitive decline
eff↑, Due to the better lipophilic and oral absorption, higher cellular uptake and a longer half-life than resveratrol, pterostilbene may have a good prospect in the future clinic application.
Half-Life↑,
TumCG↓, Special focus is placed on the oncostatic effects of pterostilbene, including inhibition of tumor growth, metastasis, angiogenesis and cancer stem cells, activation of apoptosis, and enhancement of immunotherapy.
TumMeta↓,
angioG↓,
CSCs↓, There is solid evidence that pterostilbene inhibited multiple CSCs, including breast CSCs [18,20,41,68,[110], [111], [112]], glioma CSCs [42], and lung CSCs [22]
Apoptosis↑,
eff↑, enhancement of immunotherapy
CD44↓, Pterostilbene selectively repressed CD44+/CD24− CSCs in MCF-7 cells
CD24↓,
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*antiOx↑, Quercetin has a potent antioxidant capacity, being able to capture reactive oxygen species (ROS), reactive nitrogen species (RNS), and reactive chlorine species (ROC),which act as reducing agents by chelating transition-metal ions.
*ROS↓, Quercetin is a potent scavenger of reactive oxygen species (ROS), protecting the organism against oxidative stress
*angioG↓,
*Inflam↓, anti-inflammatory properties; the ability to protect low-density lipoprotein (LDL) oxidation, and the ability to inhibit angiogenesis;
*BioAv↓, It is known that the bioavailability of quercetin is usually relatively low (0.17–7 μg/mL), less than 10% of what is consumed, due to its poor water solubility (hydrophobicity), chemical stability, and absorption profile.
*Half-Life↑, their slow elimination since their half-life ranges from 11 to 48 h, which could favor their accumulation in plasma after repeated intakes
*GSH↑, Animal and cell studies have demonstrated that quercetin induces the synthesis of GSH
*SOD↑, increase in the expression of superoxide dismutase (SOD), catalase (CAT), and GSH with quercetin pretreatment
*Catalase↑,
*Nrf1↑, quercetin accomplishes this process involves increasing the activity of the nuclear factor erythroid 2-related factor 2 (NRF2), enhancing its binding to the ARE, reducing its degradation
*BP↓, quercetin has been shown to inhibit ACE activity, reducing blood pressure
*cardioP↑, quercetin has positive effects on cardiovascular diseases
*IL10↓, Under the influence of quercetin, the levels of interleukin 10 (IL-10), IL-1β, and TNF-α were reduced.
*TNF-α↓,
*Aβ↓, quercetin’s ability to modulate the enzyme activity in clearing amyloid-beta (Aβ) plaques, a hallmark of AD pathology.
*GSK‐3β↓, quercetin can inhibit the activity of glycogen synthase kinase 3β,
*tau↓, thus reducing tau aggregation and neurofibrillary tangles in the brain
*neuroP↑,
*Pain↓, quercetin reduces pain and inflammation associated with arthritis
*COX2↓, quercetin included the inhibition of oxidative stress, production of cytokines such as cyclooxygenase-2 (COX-2) and proteoglycan degradation, and activation of the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) (Nrf2/HO-1)
*NRF2↑,
*HO-1↑,
*IL1β↓, Mechanisms included decreased levels of TNF-α, IL-1β, IL-17, and monocyte chemoattractant protein-1 (MCP-1)
*IL17↓,
*MCP1↓,
PKCδ↓, studies with human leukemia 60 (HL-60) cells report that concentrations between 20 and 30 µM are sufficient to exert an inhibitory effect on cytosolic PKC activity and membrane tyrosine protein kinase (TPK) activity.
ERK↓, 50 µM resulted in the blockade of the extracellular signal-regulated kinases (ERK1/2) pathway
BAX↓, higher doses (75–100 µM) were used, as these doses reduced the expression of proapoptotic factors such as Bcl-2-associated X protein (Bax) and caspases 3 and 9
cMyc↓, induce apoptosis at concentrations of 80 µM and also causes a downregulation of cellular myelocytomatosis (c-myc) and Kirsten RAt sarcoma (K-ras) oncogenes
KRAS↓,
ROS↓, compound’s antioxidative effect changes entirely to a prooxidant effect at high concentrations, which induces selective cytotoxicity
selectivity↑, On the other hand, when noncancerous cells are exposed to quercetin, it exerts cytoprotective effects;
tumCV↓, decrease cell viability in human glioma cultures of the U-118 MG cell line as well as an increase in death by apoptosis and cell arrest at the G2 checkpoint of the cell cycle.
Apoptosis↑,
TumCCA↑,
eff↑, quercetin combined with doxorubicin can induce multinucleation of invasive tumor cells, downregulate P-glycoprotein (P-gp) expression, increase cell sensitivity to doxorubicin,
P-gp↓,
eff↑, resveratrol, quercetin, and catechin can effectively block the cell cycle and reduce cell proliferation in vivo
eff↑, cotreatment with epigallocatechin gallate (EGCG) inhibited catechol-O-methyltransferase (COMT) activity, decreasing COMT protein content and thereby arresting the cell cycle of PC-3 human prostate cancer cells
eff↑, synergistic treatment of tamoxifen and quercetin was also able to inhibit prostate tumor formation by regulating angiogenesis
eff↑, coadministration of 2.5 μM of EGCG, genistein, and quercetin suppressed the cell proliferation of a prostate cancer cell line (CWR22Rv1) by controlling androgen receptor and NAD (P)H: quinone oxidoreductase 1 (NQO1) expression
CycB/CCNB1↓, It can also downregulate cyclin B1 and cyclin-dependent kinase-1 (CDK-1),
CDK1↓,
CDK4↓, quercetin causes a decrease in cyclins D1/Cdk4 and E/Cdk2 and an increase in p21 in vascular smooth muscle cells
CDK2↓,
TOP2↓, quercetin is known to be a potent inhibitor of topoisomerase II (TopoII), a cell cycle-associated enzyme necessary for DNA replication
Cyt‑c↑, quercetin can induce apoptosis (cell death) through caspase-3 and caspase-9 activation, cytochrome c release, and poly ADP ribose polymerase (PARP) cleavage
cl‑PARP↑,
MMP↓, quercetin induces the loss of mitochondrial membrane potential, leading to the activation of the caspase cascade and cleavage of PARP.
HSP70/HSPA5↓, apoptotic effects of quercetin may result from the inhibition of HSP kinases, followed by the downregulation of HSP-70 and HSP-90 protein expression
HSP90↓,
MDM2↓, (MDM2), an onco-protein that promotes p53 destruction, can be inhibited by quercetin
RAS↓, quercetin can prevent Ras proteins from being expressed. In one study, quercetin was found to inhibit the expression of Harvey rat sarcoma (H-Ras), K-Ras, and neuroblastoma rat sarcoma (N-Ras) in human breast cancer cells,
eff↑, there was a substantial difference in EMT markers such as vimentin, N-cadherin, Snail, Slug, Twist, and E-cadherin protein expression in response to AuNPs-Qu-5, inhibiting the migration and invasion of MCF-7 and MDA-MB cells
*Half-Life↑, elimination half-time (t1/2 ) of females (93.8 h for AP and 15.2 h for OP) was much higher than that of males t1/2 of (29.9 h for AP and 13.4 h for OP).
IL6↓, A
dose-dependent reduction of IL-6 by resveratrol led to attenuation of
matrix metalloproteinases (MMPs), including MMP2 and MMP9
MMPs↓,
MMP2↓,
MMP9↓,
BioAv↓, The most important weakness of the usual form of resveratrol is its low absorption in the intestine and its low bioavailability
Half-Life↑, some covers such as liposomes and micelles also can facilitate absorption and increase half-life
BioAv↑, another study showed that carboxymethyl chitosan can increase bioavailability by more than 3.5 times
Dose↝, low concentrations of resveratrol (lower than 50 uM) cause no remarkable toxicity for normal cells, while higher concentrations are
associated with increased oxidative injury
angioG↓, It is suggested that inhibition of STAT3, IL-10, and a reduction of vascular endothelial growth factor (VEGF) by resveratrol is involved in the suppression of macrophages and reduction of invasion and angiogenesis
IL10↓,
VEGF↓,
NF-kB↓, Inhibition of NF-kB by resveratrol can attenuate the expression of COX-2.
COX2↓,
SIRT1↑, Activation of Sirt-1 by resveratrol has a role in the suppression of NF-kB
Wnt↓, Resveratrol has also been shown that inhibit the Wnt/C-Myc pathway too
cMyc↓,
STAT3↓, Resveratrol has been shown that attenuate the expression of STAT3 through reduction of IL-6 level
PTEN↑, Downregulation of miR-17, miR-20a and miR-106b by resveratrol can activate PTEN, which leads to suppression of PI3K and induction of apoptosis in cancer cells
ROS↑, Resveratrol can trigger NOX5-induced ROS, leading to the induction of DNA damage and cancer cells senescence
RadioS↑, The combination of radiation and resveratrol has shown that has a synergic effect for stimulation of ROS
production and induction of senescence in non-small cell lung carci-
noma
Hif1a↓, Resveratrol can inhibit HIF-1α and its downstream proteins, including E-cadherin and vimentin
E-cadherin↓,
Vim↓,
angioG↓, Furthermore, resveratrol inhibits angiogenesis markers and tumor growth through the inhibition of HIF-1a
*BioAv↝, Experiments in rats demonstrated that RA applied topically to skin was absorbed percutaneously and became distributed in skin, blood, bone and muscle while intravenously administered RA was distributed in various tissues such as lung, spleen, heart a
*Half-Life↝, RA compounds (free and conjugate forms) reached a maximum concentration of 4.63 Amol/l 0.5 h after RA administration.
*Half-Life↑, e maximum COA concentration of 0.75 Amol/l was reached gradually, peaking at 8 h post-intake
*Half-Life↝, About 83% of this excretion occurred within the period 8 to 18 h after RA administration
*BioAv↑, This result shows that orally administered RA was rapidly absorbed from the digestive tract.
*antiOx↑, silymarin, demonstrating remarkable antioxidant and hepatoprotective properties in extensive preclinical investigations.
*hepatoP↑, It can protect healthy liver cells or those that have not yet sustained permanent damage by reducing oxidative stress and mitigating cytotoxicity.
*Half-Life↑, The main ingredient in silymarin, silibinin, normally takes two to four hours to reach its peak plasma concentration after oral consumption, and it has a 6‐hour plasma half‐life
*ROS↓, silibinin has potent anti‐ROS qualities,
*GSH↑, silymarin, the precursor to silibinin, can increase glutathione production in the liver and hence increase the liver tissues' antioxidant capacity
*hepatoP↑, silymarin, the precursor to silibinin, can increase glutathione production in the liver and hence increase the liver tissues' antioxidant capacity
*lipid-P↓,
*TNF-α↓, inhibit the production of pro‐inflammatory cytokines, such as TNF‐α, IFN‐γ, IL‐2, and IL‐4, which are crucial in the inflammatory cascade
*IFN-γ↓,
*IL2↓,
*IL4↓,
*NF-kB↓, Silymarin's mechanism involves suppressing NF‐κB activation,
*iNOS↓, It downregulates inflammatory mediators like interleukins, TNF‐α, and iNOS, which are involved in various diseases.
*OATPs↓, Its inhibition of transporters, including OATPs and OCTs, may also affect members of the solute carrier family
*OCT4↓,
*Inflam↓, Silymarin may have anti‐inflammatory properties that limit the production of inflammatory mediators like NF‐B and inflammatory metabolites like prostaglandin E2 (PGE2)
*PGE2↓,
MMPs↓, Silymarin significantly inhibits matrix metalloproteinases (MMPs), essential for cancer metastasis,
VEGF↓, Additionally, silymarin down‐regulates VEGF expression, contributing to anti‐angiogenic effects, and has the potential to reverse STAT‐3‐associated cancer drug resistance.
angioG↓,
STAT3↓,
*ALAT↓, The research revealed improved liver function as seen by lower levels of ALT, AST, and alkaline phosphatase, as well as a considerably lower likelihood of developing DILI four weeks after starting silymarin treatment
*AST↓,
Dose↝, The suggested dosage of silymarin has been used in clinical trials for up to 48 weeks at a dose of 2100 mg/day and for up to 4 years at a dose of up to 420 mg/day.
| - |
Review, |
AD, |
NA |
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Review, |
Stroke, |
NA |
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Review, |
ostP, |
NA |
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Review, |
IBD, |
NA |
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*MitoP↓, Experimental models consistently show that UA increases mitophagy and mitochondrial function and blunts excessive inflammatory responses.
*Strength↑, UA is a promising strategy to target health and disease conditions of aging, especially those linked to mitochondrial and muscle dysfunction.
*PINK1↑, UA can activate. PTEN-induced kinase 1 (PINK1)/Parkin-dependent mitophagy starts with the stabilization of the kinase PINK1,
*PARK2↑, which recruits and phosphorylates the ubiquitin-conjugating protein Parkin.
*Inflam↓, anti-inflammatory effect of UA was reported for the first time as a decrease in mRNA and protein levels of the inflammatory marker cyclooxygenase 2 (COX2)
*COX2↓,
*IL1β↓, In neuronal tissues, UA treatment reduced levels of IL-1β, IL-6, and TNFα in the brains of the amyloid precursor protein/presenilin 1 (APP/PS1) mouse model of AD
*IL6↓,
*TNF-α↓,
*OS↑, impact on worm longevity showed that UA extends lifespan by 45%,
*cardioP↑, reduction in IRI markers, such as circulating creatine kinase and lactate dehydrogenase levels, and by fewer apoptotic cells in the heart
*memory↑, Increased learning, memory retention, neuronal survival, and neurogenesis in the hippocampus was achieved with UA administration in the APP/PS1 mouse model of AD
*neuroG↑,
*neuroP↑, UA was shown to have neuroprotective effects in the EAE mouse model of multiple sclerosis (MS)
*Cartilage↑, In a model of osteoarthritis, an age-related and disabling joint disease caused by a slow degeneration of cartilage,
*Inflam↓, UA has protective effects against a chronic DSS-induced model of IBD, leading to reduced levels of colon inflammation markers and to better mucosal integrity.
*RenoP↑, UA consistently reduced tubular damage induced by cisplatin, as shown by histopathology and by a reduction in circulating markers of kidney damage
*eff↑, When administered as nanoparticles to increase its bioavailability, UA even improved the survival of mice that received a lethal dose of cisplatin
*Dose↝, UA showed a favorable safety profile, with no observed side effects following either single oral administration of UA up to 2000 mg or multiple oral dosing (28 days) of UA up to 1000 mg daily.
*Half-Life↑, It showed a relatively long-half life (t1/2 = 17–22 hours),
*NRF2↑, Other mechanisms of action have been proposed for UA, such as the activation of the Ahr/Nrf2 pathway and its downstream antioxidative stress response
*GutMicro↑, A recent report also showed an impact of direct UA supplementation on gut microflora in obese rats
*Risk↑, Diminished circulating concentrations of vitamin E have been demonstrated in individuals with AD. Reduced plasma levels have furthermore been associated with an increased risk of AD
*Half-Life↑, The plasma half-life of α-tocopherol is estimated at 20 hrs, which is considerably longer than that of other isoforms, particularly the tocotrienol congeners
*antiOx↑, potent antioxidant capabilities of vitamin E are well known
*BioAv↑, α-tocopherol retains a superior in vivo role in neuroprotection due to its relatively greater bioavailability and preferential retention by tissues.
*neuroP↑, includes other neuro-protective, anti-inflammatory and cholesterol-reducing properties, in addition to influencing gene expression and potentially ensuing AD pathology.
*Inflam↑,
*LDL↓,
*cognitive↑, vitamin E supplementation was associated with decreased risk of cognitive decline in a cohort of 560 AD patients from the Canadian Study of Health and Aging
Showing Research Papers: 1 to 35 of 35
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 35
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
antiOx↓, 1, antiOx↑, 1, lipid-P↑, 1, NRF2↑, 1, Prx↑, 1, ROS↓, 2, ROS↑, 8, TrxR↓, 1,
Mitochondria & Bioenergetics ⓘ
MMP↓, 1, MPT↑, 1,
Core Metabolism/Glycolysis ⓘ
cMyc↓, 2, CYP3A4↓, 1, LDL↓, 1, SIRT1↑, 1,
Cell Death ⓘ
Apoptosis↑, 5, BAX↓, 1, Casp3↑, 1, Casp8↑, 1, Cyt‑c↑, 1, JNK↑, 1, MDM2↓, 1, Myc↑, 1, TRPV1↑, 2, TumCD↑, 1,
Transcription & Epigenetics ⓘ
other↑, 1, other↝, 2, tumCV↓, 1,
Protein Folding & ER Stress ⓘ
ER Stress↑, 1, HSP70/HSPA5↓, 1, HSP90↓, 1,
DNA Damage & Repair ⓘ
cl‑PARP↑, 1,
Cell Cycle & Senescence ⓘ
CDK1↓, 1, CDK2↓, 1, CDK4↓, 1, CycB/CCNB1↓, 1, TumCCA↑, 3,
Proliferation, Differentiation & Cell State ⓘ
CD24↓, 1, CD44↓, 1, CSCs↓, 2, ERK↓, 1, FOXO↑, 1, PTEN↑, 1, RAS↓, 1, STAT3↓, 2, TOP2↓, 1, TumCG↓, 1, Wnt↓, 1,
Migration ⓘ
E-cadherin↓, 1, KRAS↓, 2, MMP2↓, 1, MMP9↓, 2, MMPs↓, 2, PKCδ↓, 1, TIMP1↑, 1, TumCI↓, 1, TumCMig↓, 1, TumCP↓, 2, TumMeta↓, 2, Vim↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 6, EGFR↓, 1, EPR↑, 3, Hif1a↓, 1, VEGF↓, 4,
Barriers & Transport ⓘ
P-gp↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 2, IL10↓, 1, IL6↓, 1, IL6↑, 1, IL8↑, 1, Imm↑, 1, NF-kB↓, 3, NK cell↑, 1, NK cell⇅, 1, PD-L1↑, 1, PSA↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 3, BioAv↑, 8, ChemoSen↑, 2, DDS↑, 4, Dose↝, 7, eff↓, 1, eff↑, 26, eff↝, 1, Half-Life↓, 1, Half-Life↑, 18, RadioS↑, 2, selectivity↑, 4,
Clinical Biomarkers ⓘ
BP↓, 1, EGFR↓, 1, IL6↓, 1, IL6↑, 1, KRAS↓, 2, Myc↑, 1, NOS2↓, 1, PD-L1↑, 1, PSA↓, 1,
Functional Outcomes ⓘ
AntiTum↑, 1, chemoP↑, 1, NP/CIPN↓, 1, OS↑, 1, Pain↓, 1, QoL↑, 1, toxicity↓, 4, toxicity↝, 1, TumVol↓, 1,
Infection & Microbiome ⓘ
Bacteria↓, 1,
Total Targets: 107
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↓, 1, antiOx↑, 7, Catalase↑, 1, GPx↑, 2, GSH↑, 4, GSR↑, 1, GSTs↓, 1, H2O2↓, 1, HDL↑, 2, HO-1↑, 2, lipid-P↓, 1, MDA↓, 1, MPO↓, 1, Nrf1↑, 1, NRF2↑, 4, PARK2↑, 1, ROS↓, 6, SOD↑, 3, TAC↑, 1, VitC↑, 2, VitE↑, 1,
Metal & Cofactor Biology ⓘ
IronCh↑, 1, TfR1/CD71↓, 1,
Mitochondria & Bioenergetics ⓘ
PINK1↑, 1,
Core Metabolism/Glycolysis ⓘ
adiP↓, 1, ALAT↓, 1, FAO↑, 1, LDL↓, 2, lipoGen↓, 1,
Cell Death ⓘ
Akt↓, 1, iNOS↓, 1, MAPK↓, 1,
Transcription & Epigenetics ⓘ
other↑, 2, other↝, 2,
Protein Folding & ER Stress ⓘ
ER Stress↓, 1,
Autophagy & Lysosomes ⓘ
MitoP↓, 1,
Proliferation, Differentiation & Cell State ⓘ
GSK‐3β↓, 1, HDAC↓, 1, neuroG↑, 1, OCT4↓, 1,
Migration ⓘ
Cartilage↑, 1, TGF-β1↑, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 1, NO↓, 2,
Barriers & Transport ⓘ
BBB↑, 3, OATPs↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 3, CRP↓, 1, IFN-γ↓, 1, IL10↓, 1, IL10↑, 1, IL17↓, 1, IL1β↓, 4, IL2↓, 1, IL4↓, 1, IL6↓, 2, Imm↑, 2, Inflam↓, 7, Inflam↑, 1, MCP1↓, 1, NF-kB↓, 2, PGE2↓, 1, TNF-α↓, 4, VitD↑, 1,
Synaptic & Neurotransmission ⓘ
AChE↓, 1, BDNF↑, 1, tau↓, 1,
Protein Aggregation ⓘ
Aβ↓, 1, BACE↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 4, BioAv↑, 8, BioAv↝, 4, Dose↝, 3, eff↓, 3, eff↑, 3, eff↝, 1, Half-Life↑, 19, Half-Life↝, 2,
Clinical Biomarkers ⓘ
ALAT↓, 1, AST↓, 1, BP↓, 2, CRP↓, 1, GutMicro↑, 2, IL6↓, 2, VitD↑, 1,
Functional Outcomes ⓘ
BOLD↑, 1, cardioP↑, 5, cognitive↑, 5, hepatoP↑, 2, memory↑, 4, neuroP↑, 8, Obesity↓, 2, OS↑, 1, Pain↓, 1, RenoP↓, 1, RenoP↑, 1, Risk↓, 3, Risk↑, 1, Strength↑, 1, toxicity↓, 2, toxicity∅, 1, Wound Healing↑, 1,
Infection & Microbiome ⓘ
Bacteria↓, 1,
Total Targets: 103
Scientific Paper Hit Count for: Half-Life, Half-Life
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include :
-low or high Dose
-format for product, such as nano of lipid formations
-different cell line effects
-synergies with other products
-if effect was for normal or cancerous cells
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