NADPH Cancer Research Results

NADPH, Nicotinamide adenine dinucleotide phosphate: Click to Expand ⟱
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NADPH (Nicotinamide adenine dinucleotide phosphate) is a crucial molecule in cellular metabolism, playing a key role in various biological processes, including energy production, antioxidant defenses, and biosynthesis.
NADPH is essential for the proper functioning of the pentose phosphate pathway, which generates NADPH and ribose-5-phosphate. Cancer cells may exploit this pathway to support their high energy demands.
Many types of cancer, including breast, lung, and colon cancer, exhibit increased NADPH levels compared to normal tissues. This increase is often associated with enhanced glucose-6-phosphate dehydrogenase (G6PD) activity, a key enzyme in the pentose phosphate pathway that generates NADPH.
Scientific Papers found: Click to Expand⟱
2327- 2DG,    2-Deoxy-d-Glucose and Its Analogs: From Diagnostic to Therapeutic Agents
- Review, Var, NA
Glycolysis↓, 2-DG inhibits glycolysis due to formation and intracellular accumulation of 2-deoxy-d-glucose-6-phosphate (2-DG6P), inhibiting the function of hexokinase and glucose-6-phosphate isomerase, and inducing cell death
HK2↓,
mt-ROS↑, 2-DG-mediated glucose deprivation stimulates reactive oxygen species (ROS) production in mitochondria, also leading to AMPK activation and autophagy stimulation.
AMPK↑,
PPP↓, 2-DG has been shown to block the pentose phosphate shunt
NADPH↓, Decreased levels of NADPH correlate with reduced glutathione levels, one of the major cellular antioxidants.
GSH↓,
Bax:Bcl2↑, Valera et al. also observed that in bladder cancer cells, 2-DG treatment modulates the Bcl-2/Bax protein ratio, driving apoptosis induction
Apoptosis↑,
RadioS↑, 2-DG radiosensitization results from its effect on thiol metabolism
eff↓, (NAC) treatment, downregulated glutamate cysteine ligase activity, or overexpression of ROS scavenging enzymes
Half-Life↓, its plasma half-life was only 48 min [117]) make 2-DG a rather poor drug candidate
other↝, Adverse effects of 2-DG administration in humans include fatigue, sweating, dizziness, and nausea, mimicking the symptoms of hypoglycemia
eff↓, Moreover, 2-DG has to be used at relatively high concentrations (≥5 mmol/L) in order to compete with blood glucose

5277- 3BP,    3-Bromopyruvate inhibits pancreatic tumor growth by stalling glycolysis, and dismantling mitochondria in a syngeneic mouse model
- in-vivo, PC, Panc02
HK2↓, It exerts potent anticancer effects by inhibiting hexokinase II enzyme (HK2) of the glycolytic pathway in cancer cells while not affecting the normal cells.
selectivity↑, it doesn’t affect the normal cells but strongly toxic to cancer cells
ATP↓, 3-BP killed 95% of Panc-2 cells at 15 μM concentration and severely inhibited ATP production by disrupting the interaction between HK2 and mitochondrial Voltage Dependent Anion Channel-1 (VDAC1) protein.
mtDam↑, Electron microscopy data revealed that 3-BP severely damaged mitochondrial membrane in cancer cells.
Dose↝, We further examined therapeutic effect of 3-BP in syngeneic mouse pancreatic cancer model by treating animals with 10, 15 and 20 mg/kg dose. 3-BP at 15 & 20 mg/kg dose level significantly reduced tumor growth by approximately 75-80% in C57BL/6 female
TumCG↓, 3-BP inhibit in vivo pancreatic tumor growth in C57BL/6 mouse model
Casp3↑, observed enhanced expression of active caspase-3 in tumor tissues exhibited apoptotic death.
Glycolysis↓, Notably, metabolomic data also revealed severe inhibition in glycolysis, NADP, ATP and lactic acid production in cancer cells treated with 40 μM 3-BP.
NADPH↓,
ATP↓,
ROS↑, 3-BP treatment produces increased levels of reactive oxygen species (ROS), which causes DNA damage with reduction of free glutathione levels [11].
DNAdam↑,
GSH↓,
Bcl-2↓, Further, treatment with 40 µM of 3-BP suppressed BCL2L1 expression and causing activation of mitochondrial caspases
Casp↑,
lactateProd↓, Metabolic inhibition of glucose consumption and lactic acid production in cancer cells treated with 3-BP

278- ALA,    The Multifaceted Role of Alpha-Lipoic Acid in Cancer Prevention, Occurrence, and Treatment
- Review, NA, NA
ROS↑, direct anticancer effect of the antioxidant ALA is manifested as an increase in intracellular ROS levels in cancer cells
NRF2↑, enhance the activity of the anti-inflammatory protein nuclear factor erythroid 2–related factor 2 (Nrf2), thereby reducing tissue damage
Inflam↓,
frataxin↑,
*BioAv↓, Oral ALA has a bioavailability of approximately 30% due to issues such as poor stability in the stomach, low solubility, and hepatic degradation.
ChemoSen↑, ALA can enhance the functionality of various other anticancer drugs, including 5-fluorouracil in colon cancer cells and cisplatin in MCF-7 breast cancer cells
Hif1a↓, it is inferred that lipoic acid may inhibit the expression of HIF-1α
eff↑, act as a synergistic agent with natural polyphenolic substances such as apigenin and genistein
FAK↓, ALA inhibits FAK activation by downregulating β1-integrin expression and reduces the levels of MMP-9 and MMP-2
ITGB1↓,
MMP2↓,
MMP9↓,
EMT↓, ALA inhibits the expression of EMT markers, including Snail, vimentin, and Zeb1
Snail↓,
Vim↓,
Zeb1↓,
P53↑, ALA also stimulates the mutant p53 protein and depletes MGMT
MGMT↓, depletes MGMT by inhibiting NF-κB signalling, thereby inducing apoptosis
Mcl-1↓,
Bcl-xL↓,
Bcl-2↓,
survivin↓,
Casp3↑,
Casp9↑,
BAX↑,
p‑Akt↓, ALA inhibits the activation of tumour stem cells by reducing Akt phosphorylation.
GSK‐3β↓, phosphorylation and inactivation of GSK3β
*antiOx↑, indirect antioxidant protection through metal chelation (ALA primarily binds Cu2+ and Zn2+, while DHLA can bind Cu2+, Zn2+, Pb2+, Hg2+, and Fe3+) and the regeneration of certain endogenous antioxidants, such as vitamin E, vitamin C, and glutathione
*ROS↓, ALA can directly quench various reactive species, including ROS, reactive nitrogen species, hydroxyl radicals (HO•), hypochlorous acid (HclO), and singlet oxygen (1O2);
selectivity↑, In normal cells, ALA acts as an antioxidant by clearing ROS. However, in cancer cells, it can exert pro-oxidative effects, inducing pathways that restrict cancer progression.
angioG↓, Combining these two hypotheses, it can be hypothesized that ALA may regulate copper and HIF-2α to limit tumor angiogenesis.
MMPs↓, ALA was shown to inhibit invasion by decreasing the mRNA levels of key matrix metalloproteinases (MMPs), specifically MMP2 and MMP9, which are crucial for the metastatic process
NF-kB↓, ALA has been shown to enhance the efficacy of the chemotherapeutic drug paclitaxel in breast and lung cancer cells by inhibiting the NF-κB signalling pathway and the functions of integrin β1/β3 [138,139]
ITGB3↓,
NADPH↓, ALA has been shown to inhibit NADPH oxidase, a key enzyme closely associated with NP, including NOX4

206- Api,    Inhibition of glutamine utilization sensitizes lung cancer cells to apigenin-induced apoptosis resulting from metabolic and oxidative stress
- in-vitro, Lung, H1299 - in-vitro, Lung, H460 - in-vitro, Lung, A549 - in-vitro, CRC, HCT116 - in-vitro, Melanoma, A375 - in-vitro, Lung, H2030 - in-vitro, CRC, SW480
Glycolysis↓, glucose consumption, lactate production, and ATP production were all strongly decreased by apigenin
lactateProd↓,
PGK1↓,
ALDOA↓,
GLUT1↓, Apigenin reduces GLUT1 expression levels.
ENO1↓,
ATP↓,
Casp9↑,
Casp3↑,
cl‑PARP↑, cleavage
PI3K/Akt↓,
HK1↓, HK1, HK2
HK2↓,
ROS↑, Apigenin causes oxidative stress leading to apoptosis. Because apoptotic signal transduction cascades involving caspase-9, -3 and PARP cleavage can be activated by increased ROS levels
Apoptosis↑,
eff↓, Cancer cells expressing high levels of GLUT1 are resistant to apigenin-induced apoptosis through metabolic compensation of glucose utilization.
NADPH↓, apigenin significantly decreased glucose utilization through suppression of GLUT1 expression, and consequently decreased NADPH production, which led to increased ROS levels.
PPP↓, inhibition of the PPP

3382- ART/DHA,    Repurposing Artemisinin and its Derivatives as Anticancer Drugs: A Chance or Challenge?
- Review, Var, NA
AntiCan↑, antimalarial drug, artemisinin that has shown anticancer activities in vitro and in vivo.
toxicity↑, safety of artemisinins in long-term cancer therapy requires further investigation.
Ferroptosis↑, Artemisinins acts against cancer cells via various pathways such as inducing apoptosis (Zhu et al., 2014; Zuo et al., 2014) and ferroptosis via the generation of reactive oxygen species (ROS) (Zhu et al., 2021) and causing cell cycle arrest
ROS↑,
TumCCA↑,
BioAv↝, absolute bioavailability was estimated to be 21.6%. ART has good solubility and is not lipophilic
eff↝, ART would not distribute well to the tissues and might be more effective in treating cancers such as leukemia, hepatocellular carcinoma (HCC), or renal cell carcinoma because the liver and kidney are highly perfused organs.
Half-Life↓, Pharmacokinetic studies showed a relatively short t1/2 of artemisinins. For ART, t1/2 was 0.41 h
Ferritin↓, Figure 3
GPx4↓,
NADPH↓,
GSH↓,
BAX↑,
Cyt‑c↑,
cl‑Casp3↑,
VEGF↓, angiogenesis
IL8↓,
COX2↓,
MMP9↓,
E-cadherin↑,
MMP2↓,
NF-kB↓,
p16↑, cell cycle arrest
CDK4↓,
cycD1/CCND1↓,
p62↓, autophagy
LC3II↑,
EMT↓, suppressing EMT and CSCs
CSCs↓,
Wnt↓, Depress Wnt/β-catenin signaling pathway
β-catenin/ZEB1↓,
uPA↓, Inhibit u-PA activity, protein and mRNA expression
TumAuto↑, Emerging evidence suggests that autophagy induction is one of the molecular mechanisms underlying anticancer activity of artemisinins
angioG↓, Inhibition of Angiogenesis
ChemoSen↑, Many studies also reported that the use of artemisinins sensitized cancer cells to conventional chemotherapy and exerted a synergistic effect on apoptosis, inhibition of cell growth, and a reduction of cell viability, leading to a lower IC50 value

5702- BRU,  BJ,    Brusatol inhibits metastasis of triple-negative breast cancer through metabolic reprogramming
- in-vitro, BC, NA
AntiTum↑, Brusatol (BRU), a natural compound with reported anti-tumor activity and low toxicity, has not been explored in the context of cancer metastasis or metabolic reprogramming.
PPP↓, BRU inhibited metabolic pathways, including the pentose phosphate pathway (PPP), glycolysis, and the tricarboxylic acid (TCA) cycle, while significantly reducing NADPH levels and exacerbating redox stress.
Glycolysis↓,
TCA↓,
NADPH↓,
ROS↑, levated levels of reactive oxygen species (ROS)
chemoP↑, enhance anti-tumor efficacy while reducing chemotherapy-associated toxicity.
e-LDH↑, BRU treatment further enhanced extracellular LDH activity in matrix-detached cells in a concentration-dependent manner
TumMeta↓, Brusatol inhibits TNBC metastasis
Glycolysis↓, BRU extensively inhibits glycolytic capacity in ECM-detached cells under metabolic stress

1640- CA,  MET,    Caffeic Acid Targets AMPK Signaling and Regulates Tricarboxylic Acid Cycle Anaplerosis while Metformin Downregulates HIF-1α-Induced Glycolytic Enzymes in Human Cervical Squamous Cell Carcinoma Lines
- in-vitro, Cerv, SiHa
GLS↓, downregulation of Glutaminase (GLS) and Malic Enzyme 1 (ME1)
NADPH↓, CA alone and co-treated with Met caused significant reduction of NADPH
ROS↑, increased ROS formation and enhanced cell death
TumCD↑,
AMPK↑, activation of AMPK
Hif1a↓, Met inhibited Hypoxia-inducible Factor 1 (HIF-1α). CA treatment at 100 μM for 24 h also inhibited HIF-1α
GLUT1↓,
GLUT3↓,
HK2↓,
PFK↓, PFKFB4
PKM2↓,
LDH↓,
cMyc↓, Met suppressed the expression of c-Myc, BAX and cyclin-D1 (CCND1) a
BAX↓,
cycD1/CCND1↓,
PDH↓, CA at a concentration of 100 µM caused inhibition of PDK activity
ROS↑, CA Regulates TCA Cycle Supply via Pyruvate Dehydrogenase Complex (PDH), Induces Mitochondrial ROS Generation and Evokes Apoptosis
Apoptosis↑,
eff↑, both drugs inhibited the expression of ACLY and FAS, but the greatest effect was detected after co-treatment
ACLY↓,
FASN↓,
Bcl-2↓,
Glycolysis↓, Met acts as a glycolytic inhibitor under normoxic and hypoxic conditions

5834- CAP,    Capsaicin and TRPV1: A Novel Therapeutic Approach to Mitigate Vascular Aging
- Study, Nor, NA
*AntiCan↑, capsaicin possesses anti-cancer, anti-inflammatory, and antioxidant properties and is used as a topical analgesic
*Inflam↓,
*antiOx↑,
*TRPV1↑, Studies demonstrate that capsaicin directly activates TRPV1 by binding to intracellular sites within the channel protein
*AMPK↑, Moreover, capsaicin and TRPV1 can activate the AMPK pathway [82, 83]
*SIRT1↑, elevating SIRT1 levels
*NADPH↓, suppressing NADPH oxidase and reducing reactive oxygen species
*ROS↓,
*MAPK↓, inhibiting MAPK pathways
*eNOS↑, activating eNOS
*Wnt/(β-catenin)↓, inhibiting the Wnt/β-catenin signaling pathway
RenoP↑, Furthermore, TRPV1 activation decreases renal perfusion pressure while increasing glomerular filtration rate and the excretion of sodium/water, thereby modulating renal hemodynamics and excretory functions

5900- CAR,  TV,    Lights and Shadows of Essential Oil-Derived Compounds: Antimicrobial and Anti-Inflammatory Properties of Eugenol, Thymol, Cinnamaldehyde, and Carvacrol
- Review, Nor, NA
*Bacteria↓, oil-derived compounds against a broad spectrum of Gram-positive and Gram-negative bacteria, including multidrug-resistant (MDR) strains
*Inflam↓, anti-inflammatory activity of these compounds is also highlighted, with emphasis on their modulation of key signaling pathways such as nuclear factor-kappa B (NF-κB)
*cardioP↑, figure 1
*neuroP↑,
*NADPH↓, thymol has been shown to inhibit NADPH production at a concentration of 200 µg/mL
*NRF2↑, thymol has been shown to activate the nuclear factor erythroid 2–related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway
*HO-1↑,
*IL1β↓, carvacrol has also shown anti-inflammatory properties [107,108], being able to inhibit pro-inflammatory mediators as IL-1β and TNF-α
*TNF-α↓,

6013- CGA,    Advances in Pharmacological Properties, Molecular Mechanisms, and Bioavailability Strategies of Chlorogenic Acid in Cardiovascular Diseases Therapy
- Review, CardioV, NA
*BioAv↝, As a dietary component, CGA exhibits moderate oral bioavailability [9], and its molecular structure remains largely intact during oral digestion
*BioAv↝, The composition of gut microbiota plays a critical role in CGA’s metabolism and absorption, producing 11 key metabolites, with the most primary products dihydrocaffeic acid, dihydroferulic acid, and 3-(3-hydroxyphenyl) propionic acid [
*BP↓, eported that CGA lowers blood pressure by relaxing vascular smooth muscle and improving endothelial function
*ROS↓, inhibiting the sources of reactive oxygen species (ROS), such as NADPH oxidase,
*NADPH↓,
*AntiAg↑, he downregulation of thromboxane A2 plays a crucial role in CGA-mediated inhibition of platelet aggregation
*TXA2↓,
*antiOx↑, cCGA exhibited the strongest antioxidant effect, which may be related to improved mitochondrial function [
*cardioP↑, CGA exerts significant cardioprotective effects by modulating multiple signaling pathways.
*Inflam↓, reduce infarct size in MI induced by left anterior descending artery (LAD) ligation in rats. It achieves this by suppressing inflammation and enhancing the activity of antioxidant enzymes, such as SOD and CAT, thereby improving cardiac function
*SOD↑,
*Catalase↑,
*Ferroptosis↓, CGA’s ability to alleviate ferroptosis
*NF-kB↓, inhibiting the NF-κB and JNK signaling pathways, highlighting its cardioprotective potential in a TAC mouse model
*JNK↓,
*NRF2↑, CGA reduces oxidative stress and ROS-induced damage by upregulating the Nrf2/HO-1 pathway, thereby mitigating doxorubicin-induced cardiotoxicity and improving cardiac tissue integrity
*HO-1↑,
*toxicity↓, which are widely used in traditional Chinese medicine [60,61], it is generally considered safe.
*BioAv↓, CGA struggles to cross lipophilic membranes, resulting in poor absorption and bioavailability [69]. Simply increasing the oral dose is not an advisable solution, as it carries significant risks.
*BioAv↑, in vitro study reported that the covalent bonding between CGA and soluble oat β-glucan significantly improved CGA’s structural stability and maximized its pharmacological potential
*BioAv↑, Studies have reported that CGA-loaded liposomes, prepared from cholesterol and phosphatidylcholine, showed a relative oral bioavailability of 129.38% compared to free CGA.
eff↑, bovine serum albumin (BSA)-decorated chlorogenic acid silver nanoparticles (AgNPs-CGA-BSA) exhibited significant antioxidant and anticancer effects both in vitro and in vivo.

2590- CHr,    Chrysin suppresses proliferation, migration, and invasion in glioblastoma cell lines via mediating the ERK/Nrf2 signaling pathway
- in-vitro, GBM, T98G - in-vitro, GBM, U251 - in-vitro, GBM, U87MG
TumCP↓, Chrysin inhibited the proliferation, migration, and invasion capacity of glioblastoma cells in dose- and time-dependent manners.
TumCMig↓,
TumCI↓,
NRF2↓, chrysin deactivated the Nrf2 signaling pathway by decreasing the translocation of Nrf2 into the nucleus
HO-1↓, suppressing the expression of hemeoxygenase-1 (HO-1) and NAD(P)H quinine oxidoreductase-1
NADPH↓,
ERK↓, Chrysin treatment downregulates the Nrf2 pathway via inhibition of ERK signaling

3795- CUR,    Curcumin: A Golden Approach to Healthy Aging: A Systematic Review of the Evidence
- Review, AD, NA
*antiOx↑, Curcumin, a natural compound with potent antioxidant and anti-inflammatory properties
*Inflam↓,
*AntiAge↑, Its potential anti-aging properties are due to its power to alter the levels of proteins associated with senescence, such as adenosine 5′-monophosphate-activated protein kinase (AMPK) and sirtuins
*AMPK↑,
*SIRT1↑,
*NF-kB↓, preventing pro-aging proteins, such as nuclear factor-kappa-B (NF-κB) and mammalian target of rapamycin (mTOR)
*mTOR↓,
*NLRP3↓, Moreover, curcumin, by inhibiting the NF-κB pathway, can directly restrain the assembly or even inhibit the activation of the NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome
*NADPH↓, by inhibiting nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and elevating the activity of antioxidant enzymes and consequently lowering reactive oxygen species (ROS)
*ROS↓,
*COX2↓, (COX-2), granulocyte colony-stimulating factor (G-CSF), and monocyte chemotactic protein-1 (MCP-1) can be decreased by curcumin
*MCP1↓,
*IL1β↓, by decreasing IL-1β, IL-17, IL-23, TNF-α, and myeloperoxidase, enhancing levels of IL-10, and downregulating activation of NF-κB
*IL17↓,
*IL23↓,
*TNF-α↓,
*MPO↓,
*IL10↑,
*lipid-P↓, curcumin showed a significant decline in lipid peroxidation and increased superoxide dismutase levels, in addition to a reduction in Aβ aggregation and tau hyperphosphorylation through the regulation of GSK3β, Cdk5, p35, and p25
*SOD↑,
*Aβ↓,
*p‑tau↓,
*GSK‐3β↓,
*CDK5↓,
*TXNIP↓, Curcumin also has an inhibitory role on the thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome pathway
*NRF2↑, well as upregulation of Nrf2, NAD(P)H quinine oxidoreductase 1 (NQO1), HO-1, and γ-glutamyl cysteine synthetase (γ-GCS) in brain cells.
*NQO1↑,
*HO-1↑,
*OS↑, significant improvement in OS, and a positive evolution in memory and spatial learning
*memory↑,
*BDNF↑, Besides that, it promoted neurogenesis through increasing brain-derived neurotrophic factor (BDNF) levels
*neuroP↑, Curcumin can promote neuroprotection
*BACE↓, Figure 7
*AChE↓, figure 7
*LDL↓, and reduced total cholesterol and LDL levels.

2654- CUR,    Oxidative Stress Inducers in Cancer Therapy: Preclinical and Clinical Evidence
- Review, Var, NA
ROS↑, ROS induction has been implicated as one of the mechanisms of the anticancer activity of curcumin and its derivatives in various cancers
Catalase↓, Curcumin induces ROS by inhibiting the activity of various ROS-related metabolic enzymes, such as CAT, SOD1, glyoxalase 1, and NAD(P)H dehydrogenase [quinone] 1 [146,149]
SOD1↓,
GLO-I↓,
NADPH↓,
TumCCA↑, ROS accumulation further mediates G1 or G2/M cell cycle arrest [146,147,150,154], senescence [146], and apoptosis.
Apoptosis↑,
Akt↓, downregulation of AKT phosphorylation [145
ER Stress↑, endoplasmic reticulum stress (namely through the PERK–ATF4–CHOP axis)
JNK↑, activation of the JNK pathway [151],
STAT3↓, and inhibition of STAT3 [155].
BioAv↑, Additionally, the combination of curcumin and piperine, a pro-oxidative phytochemical that drastically increases the bioavailability of curcumin in humans

1854- dietFMD,    How Far Are We from Prescribing Fasting as Anticancer Medicine?
- Review, Var, NA
ChemoSideEff↓, ample nonclinical evidence indicating that fasting can mitigate the toxicity of chemotherapy and/or increase the efficacy of chemotherapy.
ChemoSen↑, Fasting-Induced Increase of the Efficacy of Chemotherapy
IGF-1↓,
IGFBP1↑, biological activity of IGF-1 is further compromised due to increased levels of insulin-like growth factor binding protein 1 (IGFBP1)
adiP↑, increased levels of adiponectin stimulate the fatty acid breakdown.
glyC↓, After depletion of stored glycogen, which occurs usually 24 h after initiation of fasting, the fatty acids serve as the main fuels for most tissues
E-cadherin↑, upregulation of E-cadherin expression via activation of c-Src kinase
MMPs↓, decrease of cytokines, chemokines, metalloproteinases, growth factors
Casp3↑, increase of level of activated caspase-3
ROS↑, it is postulated that the beneficial effects of fasting are ascribed to rapid metabolic and immunological response, triggered by a temporary increase in oxidative free radical production
ATP↓, Glucose deprivation leads to ATP depletion, resulting in ROS accumulation
AMPK↑, Additionally, ROS activate AMPK
mTOR↓, Under conditions of glucose deprivation, AMPK inhibits mTORC1
ROS↑, Beyond glucose deprivation, another mechanism increasing ROS levels is the AA (amino acids) starvation
Glycolysis↓, Indeed, in cancer cells, limited glucose sources impair glycolysis, decrease glycolysis-based NADPH production due to reduced utilization of the pentose phosphate pathway [88,89,90,91],
NADPH↓,
OXPHOS↝, and shift the metabolism from glycolysis to oxidative phosphorylation (OXPHOS) (“anti-Warburg effect”), leading to ROS overload [92,93,94,95].
eff↑, Fasting compared to long-term CR causes a more profound decrease in insulin (90% versus 40%, respectively) and blood glucose (50% versus 25%, respectively).
eff↑, FMD have been demonstrated to result in alterations of the serum levels of IGF-I, IGFBP1, glucose, and ketone bodies reminiscent of those observed in fasting
*RAS↓, A plausible explanation of the differential protective effect of fasting against chemotherapy is the attenuation of the Ras/MAPK and PI3K/Akt pathways downstream of decreased IGF-1 in normal cells
*MAPK↓,
*PI3K↓,
*Akt↓,
eff↑, Starvation combined with cisplatin has been shown in vitro to protect normal cells, promoting complete arrest of cellular proliferation mediated by p53/p21 activation in AMPK-dependent and ATM-independent manner
ROS↑, generation of ROS due to paradoxical activation of the AKT/S6K, partially via the AMPK-mTORC1 energy-sensing pathways malignant cells
Akt↑, cancer cells
Casp3↑, combination of fasting and chemotherapy was in part ascribed to enhanced apoptosis due to activation of caspase 3

1955- GamB,    Gambogic acid inhibits thioredoxin activity and induces ROS-mediated cell death in castration-resistant prostate cancer
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP - in-vitro, Pca, DU145
ROS↑, GA disrupted cellular redox homeostasis, observed as elevated reactive oxygen species (ROS), leading to apoptotic and ferroptotic death.
Apoptosis↑,
Ferroptosis↑,
Trx↓, GA inhibited thioredoxin
eff↑, Auranofin (AUR), a thioredoxin reductase (TrxR) inhibitor was the one compound that demonstrated additive growth inhibition together with GA when both were combined at sub-thresh hold concentrations
TrxR↓, GA may inhibit the thioredoxin (Trx) system, which mainly composes NADPH, TrxR, and Trx.
Dose∅, GA demonstrated sub-micromolar activity (IC50 = 185nM) which was 50 times more potent than the next most active compounds, curcumin and tanshinone (CT)
MMP↓, GA treatment showed increasing loss of membrane polarity at 4 and 6 hours in PCAP-1 cells
eff↑, GA enhanced the cell killing observed for either docetaxel (DOX) or enzalutamide (ENZA)
Casp↑, These results suggest that GA initiates CASP-dependent death of PCAP-1 cells and that both iron-dependent oxidative injury and direct CASP activation contribute
NADPH↓, These results suggest that GA may inhibit the thioredoxin (Trx) system, which mainly composes NADPH, TrxR, and Trx.
TrxR↓,
ChemoSen↑, potential use of GA in combination with standard chemotherapeutic (docetaxel) and anti-androgen endocrine (enzalutamide) therapies for advanced PrCa.
AR↓, inhibit PrCa growth, in part by inhibiting AR signaling

2515- H2,    Recent Advances in Studies of Molecular Hydrogen against Sepsis
- Review, Sepsis, NA
*Sepsis↓, Molecular hydrogen exerts multiple biological effects involving anti-inflammation, anti-oxidation, anti-apoptosis, anti-shock, and autophagy regulation, which may attenuate the organ and barrier damage caused by sepsis.
*Inflam↓,
*antiOx↑,
*ROS↓, Studies have demonstrated that HRS reduces ROS production and attenuates mitochondrial dysfunction by inhibiting NADPH oxidase activity in rat cardiomyocytes
*NADPH↓,

2508- H2,    Molecular hydrogen is a promising therapeutic agent for pulmonary disease
- Review, Var, NA - Review, Sepsis, NA
*ROS↓, inhalation of 2% molecular hydrogen results in the selective scavenging of hydroxyl free radical (·OH) and peroxynitrite anion (ONOO-), significantly improving oxidative stress injury caused by cerebral ischemia/reperfusion (I/R)
eff↝, Molecular hydrogen can exert biological effects on almost all organs, including the brain, heart, lung, liver, and pancreas.
*Inflam↓, including roles in the regulation of oxidative stress and anti-inflammatory and anti-apoptotic effects
*NRF2↑, By stimulating nuclear factor erythroid 2-related factor 2 (Nrf2), which regulates the basal and induces expression of many antioxidant enzymes
*HO-1↑, hydrogen can increase the expression of heme oxygenase-1 (HO-1)
*SOD↑, increases the activity of the antioxidant enzymes SOD, CAT, and myeloperoxidase (MPO)
*Catalase↑,
*MPO↑,
*ASK1↓, Molecular hydrogen can block the apoptosis signal-regulating kinase 1 (ASK1) signaling pathway
*NADPH↓, thereby inhibiting nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity and decreasing free radical production
*Sepsis↓, Emerging evidence suggests that hydrogen can prevent sepsis, providing a novel treatment strategy for sepsis-induced ALI.
*HMGB1↓, Hydrogen attenuates tissue injury and dysfunction by inhibiting HMGB-1.
ROS↑, it has been shown that hydrogen pretreatment enhances ROS and the expression of pyroptosis-related proteins, stimulates NLRP3 inflammasome/gasdermin D (GSDMD) activation, and inhibits endometrial cancer
NLRP3↑,
GSDMD↑,
chemoP↑, Hydrogen can alleviate the side effects of conventional anti-cancer therapies, such as chemotherapy and radiotherapy, and improve quality of life
eff↑, It significantly improves the physical status of patients, reduces fatigue, insomnia, anorexia, and pain, and decreases elevated tumor markers.

3770- H2,    Role of Molecular Hydrogen in Ageing and Ageing-Related Diseases
- Review, AD, NA - Review, Park, NA
*antiOx↑, antioxidative properties as it directly neutralizes hydroxyl radicals and reduces peroxynitrite level
*NRF2↑, activates Nrf2 and HO-1, which regulate many antioxidant enzymes and proteasomes.
*HO-1↑,
*Inflam↓, hydrogen may prevent inflammation
*neuroP↑, prevention and treatment of various ageing-related diseases, such as neurodegenerative disorders, cardiovascular disease, pulmonary disease, diabetes, and cancer.
*cardioP↑,
*other↓, It also prevented ischemia-reperfusion (I/R) injury and stroke in a rat model
*ROS↓, H2 has been shown to exert its beneficial effects in various pathological conditions that involve free radicals and oxidative stress
*NADPH↓, figure 2, H2 Inhibits NADPH Oxidase Activity
*Catalase↑,
*GPx1↑,
*NO↓, H2 Indirectly Reduces Nitric Oxide (NO) Production
*mt-ROS↓, H2 Decreases Mitochondrial ROS
*SIRT3↑, In the kidneys, H2 suppressed the downregulated Sirt3 expression, which is the most abundant member of the sirtuin family, by reducing oxidative stress reactions
*SIRT1↑, In the liver, H2 elevated HO-1 to induce Sirt1 expression
*TLR4↓, H2 inhibits TLR4, which involves hyperglycemia in type 2 diabetes mellitus
*mTOR↓, For example, H2 inhibits mTOR, activates autophagy, and alleviates cognitive impairment resulting from sepsis
*cognitive↑,
*Sepsis↓,
*PTEN↓, It inhibits the activation of the PTEN/AKT/mTOR pathway and alleviates peritoneal fibrosis
*Akt↓,
*NLRP3↓, It also facilitates autophagy-mediated NLRP3 inflammasome inactivation and alleviates mitochondrial dysfunction and organ damage
*AntiAg↑, antiageing mechanism of H2 and the influence on ageing hallmarks are summarized in Figure 3.
*IL6↓, significantly suppressed inflammatory cytokines (IL-6, TNF-α, and IL-1β), MDA, and 8-OHdG, and improved memory dysfunction
*TNF-α↓,
*IL1β↓,
*MDA↓,
*memory↑,
*FOXO3↑, HRW can also upregulate Sirt1-Forkhead box protein O3a (FOXO3a
TumCG↓, H2 inhibits lung cancer progression
*LDL↓, Decreases oxidized LDL; improves HDL function

3773- H2,    Role and mechanism of molecular hydrogen in the treatment of Parkinson’s diseases
- Review, Park, NA
*neuroP↑, potential neuroprotective effects, attributed to its selective antioxidant and anti-inflammatory properties.
*antiOx↑,
*Inflam↓,
*ROS↓, potential of molecular hydrogen to attenuate oxidative stress,
*NADPH↓, via the inhibition of NADPH oxidase activity
*NRF2↑, it also enhances the endogenous defense system by modulating the Nrf2/ARE pathway.
*BBB↑, easily penetrate the blood–brain barrier
*IL1β↓, H₂ significantly reduces the release of pro-inflammatory factors, including IL-1β, IL-6, TNF-α, NF-κB, and HMGB1,
*IL6↓,
*TNF-α↓,
*NF-kB↓,
*NLRP3↓, hydrogen can mitigate neuroinflammation by inhibiting the NLRP3 inflammasome pathway
*Sepsis↓, hydrogen intervention in sepsis models
*p‑mTOR↓, inhibits the phosphorylation level of mTOR (indicated by a decrease in the p-mTOR/mTOR ratio) while activating the AMPK s
*AMPK↑,
*SIRT1↑, hydrogen-rich water alleviates intestinal oxidative stress by upregulating the expression of SIRT1, Nrf2, and HO-1
*HO-1↑,

2868- HNK,    Honokiol: A review of its pharmacological potential and therapeutic insights
- Review, Var, NA - Review, Sepsis, NA
*P-gp↓, reduction in the expression of defective proteins like P-glycoproteins, inhibition of oxidative stress, suppression of pro-inflammatory cytokines (TNF-α, IL-10 and IL-6),
*ROS↓,
*TNF-α↓,
*IL10↓,
*IL6↓,
eIF2α↑, Bcl-2, phosphorylated eIF2α, CHOP,GRP78, Bax, cleaved caspase-9 and phosphorylated PERK
CHOP↑,
GRP78/BiP↑,
BAX↑,
cl‑Casp9↑,
p‑PERK↑,
ER Stress↑, endoplasmic reticulum stress and proteins in apoptosis in 95-D and A549 cells
Apoptosis↑,
MMPs↓, decrease in levels of matrix metal-mloproteinases, P-glycoprotein expression, the formation of mammosphere, H3K27 methyltransferase, c-FLIP, level of CXCR4 receptor,pluripotency-factors, Twist-1, class I histone deacetylases, steroid receptor co
cFLIP↓,
CXCR4↓,
Twist↓,
HDAC↓,
BMPs↑, enhancement in Bax protein, and (BMP7), as well as interference with an activator of transcription 3 (STAT3), (mTOR), (EGFR), (NF-kB) and Shh
p‑STAT3↓, secreased the phosphorylation of STAT3
mTOR↓,
EGFR↓,
NF-kB↓,
Shh↓,
VEGF↓, induce apoptosis, and regulate the vascular endothelial growth factor-A expression (VEGF-A)
tumCV↓, human glioma cell lines (U251 and U-87 MG) through inhibition of colony formation, glioma cell viability, cell migration, invasion, suppression of ERK and AKT signalling cascades, apoptosis induction, and reduction of Bcl-2 expression.
TumCMig↓,
TumCI↓,
ERK↓,
Akt↓,
Bcl-2↓,
Nestin↓, increased the Bax expression, lowered the CD133, EGFR, and Nesti
CD133↓,
p‑cMET↑, HKL through the downregulating the phosphorylation of c-Met phosphorylation and stimulation of Ras,
RAS↑,
chemoP↑, Cheng and coworker determined the chemopreventive role of HKL against the proliferation of renal cell carcinoma (RCC) 786‑0 cells through multiple mechanism
*NRF2↑, , HKL also effectively activate the Nrf2/ARE pathway and reverse this pancreatic dysfunction in in vivo and in vitro model
*NADPH↓, (HUVECs) such as inhibition of NADPH oxidase activity, suppression of p22 (phox) protein expression, Rac-1 phosphorylation, reactive oxygen species production, inhibition of degradation of Ikappa-B-alpha, and suppression of activity of of NF-kB
*p‑Rac1↓,
*ROS↓,
*IKKα↑,
*NF-kB↓,
*COX2↓, Furthermore, HKL treatment the inhibited cyclooxygenase (COX-2) upregulation, reduces prostaglandin E2 production, enhanced caspase-3 activity reduction
*PGE2↓,
*Casp3↓,
*hepatoP↑, compound also displayed hepatoprotective action against oxidative injury in tert-butyl hydroperoxide (t-BHP)-injured AML12 liver cells in in vitro model
*antiOx↑, compound reduces the level of acetylation on SOD2 to stimulate its antioxidative action, which results in reduced reactive oxygen species aggregation in AML12 cells
*GSH↑, HKL prevents oxidative damage induced by H2O2 via elevating antioxidant enzymes levels which includes glutathione and catalase and promotes translocation and activation transcription factor Nrf2
*Catalase↑,
*RenoP↑, imilarly, the compound protects renal reperfusion/i-schemia injury (IRI) in adult male albino Wistar rats via reducing theactivities of serum alkaline phosphatase (ALP), aspartate aminotrans- ferase (AST) and alanine aminotransferase (ALT)
*ALP↓,
*AST↓,
*ALAT↓,
*neuroP↑, Several reports and works have shown that HKL displays some neuroprotective properties
*cardioP↑, Cardioprotection
*HO-1↑, the expression level of heme oxygenase-1 (HO-1)was remarkably up-regulated and miR-218-5p was significantly down-regulated in septic mice treated with HKL
*Inflam↓, anti-inflammatory action of HKL at dose of 10 mg/kg in the muscle layer of mice

2891- HNK,    Honokiol, an Active Compound of Magnolia Plant, Inhibits Growth, and Progression of Cancers of Different Organs
- Review, Var, NA
AntiCan↑, honokiol possesses anti-carcinogenic, anti-inflammatory, anti-oxidative, anti-angiogenic as well as inhibitory effect on malignant transformation of papillomas to carcinomas in vitro and in vivo animal models without any appreciable toxicity.
Inflam↓,
antiOx↑,
selectivity↑,
*toxicity↓,
cycD1/CCND1↓, honokiol resulted in inhibition of UVB-induced expression levels of cyclins (cyclins D1, D2, and E) and CDKs in skin tumors
cycE/CCNE↓,
CDK2↓,
CDK4↓,
TumMeta↓, Honokiol Inhibits Metastatic Potential of Melanoma Cells
NADPH↓, Honokiol not only reduces the NADPH oxidase activity
MMP2↓, honokiol treatment reduces the expression of MMP-2 and MMP-9
MMP9↓,
p‑mTOR↓, honokiol caused significant downregulation of mTOR phosphorylation
EGFR↓, honokiol decreases the expression levels of total EGFR
EMT↓, honokiol effectively inhibits EMT in breast cancer cells
SIRT1↑, onokiol increases the expressions of SIRT1 and SIRT3,
SIRT3↑,
EZH2↓, depletion of EZH2 by honokiol treatment inhibited cell proliferation
Snail↓, significantly down regulates Snail, vimentin, N-cadherin expression, and upregulates cytokeratin-18 and E-cadherin expression
Vim↓,
N-cadherin↓,
E-cadherin↑,
COX2↓, honokiol as an inhibitor of COX-2 expression
NF-kB↓, inhibited transcriptional activity of NF-jB,
*ROS↓, Inhibition of UVR-induced inflammatory mediators as well as ROS by honokiol treatment contributes to the prevention of UVR-induced skin tumor development
Ca+2↑, excessive influx of cytosolic calcium ion into the mitochondria triggers dysfunction of the mitochon- drial membrane permeabilization with mitochondrial ROS induction
ROS↑,

4209- Hup,    Huperzine A, reduces brain iron overload and alleviates cognitive deficit in mice exposed to chronic intermittent hypoxia
- in-vivo, NA, NA
*ROS↓, HuA improves synaptic plasticity and decreases ROS level in CIH mice
*cognitive↑, HuA significantly improved cognitive impairment and neuronal damage in the hippocampus of CIH mice via increasing the ratio of Bcl-2/Bax and inhibiting caspase-3 cleavage.
*neuroP↑,
*Bax:Bcl2↓,
*Casp3↑,
*NADPH↓, HuA considerably decreased ROS levels by downregulating the high levels of NADPH oxidase (NOX 2, NOX 4) mediated by CIH.
*NOX↓,
*TfR1/CD71↓, Decreased levels of TfR1 and FTL proteins observed in HuA treated CIH group, could reduce iron overload in hippocampus. HuA increased PSD 95 protein expression, CREB activation and BDNF protein expression
*Iron↓,
*PSD95↑,
*BDNF↑,

2540- M-Blu,    Alternative mitochondrial electron transfer for the treatment of neurodegenerative diseases and cancers: Methylene blue connects the dots
- Review, Var, NA - Review, AD, NA
*OCR↑, MB was found to increase oxygen consumption of normal tissues having aerobic glycolysis and of tumors
*Glycolysis↓, Methylene blue increases oxygen consumption, decrease glycolysis, and increases glucose uptake in vitro.
*GlucoseCon↑, Methylene blue enhances glucose uptake and regional cerebral blood flow in rats upon acute treatment.
neuroP↑, methylene blue provides protective effect in neuron and astrocyte against various insults in vitro and in rodent models of Alzheimer’s, Parkinson’s, and Huntington’s disease.
Warburg↓, In glioblastoma cells, methylene blue reverses Warburg effect by enhancing mitochondrial oxidative phosphorylation, arrests glioma cell cycle at s-phase, and inhibits glioma cell proliferation.
mt-OXPHOS↑,
TumCCA↑,
TumCP↓,
ROS⇅, MB has very unique redox property that exists in equilibrium between oxidized state in dark blue (MB) and colorless reduced state (leucomethylene blue), making it both prooxidant and antioxidant under different conditions.
*cognitive↑, Methylene blue feeding improved water-maze and bridge walking performance in 5 X FAD mice. MB enhances memory function in normal rodents potentially through neurometabolic mechanisms
*mTOR↓, MB has been demonstrated to induce autophagy and attenuate tauopathy through inhibition of mTOR signaling both in vitro and in vivo
*mt-antiOx↑, Secondly, the distinct redox property enables MB as a regenerable anti-oxidant in mitochondria that distinct from the traditional free radical scavenges
*memory↑, , MB has been found to improve various experimental memory tasks in rodents
*BBB↑, MB can cross BBB and reach brain at concentrations 10 times higher than that in the circulation
*eff↝, In fibroblast cells, MB has been shown to stimulate 2-deoxyglucose uptake (Louters et al., 2006; Roelofs et al., 2006). Using MRI and PET, we demonstrated that acute treatment of MB significantly enhance glucose uptake
*ECAR↓, MB increased oxygen consumption rate and decreased extracellular acidification rate in both neuronal cells and astrocytes
eff↑, MB has also been used as a tracer for cancer diagnosis and as a photosensitizer for cancer treatment
lactateProd↓, MB increase oxygen consumption rate, decrease lactic acid production and extracellular acidification rate, reduce NADPH, and inhibit proliferation
NADPH↓,
OXPHOS↑, increases oxidative phosphorylation, decreases glycolytic flux and metabolic intermediates, hence, exhausts the building brick for cancer cell proliferation.
AMPK↑, MB is capable of activating AMPK signal pathway
selectivity↑, with low toxicity, and the high affinity to both neuronal and cancer tissues

3927- PTS,    Effects of Pterostilbene on Cardiovascular Health and Disease
- Review, AD, NA - Review, Stroke, NA
*Inflam↓, remarkable anti-inflammatory and antioxidant effects.
*antiOx↑,
*BioAv↑, high bioavailability and low toxicity in many species has contributed to its promising research prospects.
*toxicity↓,
*NADPH↓, Pterostilbene significantly down-regulates nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX),
*ROS↓, which is the key enzyme family that induces the release of reactive oxygen species (ROS)
*Catalase↑, pterostilbene treatment as it increases the expression levels of catalase (CAT), glutathione (GSH), superoxide dismutase (SOD), and other antioxidants in diabetic rats [
*GSH↑,
*SOD↑,
*TNF-α↓, (tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-4), matrix metalloproteinases (MMPs), and cyclooxygenase (COX)-2 are all suppressed by pterostilbene treatment.
*IL1β↓,
*IL4↓,
*MMPs↓,
*COX2↓,
*MAPK↝, anti-inflammatory action of pterostilbene has been proved to be associated with modulating mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) pathways
*NF-kB↓,
*IL8↓, pterostilbene can successfully reverse the elevation of related pro-inflammatory cytokines (IL-8, monocyte chemoattractant protein (MCP)-1, and E-selectin)
*MCP1↓,
*E-sel↓,
*lipid-P↓, Pterostilbene has been demonstrated to reduce lipid peroxidation by regulating the expression of Nrf2, exhibiting anti-peroxidation and anti-hyperlipidemic effects
*NRF2↑,
*PPARα↑, Pterostilbene acts as a potent PPAR-α agonist
*LDL↓, pterostilbene could effectively reduce the plasma low-density lipoprotein (LDL) cholesterol levels of hamsters by 29% and increase the plasma high-density lipoprotein (HDL) cholesterol levels by almost 7%
other↓, Ability to Protect against Stroke

3347- QC,    Recent Advances in Potential Health Benefits of Quercetin
- Review, Var, NA - Review, AD, NA
*antiOx↑, Its strong antioxidant properties enable it to scavenge free radicals, reduce oxidative stress, and protect against cellular damage.
*ROS↓,
*Inflam↓, Quercetin’s anti-inflammatory properties involve inhibiting the production of inflammatory cytokines and enzymes,
TumCP↓, exhibits anticancer effects by inhibiting cancer cell proliferation and inducing apoptosis.
Apoptosis↑,
*cardioP↑, cardiovascular benefits such as lowering blood pressure, reducing cholesterol levels, and improving endothelial function
*BP↓, Quercetin‘s ability to reduce blood pressure was also supported by a different investigation
TumMeta↓, The most important impact of quercetin is its ability to inhibit the spread of certain cancers including those of the breast, cervical, lung, colon, prostate, and liver
MDR1↓, quercetin decreased the expression of genes multidrug resistance protein 1 and NAD(P)H quinone oxidoreductase 1 and sensitized MCF-7 cells to the chemotherapy medication doxorubicin
NADPH↓,
ChemoSen↑,
MMPs↓, Inhibiting CT26 cells’ migration and invasion abilities by inhibiting their expression of tissue inhibitors of metalloproteinases (TIMPs) inhibits their invasion and migration abilities
TIMP2↑,
*NLRP3↓, inhibited NLRP3 by acting on this inflammasome
*IFN-γ↑, quercetin significantly upregulates the gene expression and production of interferon-γ (IFN-γ), which is obtained from T helper cell 1 (Th1), and downregulates IL-4, which is obtained from Th2.
*COX2↓, quercetin is known to decrease the production of inflammatory molecules COX-2, nuclear factor-kappa B (NF-κB), activator protein 1 (AP-1), mitogen-activated protein kinase (MAPK), reactive nitric oxide synthase (NOS), and reactive C-protein (CRP)
*NF-kB↓,
*MAPK↓,
*CRP↓,
*IL6↓, Quercetin suppressed the production of inflammatory cytokines such as IL-6, TNF-α, and IL-1β via upregulating TLR4.
*TNF-α↓,
*IL1β↓,
*TLR4↑,
*PKCδ↓, Quercetin employed suppression on the phosphorylation of PKCδ to control the PKCδ–JNK1/2–c-Jun pathway.
*AP-1↓, This pathway arrested the accumulation of AP-1 transcription factor in the target genes, thereby resulting in reduced ICAM-1 and inflammatory inhabitation
*ICAM-1↓,
*NRF2↑, Quercetin overexpressed Nrf2 and targeted its downstream gene, contributing to increased HO-1 levels responsible for the down-regulation of TNF-α, iNOS, and IL-6
*HO-1↑,
*lipid-P↓, Quercetin acts as a potent antioxidant by scavenging ROS, inhibiting lipid peroxidation, and enhancing the activity of antioxidant enzymes
*neuroP↑, This helps to counteract oxidative stress and protect against neurodegenerative processes that contribute to AD
*eff↑, rats treated with chronic rotenone or 3-nitropropionic acid showed enhanced neuroprotection when quercetin and fish oil were taken orally
*memory↑, Both memory and learning abilities in the test animals increased
*cognitive↑,
*AChE↓, The increase in AChE activity brought on by diabetes was prevented in the cerebral cortex and hippocampus by quercetin at a level of 50 mg/kg body weight.
*BioAv↑, consumption of fried onions compared to black tea, suggesting that the form of quercetin present in onions is better absorbed than that in tea
*BioAv↑, This suggests that dietary fat can increase the absorption of quercetin [180]
*BioAv↑, potential of liposomes to enhance the bioactivity and bioavailability of quercetin has been the subject of several investigations
*BioAv↑, several emulsion types that may be employed to encapsulate quercetin, but oil-in-water (O/W) emulsions are the most widely utilized.
*BioAv↑, the kind of oil (triglyceride oils made up of either long-chain or medium-chain fatty acids) affected the bioaccessibility of quercetin and gastrointestinal stability, emphasizing the significance of picking a suitable oil phase

3336- QC,    Neuroprotective Effects of Quercetin in Alzheimer’s Disease
- Review, AD, NA
*neuroP↑, Neuroprotection by quercetin has been reported in several in vitro studies
*lipid-P↓, It has been shown to protect neurons from oxidative damage while reducing lipid peroxidation.
*antiOx↑, In addition to its antioxidant properties, it inhibits the fibril formation of amyloid-β proteins, counteracting cell lyses and inflammatory cascade pathways.
*Aβ↓,
*Inflam↓,
*BBB↝, It also has low BBB penetrability, thus limiting its efficacy in combating neurodegenerative disorders.
*NF-kB↓, downregulating pro-inflammatory cytokines, such as NF-kB and iNOS, while stimulating neuronal regeneration
*iNOS↓,
*memory↑, Quercetin has shown therapeutic efficacy, improving learning, memory, and cognitive functions in AD
*cognitive↑,
*AChE↓, Quercetin administration resulted in the inhibition of AChE
*MMP↑, quercetin ameliorates mitochondrial dysfunction by restoring mitochondrial membrane potential, decreases ROS production, and restores ATP synthesis
*ROS↓,
*ATP↑,
*AMPK↑, It also increased the expression of AMP-activated protein kinase (AMPK), which is a key cell regulator of energy metabolism.
*NADPH↓, Activated AMPK can decrease ROS generation by inhibiting NADPH oxidase activity
*p‑tau↓, Inhibition of AβAggregation and Tau Phosphorylation

3338- QC,    Quercetin: Its Antioxidant Mechanism, Antibacterial Properties and Potential Application in Prevention and Control of Toxipathy
- Review, Var, NA - Review, Stroke, NA
*antiOx↑, The antioxidant mechanism of quercetin in vivo is mainly reflected in its effects on glutathione (GSH), signal transduction pathways, reactive oxygen species (ROS), and enzyme activities.
*GSH↑,
*ROS↓,
*Dose↑, antioxidant properties of quercetin show a concentration dependence in the low dose range but too much of the antioxidant brings about the opposite result
*NADPH↓, quercetin counteracts atherosclerosis by reversing the increased expression of NADPH oxidase i
*AMP↓, decreases in activation of AMP-activated protein kinase, thereby inhibiting NF-κB signaling
*NF-kB↓,
*p38↑, quercetin improves the antioxidant capacity of cells by activating the intracellular p38 MAPK pathway, increasing intracellular GSH levels and providing a source of hydrogen donors in the scavenging of free radical reactions.
*MAPK↑,
*SOD↑, quercetin achieves protection against acute spinal cord injury by up-regulating the activity of SOD, down-regulating the level of malondialdehyde (MDA), and inhibiting the p38MAPK/iNOS signaling pathway
*MDA↓,
*iNOS↓,
*Catalase↑, quercetin reduces imiquimod (IMQ)-induced MDA levels in skin tissues and enhances catalase, SOD, and GSH activities, which together improve the antioxidant properties of the body
*PI3K↑, It also controls the development of atherosclerosis induced by high fructose diet by enhancing PI3K/AKT and inhibiting ROS
*Akt↑,
*lipid-P↓, Quercetin enhances antioxidant activity and inhibits lipid cultivation, and it is effective in the treatment of oxidative liver damag
*memory↑, reversed hypoxia-induced memory impairment
*radioP↑, Quercetin protects cells from radiation and genotoxicity-induced damage by increasing endogenous antioxidant and scavenging free radical levels
*neuroP↑, This suggests that quercetin may be a potential neuroprotective agent against ischemia, which protects CA1 vertebral neurons from I/R injury in the hippocampal region of animals
*MDA↓, quercetin significantly reduced MDA levels and increased SOD and catalase levels.

3026- RosA,    Modulatory Effect of Rosmarinic Acid on H2O2-Induced Adaptive Glycolytic Response in Dermal Fibroblasts
- in-vitro, Nor, NA
*ROS↓, H2O2 caused a significant ROS increase in the cells, and pre-treatment with rosmarinic acid (5–50 µM) decreased ROS significantly in the presence of glutathione
*ATP↑, The rosmarinic acid also recovered intracellular ATP and decreased NADPH production via the pentose phosphate pathway.
*NADPH↓,
*HK2↓, (HK-2), phosphofructokinase-2 (PFK-2), and lactate dehydrogenase A (LDHA), were downregulated in cells treated with rosmarinic acid
*PFK2↓,
*LDHA↓,
*GSR↑, GSR), glutathione peroxidase-1 (GPx-1), and peroxiredoxin-1 (Prx-1) and redox protein thioredoxin-1 (Trx-1) were upregulated in treated cells compared to control cells.
*GPx↑,
*Prx↑,
*Trx↑,
*antiOx↑, To sum up, the rosmarinic acid could be used as an antioxidant against H2O2-induced adaptive responses in fibroblasts by modulating glucose metabolism, glycolytic genes, and GSH production.
*GSH↑, The pre-treatment of rosmarinic acid could raise intracellular GSH to protect cells from ROS
*ROS↓, rosmarinic acid pre-treatment reduced the amount of ROS in the fibroblasts upon the addition of H2O2
*GlucoseCon↓, both compounds also decreased glucose consumption and lactate production
*lactateProd↓,
*Glycolysis↝, The results indicated that rosmarinic acid is able to shape cellular glucose utilization, glycolysis, and GSH.
*ATP↑, The rosmarinic acid also recovered intracellular ATP and decreased NADPH production via the pentose phosphate pathway.
*NADPH↓,
*PPP↓,

4908- Sal,    Salinomycin triggers prostate cancer cell apoptosis by inducing oxidative and endoplasmic reticulum stress via suppressing Nrf2 signaling
- in-vitro, Pca, PC3 - in-vitro, Pca, DU145
tumCV↓, salinomycin inhibited the viability and induced the apoptosis of PC-3 and DU145 cells in a dose-dependent manner
ROS↑, salinomycin increased the production of reactive oxygen species (ROS) and 8-hydroxy-2'-deoxyguanosine (8-OH-dG) and the lipid peroxidation.
lipid-P↑,
UPR↑, salinomycin induced the activation of unfolded protein response and endoplasmic reticulum stress in DU145 and PC-3 cells
ER Stress↑,
NRF2↓, salinomycin significantly downregulated the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1, NAD(P)H quinone dehydrogenase 1
NADPH↓,
HO-1↓,
SOD↓, and decreased the activity of the antioxidant enzymes superoxide dismutase, catalase and glutathione peroxidase in PC-3 and DU145 cells.
Catalase↓,
GPx↓,
eff↓, Nrf2 activator, tert-butylhydroquinone, significantly reversed the therapeutic effects of salinomycin by stimulating the Nrf2 pathway and increasing the activity of antioxidant enzymes.
TumCP↓, proliferation of PC-3 and DU145 cells was significantly decreased following treatment with salinomycin (2-50 µM

3309- SIL,    Silymarin as a Natural Antioxidant: An Overview of the Current Evidence and Perspectives
- Review, NA, NA
*ROS↓, (1) Direct scavenging free radicals and chelating free Fe and Cu are mainly effective in the gut.
*IronCh↑,
*MMP↑, (2) Preventing free radical formation by inhibiting specific ROS-producing enzymes, or improving an integrity of mitochondria in stress conditions, are of great importance.
*NRF2↑, (3) Maintaining an optimal redox balance in the cell by activating a range of antioxidant enzymes and non-enzymatic antioxidants, mainly via Nrf2 activation
*Inflam↓, (4) Decreasing inflammatory responses by inhibiting NF-κB pathways is an emerging mechanism of SM protective effects in liver toxicity and various liver diseases.
*hepatoP↑,
*HSPs↑, (5) Activating vitagenes, responsible for synthesis of protective molecules, including heat shock proteins (HSPs), thioredoxin and sirtuins
*Trx↑,
*SIRT2↑, increased expression of protective molecules (GSH, Thioredoxins, heat shock proteins (HSPs), sirtuins, etc.)
*GSH↑,
*ROS↑, Similarly, production of O2− and NO in isolated rat Kupffer cells were inhibited by silibinin in a dose-dependent manner, with IC50 80 μM
*NADPH↓, It also decreased the NADPH oxidase, iNOS and NF-κB over expression by As and upregulated the Nrf2 expression in the renal tissue.
*iNOS↓,
*NF-kB↓,
*BioAv↓, active free silibinin concentration in plasma after oral consumption of SM, depending on dose of supplementation, could be in the range 0.2–2.0 μM.
*Dose↝, healthy volunteers, after an oral administration of SM (equivalent to 120 mg silibinin), total (unconjugated + conjugated) silibinin concentration in plasma was 1.1–1.3 μg/mL
*BioAv↑, For example, silibinin concentration in the gut could reach 800 μM

964- SIL,    Silibinin inhibits hypoxia-induced HIF-1α-mediated signaling, angiogenesis and lipogenesis in prostate cancer cells: In vitro evidence and in vivo functional imaging and metabolomics
- vitro+vivo, Pca, LNCaP - in-vitro, Pca, 22Rv1
TumCP↓,
Hif1a↓, strongly decreased hypoxia-induced HIF-1α expression
NADPH↓,
angioG↓,
FASN↓,
ACC↓,

5089- SSE,  Se,    Redox-mediated effects of selenium on apoptosis and cell cycle in the LNCaP human prostate cancer cell line
- in-vitro, Pca, LNCaP
ROS↑, Our results demonstrated that oxidative stress was induced by sodium selenite at high concentrations in both acute and chronic treatments, but outcomes were different.
mtDam↑, After acute exposure to selenite, cells exhibited mitochondrial injury and cell death, mainly apoptosis.
TumCD↑,
Apoptosis↑,
TumCCA↑, After chronic exposure to selenite, cells showed growth inhibition caused by cell cycle arrest, increased numbers of mitochondria and levels of mitochondrial enzymes, and only minimal induction of apoptosis
Trx↓, production of ROS, regulation of the Trx redox system, regulation of the cell cycle, and inhibition of angiogenes
angioG↓,
GSH⇅, intracellular levels of GSH were increased at doses of 0.5 and 1.5 uM selenite and decreased at doses of 2 and 2.5 uM selenite
NADPH↓, In addition, GSH and NADPH are consumed
GPx↑, GPX activities in the selenite-adapted cells were significantly increased (2- to 3-fold induction

5085- SSE,    Intravenous Infusion of High Dose Selenite in End-Stage Cancer Patients: Analysis of Systemic Exposure to Selenite and Seleno-Metabolites
- Review, Var, NA
toxicity↝, selenite is safe and tolerable with an unexpectable high maximum tolerated dose (MTD) and short half-life.
Half-Life↝, half-life was short (18.5 h)
ROS↑, Selenide efficiently redox cycles with oxygen, producing reactive oxygen species (ROS) until the system is exhausted of thiols and/or NADPH
Thiols↓,
NADPH↓,
toxicity↝, trimethylselenonium may serve as a urinary biomarker for both excessive selenium intake and body burden as well as a toxic dose of selenium
other↝, Selenoprotein P (SELENOP) is a proven biomarker of Se status

3431- TQ,    PI3K-AKT Pathway Modulation by Thymoquinone Limits Tumor Growth and Glycolytic Metabolism in Colorectal Cancer
- in-vitro, CRC, HCT116 - in-vitro, CRC, SW48
Glycolysis↓, we provide evidence that thymoquinone inhibits glycolytic metabolism (Warburg effect) in colorectal cancer cell lines.
Warburg↓,
HK2↓, was due, at least in part, to the inhibition of the rate-limiting glycolytic enzyme, Hexokinase 2 (HK2),
ATP↓, such reduction in glucose fermentation capacity also led to a significant reduction in overall ATP production as well as maintaining the redox state (NADPH production) of these cells
NADPH↓, showed a significant reduction in glucose fermentation, ATP and NADPH production rates
PI3K↓, reduction in HK2 levels upon TQ treatment coincided with significant inhibition in PI3K-AKT activation
Akt↓,
TumCP↓, Thymoquinone Inhibits Cell Migration and Invasion via Modulating Glucose Metabolic Reprogramming
E-cadherin↑, TQ was able to induce E-cadherin while inhibiting N-cadherin expression
N-cadherin↓,
Hif1a↓, TQ is reported to induce cell death in renal cell carcinoma [81] and pancreatic cancers [82] via inhibiting HIF1α and pyruvate kinase M2 (PKM2)-mediated glycolysis
PKM2↓,
GlucoseCon↓, TQ treatment inhibited the glucose uptake and subsequent lactate production in HCT116 and SW480 cells
lactateProd↓,
EMT↓, TQ inhibits cell proliferation, clonogenicity and epithelial-mesenchymal transition (EMT) in CRC cells (HCT116 and SW480)


Showing Research Papers: 1 to 34 of 34

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 34

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↓, 2,   Ferroptosis↑, 2,   frataxin↑, 1,   GPx↓, 1,   GPx↑, 1,   GPx4↓, 1,   GSH↓, 3,   GSH⇅, 1,   HK1↓, 1,   HO-1↓, 2,   lipid-P↑, 1,   NRF2↓, 2,   NRF2↑, 1,   OXPHOS↑, 1,   OXPHOS↝, 1,   mt-OXPHOS↑, 1,   ROS↑, 17,   ROS⇅, 1,   mt-ROS↑, 1,   SIRT3↑, 1,   SOD↓, 1,   SOD1↓, 1,   Thiols↓, 1,   Trx↓, 2,   TrxR↓, 2,  

Metal & Cofactor Biology ⓘ

Ferritin↓, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 5,   MMP↓, 1,   mtDam↑, 2,  

Core Metabolism/Glycolysis ⓘ

ACC↓, 1,   ACLY↓, 1,   adiP↑, 1,   ALDOA↓, 1,   AMPK↑, 4,   cMyc↓, 1,   ENO1↓, 1,   FASN↓, 2,   GLO-I↓, 1,   GLS↓, 1,   GlucoseCon↓, 1,   glyC↓, 1,   Glycolysis↓, 8,   HK2↓, 5,   lactateProd↓, 4,   LDH↓, 1,   e-LDH↑, 1,   NADPH↓, 19,   PDH↓, 1,   PFK↓, 1,   PGK1↓, 1,   PI3K/Akt↓, 1,   PKM2↓, 2,   PPP↓, 3,   SIRT1↑, 1,   TCA↓, 1,   Warburg↓, 2,  

Cell Death ⓘ

Akt↓, 3,   Akt↑, 1,   p‑Akt↓, 1,   Apoptosis↑, 8,   BAX↓, 1,   BAX↑, 3,   Bax:Bcl2↑, 1,   Bcl-2↓, 4,   Bcl-xL↓, 1,   Casp↑, 2,   Casp3↑, 5,   cl‑Casp3↑, 1,   Casp9↑, 2,   cl‑Casp9↑, 1,   cFLIP↓, 1,   Cyt‑c↑, 1,   Ferroptosis↑, 2,   GSDMD↑, 1,   JNK↑, 1,   Mcl-1↓, 1,   survivin↓, 1,   TumCD↑, 2,  

Transcription & Epigenetics ⓘ

EZH2↓, 1,   other↓, 1,   other↝, 2,   tumCV↓, 2,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   eIF2α↑, 1,   ER Stress↑, 3,   GRP78/BiP↑, 1,   p‑PERK↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes ⓘ

LC3II↑, 1,   p62↓, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   MGMT↓, 1,   p16↑, 1,   P53↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 2,   cycD1/CCND1↓, 3,   cycE/CCNE↓, 1,   TumCCA↑, 4,  

Proliferation, Differentiation & Cell State ⓘ

CD133↓, 1,   p‑cMET↑, 1,   CSCs↓, 1,   EMT↓, 4,   ERK↓, 2,   GSK‐3β↓, 1,   HDAC↓, 1,   IGF-1↓, 1,   IGFBP1↑, 1,   mTOR↓, 2,   p‑mTOR↓, 1,   Nestin↓, 1,   PI3K↓, 1,   RAS↑, 1,   Shh↓, 1,   STAT3↓, 1,   p‑STAT3↓, 1,   TumCG↓, 2,   Wnt↓, 1,  

Migration ⓘ

Ca+2↑, 1,   E-cadherin↑, 4,   FAK↓, 1,   ITGB1↓, 1,   ITGB3↓, 1,   MMP2↓, 3,   MMP9↓, 3,   MMPs↓, 4,   N-cadherin↓, 2,   Snail↓, 2,   TIMP2↑, 1,   TumCI↓, 2,   TumCMig↓, 2,   TumCP↓, 6,   TumMeta↓, 3,   Twist↓, 1,   uPA↓, 1,   Vim↓, 2,   Zeb1↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 4,   EGFR↓, 2,   Hif1a↓, 4,   VEGF↓, 2,  

Barriers & Transport ⓘ

GLUT1↓, 2,   GLUT3↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   CXCR4↓, 1,   IL8↓, 1,   Inflam↓, 2,   NF-kB↓, 4,  

Protein Aggregation ⓘ

NLRP3↑, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   BioAv↝, 1,   ChemoSen↑, 5,   Dose↝, 1,   Dose∅, 1,   eff↓, 4,   eff↑, 10,   eff↝, 2,   Half-Life↓, 2,   Half-Life↝, 1,   MDR1↓, 1,   RadioS↑, 1,   selectivity↑, 4,  

Clinical Biomarkers ⓘ

AR↓, 1,   BMPs↑, 1,   EGFR↓, 2,   EZH2↓, 1,   Ferritin↓, 1,   LDH↓, 1,   e-LDH↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 2,   AntiTum↑, 1,   chemoP↑, 3,   ChemoSideEff↓, 1,   neuroP↑, 1,   RenoP↑, 1,   toxicity↑, 1,   toxicity↝, 2,  
Total Targets: 182

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 13,   mt-antiOx↑, 1,   Catalase↑, 6,   Ferroptosis↓, 1,   GPx↑, 1,   GPx1↑, 1,   GSH↑, 5,   GSR↑, 1,   HO-1↑, 8,   Iron↓, 1,   lipid-P↓, 5,   MDA↓, 3,   MPO↓, 1,   MPO↑, 1,   NQO1↑, 1,   NRF2↑, 10,   Prx↑, 1,   ROS↓, 19,   ROS↑, 1,   mt-ROS↓, 1,   SIRT3↑, 1,   SOD↑, 5,   Trx↑, 2,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,   TfR1/CD71↓, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 3,   MMP↑, 2,   OCR↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   AMP↓, 1,   AMPK↑, 4,   ECAR↓, 1,   GlucoseCon↓, 1,   GlucoseCon↑, 1,   Glycolysis↓, 1,   Glycolysis↝, 1,   HK2↓, 1,   lactateProd↓, 1,   LDHA↓, 1,   LDL↓, 3,   NADPH↓, 16,   PFK2↓, 1,   PPARα↑, 1,   PPP↓, 1,   SIRT1↑, 4,   SIRT2↑, 1,  

Cell Death ⓘ

Akt↓, 2,   Akt↑, 1,   ASK1↓, 1,   Bax:Bcl2↓, 1,   Casp3↓, 1,   Casp3↑, 1,   Ferroptosis↓, 1,   iNOS↓, 3,   JNK↓, 1,   MAPK↓, 3,   MAPK↑, 1,   MAPK↝, 1,   p38↑, 1,   TRPV1↑, 1,  

Transcription & Epigenetics ⓘ

other↓, 1,  

Protein Folding & ER Stress ⓘ

HSPs↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

FOXO3↑, 1,   GSK‐3β↓, 1,   mTOR↓, 3,   p‑mTOR↓, 1,   PI3K↓, 1,   PI3K↑, 1,   PTEN↓, 1,   RAS↓, 1,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

AntiAg↑, 2,   AP-1↓, 1,   CDK5↓, 1,   E-sel↓, 1,   MMPs↓, 1,   PKCδ↓, 1,   p‑Rac1↓, 1,   TXNIP↓, 1,  

Angiogenesis & Vasculature ⓘ

eNOS↑, 1,   NO↓, 1,   TXA2↓, 1,  

Barriers & Transport ⓘ

BBB↑, 2,   BBB↝, 1,   P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 4,   CRP↓, 1,   HMGB1↓, 1,   ICAM-1↓, 1,   IFN-γ↑, 1,   IKKα↑, 1,   IL10↓, 1,   IL10↑, 1,   IL17↓, 1,   IL1β↓, 6,   IL23↓, 1,   IL4↓, 1,   IL6↓, 4,   IL8↓, 1,   Inflam↓, 13,   MCP1↓, 2,   NF-kB↓, 9,   PGE2↓, 1,   TLR4↓, 1,   TLR4↑, 1,   TNF-α↓, 7,  

Cellular Microenvironment ⓘ

NOX↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 3,   BDNF↑, 2,   PSD95↑, 1,   p‑tau↓, 2,  

Protein Aggregation ⓘ

Aβ↓, 2,   BACE↓, 1,   NLRP3↓, 4,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 3,   BioAv↑, 9,   BioAv↝, 2,   Dose↑, 1,   Dose↝, 1,   eff↑, 1,   eff↝, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   ALP↓, 1,   AST↓, 1,   BP↓, 2,   CRP↓, 1,   IL6↓, 4,  

Functional Outcomes ⓘ

AntiAge↑, 1,   AntiCan↑, 1,   cardioP↑, 5,   cognitive↑, 5,   hepatoP↑, 2,   memory↑, 6,   neuroP↑, 9,   OS↑, 1,   radioP↑, 1,   RenoP↑, 1,   toxicity↓, 3,  

Infection & Microbiome ⓘ

Bacteria↓, 1,   Sepsis↓, 4,  
Total Targets: 140

Scientific Paper Hit Count for: NADPH, Nicotinamide adenine dinucleotide phosphate
4 Hydrogen Gas
3 Quercetin
2 Curcumin
2 Honokiol
2 Silymarin (Milk Thistle) silibinin
2 Selenite (Sodium)
1 2-DeoxyGlucose
1 3-bromopyruvate
1 Alpha-Lipoic-Acid
1 Apigenin (mainly Parsley)
1 Artemisinin
1 brusatol
1 Brucea javanica
1 Caffeic acid
1 Metformin
1 Capsaicin
1 Carvacrol
1 Thymol-Thymus vulgaris
1 Chlorogenic acid
1 Chrysin
1 diet FMD Fasting Mimicking Diet
1 Gambogic Acid
1 Huperzine A/Huperzia serrata
1 Methylene blue
1 Pterostilbene
1 Rosmarinic acid
1 salinomycin
1 Selenium
1 Thymoquinone
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

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:624  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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