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⟱
3269- ALA,    Sulfur-containing therapeutics in the treatment of Alzheimer’s disease
- NA, AD, NA
*AChE↓, ALA activated AChE and increased glucose uptake, thus providing more acetyl-CoA to generate acetylcholine (ACh). (note activated AChE in this review likely should say inhibited!!!)
*GlucoseCon↑,
*ACC↑,
*GSH↑, ALA increased intracellular GSH levels by chelating redox-active transition metals, thus inhibiting the formation of hydroxyl radicals and Aβ aggregation.
*Aβ↓,
*Catalase↑, Levels of several antioxidant enzymes including catalase, GR, glutathione-S-transferase (GST), NADPH, and quinone oxidoreductase-1 (NQO1) were enhanced by ALA
*GSR↑,
*GSTs↑,
*NADPH↑,
*NQO1↑,
*iNOS↓, LA prevented the induction of iNOS, inhibited TNFα-induced activation of NF-κB [42], levels of which are increased in AD.
*NF-kB↓,
*lipid-P↓, ALA reduced the levels of lipid peroxidation products
*BBB↑, ALA could easily cross the blood–brain barrier (BBB)
*memory↑, ALA treatment significantly improved the spatial memory and cognition capacity of the mice in the Morris water maze and novel object recognition test.
*cognitive↑,
*antiOx↑, antioxidant and anti-inflammatory activities of ALA
*Inflam↓,

2639- Api,    Plant flavone apigenin: An emerging anticancer agent
- Review, Var, NA
*antiOx↑, Apigenin (4′, 5, 7-trihydroxyflavone), a major plant flavone, possessing antioxidant, anti-inflammatory, and anticancer properties
*Inflam↓,
AntiCan↑,
ChemoSen↑, Studies demonstrate that apigenin retain potent therapeutic properties alone and/or increases the efficacy of several chemotherapeutic drugs in combination on a variety of human cancers.
BioEnh↑, Apigenin’s anticancer effects could also be due to its differential effects in causing minimal toxicity to normal cells with delayed plasma clearance and slow decomposition in liver increasing the systemic bioavailability in pharmacokinetic studies.
chemoPv↑, apigenin highlighting its potential activity as a chemopreventive and therapeutic agent.
IL6↓, In taxol-resistant ovarian cancer cells, apigenin caused down regulation of TAM family of tyrosine kinase receptors and also caused inhibition of IL-6/STAT3 axis, thereby attenuating proliferation.
STAT3↓,
NF-kB↓, apigenin treatment effectively inhibited NF-κB activation, scavenged free radicals, and stimulated MUC-2 secretion
IL8↓, interleukin (IL)-6, and IL-8
eff↝, The anti-proliferative effects of apigenin was significantly higher in breast cancer cells over-expressing HER2/neu but was much less efficacious in restricting the growth of cell lines expressing HER2/neu at basal levels
Akt↓, Apigenin interferes in the cell survival pathway by inhibiting Akt function by directly blocking PI3K activity
PI3K↓,
HER2/EBBR2↓, apigenin administration led to the depletion of HER2/neu protein in vivo
cycD1/CCND1↓, Apigenin treatment in breast cancer cells also results in decreased expression of cyclin D1, D3, and cdk4 and increased quantities of p27 protein
CycD3↓,
p27↑,
FOXO3↑, In triple-negative breast cancer cells, apigenin induces apoptosis by inhibiting the PI3K/Akt pathway thereby increasing FOXO3a expression
STAT3↓, In addition, apigenin also down-regulated STAT3 target genes MMP-2, MMP-9, VEGF and Twist1, which are involved in cell migration and invasion of breast cancer cells [
MMP2↓,
MMP9↓,
VEGF↓, Apigenin acts on the HIF-1 binding site, which decreases HIF-1α, but not the HIF-1β subunit, thereby inhibiting VEGF.
Twist↓,
MMP↓, Apigenin treatment of HGC-27 and SGC-7901 gastric cancer cells resulted in the inhibition of proliferation followed by mitochondrial depolarization resulting in apoptosis
ROS↑, Further studies revealed apigenin-induced apoptosis in hepatoma tumor cells by utilizing ROS generated through the activation of the NADPH oxidase
NADPH↑,
NRF2↓, Apigenin significantly sensitized doxorubicin-resistant BEL-7402 (BEL-7402/ADM) cells to doxorubicin (ADM) and increased the intracellular concentration of ADM by reducing Nrf2-
SOD↓, In human cervical epithelial carcinoma HeLa cells combination of apigenin and paclitaxel significantly increased inhibition of cell proliferation, suppressing the activity of SOD, inducing ROS accumulation leading to apoptosis by activation of caspas
COX2↓, melanoma skin cancer model where apigenin inhibited COX-2 that promotes proliferation and tumorigenesis
p38↑, Additionally, it was shown that apigenin treatment in a late phase involves the activation of p38 and PKCδ to modulate Hsp27, thus leading to apoptosis
Telomerase↓, apigenin inhibits cell growth and diminishes telomerase activity in human-derived leukemia cells
HDAC↓, demonstrated the role of apigenin as a histone deacetylase inhibitor. As such, apigenin acts on HDAC1 and HDAC3
HDAC1↓,
HDAC3↓,
Hif1a↓, Apigenin acts on the HIF-1 binding site, which decreases HIF-1α, but not the HIF-1β subunit, thereby inhibiting VEGF.
angioG↓, Moreover, apigenin was found to inhibit angiogenesis, as suggested by decreased HIF-1α and VEGF expression in cancer cells
uPA↓, Furthermore, apigenin intake resulted in marked inhibition of p-Akt, p-ERK1/2, VEGF, uPA, MMP-2 and MMP-9, corresponding with tumor growth and metastasis inhibition in TRAMP mice
Ca+2↑, Neuroblastoma SH-SY5Y cells treated with apigenin led to induction of apoptosis, accompanied by higher levels of intracellular free [Ca(2+)] and shift in Bax:Bcl-2 ratio in favor of apoptosis, cytochrome c release, followed by activation casp-9, 12
Bax:Bcl2↑,
Cyt‑c↑,
Casp9↑,
Casp12↑,
Casp3↑, Apigenin also augmented caspase-3 activity and PARP cleavage
cl‑PARP↑,
E-cadherin↑, Apigenin treatment resulted in higher levels of E-cadherin and reduced levels of nuclear β-catenin, c-Myc, and cyclin D1 in the prostates of TRAMP mice.
β-catenin/ZEB1↓,
cMyc↓,
CDK4↓, apigenin exposure led to decreased levels of cell cycle regulatory proteins including cyclin D1, D2 and E and their regulatory partners CDK2, 4, and 6
CDK2↓,
CDK6↓,
IGF-1↓, A reduction in the IGF-1 and increase in IGFBP-3 levels in the serum and the dorsolateral prostate was observed in apigenin-treated mice.
CK2↓, benefits of apigenin as a CK2 inhibitor in the treatment of human cervical cancer by targeting cancer stem cells
CSCs↓,
FAK↓, Apigenin inhibited the tobacco-derived carcinogen-mediated cell proliferation and migration involving the β-AR and its downstream signals FAK and ERK activation
Gli↓, Apigenin inhibited the self-renewal capacity of SKOV3 sphere-forming cells (SFC) by downregulating Gli1 regulated by CK2α
GLUT1↓, Apigenin induces apoptosis and slows cell growth through metabolic and oxidative stress as a consequence of the down-regulation of glucose transporter 1 (GLUT1).

3160- Ash,    Withaferin A: A Pleiotropic Anticancer Agent from the Indian Medicinal Plant Withania somnifera (L.) Dunal
- Review, Var, NA
TumCCA↑, withaferin A suppressed cell proliferation in prostate, ovarian, breast, gastric, leukemic, and melanoma cancer cells and osteosarcomas by stimulating the inhibition of the cell cycle at several stages, including G0/G1 [86], G2, and M phase
H3↑, via the upregulation of phosphorylated Aurora B, H3, p21, and Wee-1, and the downregulation of A2, B1, and E2 cyclins, Cdc2 (Tyr15), phosphorylated Chk1, and Chk2 in DU-145 and PC-3 prostate cancer cells.
P21↑,
cycA1/CCNA1↓,
CycB/CCNB1↓,
cycE/CCNE↓,
CDC2↓,
CHK1↓,
Chk2↓,
p38↑, nitiated cell death in the leukemia cells by increasing the expression of p38 mitogen-activated protein kinases (MAPK)
MAPK↑,
E6↓, educed the expression of human papillomavirus E6/E7 oncogenes in cervical cancer cells
E7↓,
P53↑, restored the p53 pathway causing the apoptosis of cervical cancer cells.
Akt↓, oral dose of 3–5 mg/kg withaferin A attenuated the activation of Akt and stimulated Forkhead Box-O3a (FOXO3a)-mediated prostate apoptotic response-4 (Par-4) activation,
FOXO3↑,
ROS↑, the generation of reactive oxygen species, histone H2AX phosphorylation, and mitochondrial membrane depolarization, indicating that withaferin A can cause the oxidative stress-mediated killing of oral cancer cells [
γH2AX↑,
MMP↓,
mitResp↓, withaferin A inhibited the expansion of MCF-7 and MDA-MB-231 human breast cancer cells by ROS production, owing to mitochondrial respiration inhibition
eff↑, combination treatment of withaferin A and hyperthermia induced the death of HeLa cells via a decrease in the mitochondrial transmembrane potential and the downregulation of the antiapoptotic protein myeloid-cell leukemia 1 (MCL-1)
TumCD↑,
Mcl-1↓,
ER Stress↑, . Withaferin A also attenuated the development of glioblastoma multiforme (GBM), both in vitro and in vivo, by inducing endoplasmic reticulum stress via activating the transcription factor 4-ATF3-C/EBP homologous protein (ATF4-ATF3-CHOP)
ATF4↑,
ATF3↑,
CHOP↑,
NOTCH↓, modulating the Notch-1 signaling pathway and the downregulation of Akt/NF-κB/Bcl-2 . withaferin A inhibited the Notch signaling pathway
NF-kB↓,
Bcl-2↓,
STAT3↓, Withaferin A also constitutively inhibited interleukin-6-induced phosphorylation of STAT3,
CDK1↓, lowering the levels of cyclin-dependent Cdk1, Cdc25C, and Cdc25B proteins,
β-catenin/ZEB1↓, downregulation of p-Akt expression, β-catenin, N-cadherin and epithelial to the mesenchymal transition (EMT) markers
N-cadherin↓,
EMT↓,
Cyt‑c↑, depolarization and production of ROS, which led to the release of cytochrome c into the cytosol,
eff↑, combinatorial effect of withaferin A and sulforaphane was also observed in MDA-MB-231 and MCF-7 breast cancer cells, with a dramatic reduction of the expression of the antiapoptotic protein Bcl-2 and an increase in the pro-apoptotic Bax level, thus p
CDK4↓, downregulates the levels of cyclin D1, CDK4, and pRB, and upregulates the levels of E2F mRNA and tumor suppressor p21, independently of p53
p‑RB1↓,
PARP↑, upregulation of Bax and cytochrome c, downregulation of Bcl-2, and activation of PARP, caspase-3, and caspase-9 cleavage
cl‑Casp3↑,
cl‑Casp9↑,
NRF2↑, withaferin A binding with Keap1 causes an increase in the nuclear factor erythroid 2-related factor 2 (Nrf2) protein levels, which in turn, regulates the expression of antioxidant proteins that can protect the cells from oxidative stress.
ER-α36↓, Decreased ER-α
LDHA↓, inhibited growth, LDHA activity, and apoptotic induction
lipid-P↑, induction of oxidative stress, increased lipid peroxidation,
AP-1↓, anti-inflammatory qualities of withaferin A are specifically attributed to its inhibition of pro-inflammatory molecules, α-2 macroglobulin, NF-κB, activator protein 1 (AP-1), and cyclooxygenase-2 (COX-2) inhibition,
COX2↓,
RenoP↑, showing strong evidence of the renoprotective potential of withaferin A due to its anti-inflammatory activity
PDGFR-BB↓, attenuating the BB-(PDGF-BB) platelet growth factor
SIRT3↑, by increasing the sirtuin3 (SIRT3) expression
MMP2↓, withaferin A inhibits matrix metalloproteinase-2 (MMP-2) and MMP-9,
MMP9↓,
NADPH↑, but also provokes mRNA stimulation for a set of antioxidant genes, such as NADPH quinone dehydrogenase 1 (NQO1), glutathione-disulfide reductase (GSR), Nrf2, heme oxygenase 1 (HMOX1),
NQO1↑,
GSR↑,
HO-1↑,
*SOD2↑, cardiac ischemia-reperfusion injury model. Withaferin A triggered the upregulation of superoxide dismutase SOD2, SOD3, and peroxiredoxin 1(Prdx-1).
*Prx↑,
*Casp3?, and ameliorated cardiomyocyte caspase-3 activity
eff↑, combination with doxorubicin (DOX), is also responsible for the excessive generation of ROS
Snail↓, inhibition of EMT markers, such as Snail, Slug, β-catenin, and vimentin.
Slug↓,
Vim↓,
CSCs↓, highly effective in eliminating cancer stem cells (CSC) that expressed cell surface markers, such as CD24, CD34, CD44, CD117, and Oct4 while downregulating Notch1, Hes1, and Hey1 genes;
HEY1↓,
MMPs↓, downregulate the expression of MMPs and VEGF, as well as reduce vimentin, N-cadherin cytoskeleton proteins,
VEGF↓,
uPA↓, and protease u-PA involved in the cancer cell metastasis
*toxicity↓, A was orally administered to Wistar rats at a dose of 2000 mg/kg/day and had no adverse effects on the animals
CDK2↓, downregulated the activation of Bcl-2, CDK2, and cyclin D1
CDK4↓, Another study also demonstrated the inhibition of Hsp90 by withaferin A in a pancreatic cancer cell line through the degradation of Akt, cyclin-dependent kinase 4 Cdk4,
HSP90↓,

5552- BBM,    Effects of berbamine against myocardial ischemia/reperfusion injury: Activation of the 5' adenosine monophosphate‐activated protein kinase/nuclear factor erythroid 2‐related factor pathway and changes in the mitochondrial state
- in-vivo, Stroke, NA
*eff↑, BA significantly improved post‐ischemic cardiac function, reduced infarct size and apoptotic cell death, decreased oxidative stress, and improved the mitochondrial state.
*ROS↓,
*mtDam↓,
*AMPK↑, Furthermore, BA markedly increased AMPK activation, Nrf2 nuclear translocation, and the levels of NAD(P)H quinone dehydrogenase and heme oxygenase‐1.
*NRF2↑,
*NADPH↑,
*HO-1↑,
*cardioP↑, berbamine (BA)‐induced cardioprotective effects

2652- CAP,    Oxidative Stress Inducers in Cancer Therapy: Preclinical and Clinical Evidence
- Review, Var, NA
chemoPv↑, capsaicin has been reported as both a chemopreventive and as an anticancer agent
AntiCan↑,
ROS↑, Capsaicin has been reported to induce ROS-dependent cell death in various cancers, including colorectal [63], prostate [64,65], bladder [66,67,68], and pancreatic [69,70] cancers.
TumCG↓, reported to inhibit tumor growth in vivo in mouse xenograft models of prostate [64] and bladder [66] cancers.
ROS↑, Mechanistically, capsaicin-mediated ROS accumulation
MMP↑, leads to mitochondrial membrane depolarization [63,64,66],
Apoptosis↑, which further triggers mitochondria-dependent apoptosis
TumCCA↑, as well as G0/G1 cell cycle arrest
JNK↑, in bladder cancer cells, capsaicin induces JNK activation in an ROS-dependent manner
SOD↓, (1) inhibition of the activity of antioxidant enzymes SOD, catalase (CAT), and glutathione peroxidase [70];
Catalase↓,
GPx↓,
other↓, (2) inhibition of the activity of mitochondrial complex-I and complex-III in the electron transport chain [70];
SIRT1↓, (3) downregulation of the expression of sirtuin-1, a NAD-dependent deacetylase that regulates the expression of various antioxidant enzymes [69];
NADPH↑, (4) upregulation of the expression of NADPH oxidase 4, which generates superoxide [69];
FOXO3↑, (5) increased expression of FOXO3a, which is a transcription factor that regulates the oxidative stress response [68].

6108- Chol,    Trimethylamine-N-Oxide (TMAO) as a Rising-Star Metabolite: Implications for Human Health
- Review, Nor, NA - Review, AD, NA
*TMAO↑, The gut microbiota’s role in metabolizing phytoestrogens suggests that these compounds can modulate the microbial community structure, potentially affecting the production of TMAO from dietary choline and carnitine [5].
*ROS↑, TMAO has the ability to induce oxidative stress in cells by promoting the production of reactive oxygen species (ROS).
*NADPH↑, TMAO has been shown to increase the activity of NADPH oxidase [30], an enzyme that generates ROS as part of its normal function.
*Ca+2↑, TMAO enters platelets and facilitates the release of calcium ions (Ca2+) from intracellular stores.
*AntiAg↓, Calcium serves as a critical secondary messenger in platelet activation, and its elevated levels promote platelet aggregation and thrombus formation
*cognitive↓, TMAO has been linked to cognitive decline and neurodegenerative disorders, including Alzheimer’s disease (AD). Through an integrated analysis of genetic, epigenetic, pathological, and biochemical data, Xu et al. identified a correlation between gut m
*TJ↓, However, excessive TMAO concentrations disrupt BBB integrity by inhibiting tight junction proteins, including claudin-5 and zonula occludens-1
*CLDN1↓,
*ZO-1↓,
*Inflam↑, TMAO also triggers neuroinflammation by activating the NLRP3 inflammasome,
*NLRP3↑,
*ER Stress↑, TMAO enhances the ER stress response by activating the PERK-eIF2α pathway, which is known to impair synaptic plasticity and neuronal function, processes strongly implicated in AD progression
*cognitive↓, TMAO has been identified as the most predictive biomarker for memory impairment and cognitive decline among 56 microbiota-derived metabolic markers
*Dose↝, use of cooking methods such as boiling or stewing instead of grilling, which can produce higher amounts of TMAO
*eff↑, Studies suggest that Lactobacillus plantarum ZDY04 could help reduce TMAO concentrations and prevent TMAO-induced atherosclerosis in animal models
*other↝, Currently, no medications specifically designed to reduce blood TMAO levels exist
*other↝, a review published in 2025 has highlighted the potential role of statins in lowering TMAO levels independently of their cholesterol-lowering effects
*other↝, scientific evidence suggests that statins selectively inhibit the growth of pathogenic bacteria, such as Clostridium and Ruminococcus, while promoting beneficial species, such as Bifidobacterium and Lactobacillus

2786- CHr,    Chemopreventive and therapeutic potential of chrysin in cancer: mechanistic perspectives
- Review, Var, NA
Apoptosis↑, chrysin inhibits cancer growth through induction of apoptosis, alteration of cell cycle and inhibition of angiogenesis, invasion and metastasis without causing any toxicity and undesirable side effects to normal cells
TumCCA↑,
angioG↓,
TumCI↓,
TumMeta↑,
*toxicity↓,
selectivity↑,
chemoPv↑, Induction of phase II detoxification enzymes, such as glutathione S-transferase (GST) or NAD(P)H:quinone oxidoreductase (QR) is one of the major mechanism of protection against initiation of carcinogenesis
*GSTs↑,
*NADPH↑,
*GSH↑, upregulation of antioxidant and carcinogen detoxification enzymes (glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR), GST and QR)
HDAC8↓, inhibits of HDAC8 enzymatic activity
Hif1a↓, Prostate DU145: Inhibits HIF-1a expression through Akt signaling and abrogation of VEGF expression
*ROS↓, chrysin (20 and 40 mg/kg) was shown to exhibit chemopreventive activity by ameliorating oxidative stress and inflammation via NF-kB pathway
*NF-kB↓,
SCF↓, Chrysin has also been reported to have the ability to abolish the stem cell factor (SCF)/c-Kit signaling in human myeloid leukemia cells by preventing the PI3 K pathway
cl‑PARP↑, (PARP) and caspase-3 and concurrently decreasing pro-survival proteins survivin and XIAP
survivin↓,
XIAP↓,
Casp3↑, activation of caspase-3 and -9.
Casp9↑,
GSH↓, chrysin sustains a significant depletion of intracellular GSH concentrations in human NSCLC cells
ChemoSen↑, chrysin potentiates cisplatin toxicity, in part, via synergizing pro-oxidant effects of cisplatin by inducing mitochondrial dysfunction, and by depleting cellular GSH, an important antioxidant defense
Fenton↑, ability to participate in a fenton type chemical reaction
P21↑, upregulation of p21 independent of p53 status and decrease in cyclin D1, CDK2 protein levels
P53↑,
cycD1/CCND1↓,
CDK2↓,
STAT3↓, chrysin inhibits angiogenesis through inhibition of STAT3 and VEGF release mediated by hypoxia through Akt signaling pathway
VEGF↓,
Akt↓,
NRF2↓, Chrysin treatment significantly reduced nrf2 expression in cells at both the mRNA and protein levels through down-regulation of PI3K-Akt and ERK pathways.

1485- CUR,  Chemo,  Rad,    Curcumin, the golden spice from Indian saffron, is a chemosensitizer and radiosensitizer for tumors and chemoprotector and radioprotector for normal organs
- Review, Var, NA
ChemoSen↑, Such effects of curcumin were due to its ability to sensitize cancer cells for increased production of ROS
NF-kB↓, it downregulates various growth regulatory pathways and specific genetic targets including genes for NF-κB, STAT3, COX2, Akt
*STAT3↓, curcumin acts as a chemosensitizer and radiosensitizer has also been studied extensively. For example, it downregulates various growth regulatory pathways and specific genetic targets including genes for NF-kB, STAT3, COX2, Akt,
*COX2↓,
*Akt↓,
*NRF2↑, The protective effects of curcumin appear to be mediated through its ability to induce the activation of NRF2 and induce the expression of antioxidant enzymes (e.g., hemeoxygenase-1, glutathione peroxidase
*HO-1↑,
*GPx↑,
*NADPH↑,
*GSH↑, increase glutathione (a product of the modulatory subunit of gamma-glutamyl-cysteine ligase)
*ROS↓, dietary curcumin can inhibit chemotherapy-induced apoptosis via inhibition of ROS generation and blocking JNK signaling
*p300↓, inhibit p300 HAT activity
radioP↑, radioprotector for normal organs
chemoP↑, curcumin has also been shown to protect normal organs such as liver, kidney, oral mucosa, and heart from chemotherapy and radiotherapy-induced toxicity.
RadioS↑,

2873- HNK,    Honokiol Alleviates Oxidative Stress-Induced Neurotoxicity via Activation of Nrf2
- in-vitro, Nor, PC12
*neuroP↑, multiple pharmacological functions, including neuroprotection.
*GSH↑, Hon attenuates the H2O2- or 6-hydroxydopamine (6-OHDA)-induced apoptosis of PC12 cells by increasing the glutathione level
*HO-1↑, and upregulating a multitude of cytoprotective proteins, including heme oxygenase 1, NAD(P)H:quinone oxidoreductase 1, thioredoxin 1, and thioredoxin reductase 1.
*NADPH↑,
*Trx1↑,
*TrxR1↑,
*NRF2↑, Hon promotes transcription factor Nrf2 nuclear translocation and activation.
*ROS↓, Hon is promising for further development as a therapeutic drug against oxidative stress-related neurodegenerative disorders. Inhibition of ROS accumulation
*antiOx↑, Upregulation of antioxidant species in PC12 cells
*BBB↑, Hon has the ability to cross the BBB
Dose↓, We demonstrated here that Hon, at the concentration as low as 5 μM, significantly rescues the cells from H2O2- or 6-OHDA-induced oxidative damage

5156- PTL,    Rational Design of a Parthenolide-based Drug Regimen That Selectively Eradicates Acute Myelogenous Leukemia Stem Cells
- in-vitro, AML, NA
NADPH↑, parthenolide leads to induction of compensatory mechanisms that include up-regulated NADPH production via the pentose phosphate pathway
PPP↑, Metabolomic analyses reveal increased PPP activity for NADPH production in PTL-treated AML cells. compensatory mechanisms
NRF2↑, activation of the Nrf2-mediated oxidative stress response pathway. compensatory mechanisms
ROS↑,
CSCs↓, parthenolide, 2-deoxyglucose, temsirolimus (termed PDT) regimen is a potent means of targeting AML stem cells but has little to no effect on normal stem cells
selectivity↑,
other↝, combined with 2-deoxyglucose (D) and temsirolimus (T), drugs chosen for their ability to inhibit the PPP and the Nrf-2 mediated anti-oxidant response, respectively

1985- PTL,    KEAP1 Is a Redox Sensitive Target That Arbitrates the Opposing Radiosensitive Effects of Parthenolide in Normal and Cancer Cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, DU145 - in-vitro, Nor, PrEC - in-vivo, NA, NA
ROS↑, parthenolide enhances ROS production in prostate cancer cells through activation of NADPH oxidase
NADPH↑,
RadioS↑, In vivo, parthenolide increases radiosensitivity of mouse xenograft tumors but protects normal prostate and bladder tissues against radiation-induced injury
radioP↑, DMAPT, the water soluble prodrug of parthenolide, is a promising agent for selectively enhancing the sensitivity of prostate cancer cells to radiation while protecting normal tissues from damage caused by radiation.
Trx↓, causes oxidation of thioredoxin (TrX) in prostate cancer cells
*ox-Keap1↑, three normal cell lines, parthenolide increased the oxidized form of Keap1 but decreased the reduced form of Keap1
ox-Keap1↓, results from the three cancer cell lines appeared to be completely opposite to results observed in normal cells treated with parthenolide
rd-Keap1↑, in vivo results show that parthenolide decreased the oxidized form of Keap1 but increased the reduced form of Keap1 in the tumors
*NRF2↑, Oxidization of Keap1 leads to activation of the Nrf2 pro-survival pathway in normal cells. Nrf2 pathway is a major mechanism by which parthenolide protects normal cells against radiation injury
NRF2∅, but no changes were observed in the three cancer cell lines.
NF-kB↓, It has been reported that parthenolide is a potent inhibitor of NF-κB

1987- PTL,  Rad,    A NADPH oxidase dependent redox signaling pathway mediates the selective radiosensitization effect of parthenolide in prostate cancer cells
- in-vitro, Pca, PC3 - in-vitro, Nor, PrEC
selectivity↑, parthenolide (PN), a sesquiterpene lactone, selectively exhibits a radiosensitization effect on prostate cancer PC3 cells but not on normal prostate epithelial PrEC cells.
RadioS↑,
ROS↑, oxidative stress in PC3 cells but not in PrEC cells
*ROS∅, oxidative stress in PC3 cells but not in PrEC cells
NADPH↑, In PC3 but not PrEC cells, PN activates NADPH oxidase leading to a decrease in the level of reduced thioredoxin, activation of PI3K/Akt and consequent FOXO3a phosphorylation, which results in the downregulation of FOXO3a targets, MnSOD, CAT
Trx↓,
PI3K↑,
Akt↑,
p‑FOXO3↓, downregulation of FOXO3a targets, antioxidant enzyme manganese superoxide dismutase (MnSOD) and catalase
SOD2↓, MnSOD
Catalase↓,
radioP↑, when combined with radiation, PN further increases ROS levels in PC3 cells, while it decreases radiation-induced oxidative stress in PrEC cells
*NADPH∅, Parthenolide activates NADPH oxidase in PC3 cells but not in PrEC cells
*GSH↑, increases glutathione (GSH) in PrEC cells(normal cells)
*GSH/GSSG↑, GSH/GSSG ratio is not significantly changed by parthenolide in PC3 cells but is increased 2.4 fold in PrEC cells (normal cells)
*NRF2↑, The induction of GSH may be due to the activation of the Nrf2/ARE (antioxidant/electrophile response element) pathway

3079- RES,    Therapeutic role of resveratrol against hepatocellular carcinoma: A review on its molecular mechanisms of action
- Review, Var, NA
angioG↓, Resveratrol suppresses angiogenesis and metastatic markers to reverse cancer spread.
TumMeta↓,
ChemoSen↑, Resveratrol chemosensitizes chemotherapy and synergizes anti-cancer phytochemicals.
NADPH↑, Both in vitro and in vivo studies indicates that resveratrol enhances various redox enzymes activity, especially nicotinamide adenine dinucleotide phosphate (NADPH)
SIRT1↑, resveratrol effectively modulates both the cytokine and chemokine profiles in immune and endothelial cells by the upregulation of sirtuin-1 (SIRT1)
NF-kB↓, suppression of NF-κB and prevention of the activation of NOD-like receptor family (Nrf) pyrin domain containing-3 inflammasome [
NLRP3↓,
Dose↝, The optimal dose of resveratrol being around 150 mg per day is considered safe by all means.
COX2↓, Cox2 ↓; MMP9 ↓
MMP9↓,
PGE2↓, Cox1 and 2; PGE2↓
TIMP1↑, Resveratrol suppresses the PMA-induced MMP activity in HepG2 cell line, while it also upregulates tissue inhibitor proteins of MMP, namely, TIMP1 and TIMP2, in dose-dependent manner
TIMP2↑,
Sp1/3/4↓, Resveratrol mitigates the expression of SP-1 by inhibiting both phosphorylation of JNK1/2 and expression of urokinase-type plasminogen activator in Huh-7 cell line
p‑JNK↓,
uPAR↓,
ROS↓, Resveratrol attenuates the excessive ROS production and inflammatory cytokine, IL-6, and CXCR4 receptor expression by downregulating Gli-1 expression.
CXCR4↓,
IL6↓,
Gli1↓,
*ROS↓, redox imbalance may be attenuated by resveratrol via downregulating ROS production and simultaneously inducing antioxidant enzymes, GST, SOD, CAT and GPx activities in the cells
*GSTs↑,
*SOD↑,
*Catalase↑,
*GPx↑,
*lipid-P↓, [72] observed that resveratrol treatment not only reduces lipid peroxidation but also increases GSH and GST serum levels in CCl4-treated rats as compared to the CCl4-control animals
*GSH↑,
eff↑, Resveratrol, in combination with thymoquinone (TQ), has been demonstrated to provide a synergistic antiproliferative efficacy against HCC cell lines as reported by Ismail et al.
eff↑, Curcumin, a potential anticancer phytochemical, in combination with resveratrol has been reported to trigger synergistic apoptotic effects against Hepa1–6 cells
eff↑, berberine in combination with resveratrol lowers the cell viability and cell adhesion. At low concentration, berberine significantly induces cell death while resveratrol inhibits cell migration in HepG2 cells

3184- SFN,    The Integrative Role of Sulforaphane in Preventing Inflammation, Oxidative Stress and Fatigue: A Review of a Potential Protective Phytochemical
- Review, Nor, NA
*NRF2↑, SFN treatment modulates redox balance via activating redox regulator nuclear factor E2 factor-related factor (Nrf2).
*Inflam↓, SFN reduces inflammation by suppressing centrally involved inflammatory regulator nuclear factor-kappa B (NF-κB),
*NF-kB↓,
*ROS↓, SFN in preventing fatigue, inflammation, and oxidative stress,
*BioAv↝, It was identified that the lowest oral dose of SFN (2.8 µmol/kg or 0.5 mg/kg) has an absolute bioavailability of more than 80%, whilst with the highest dose (28 µmol/kg or 5 mg/kg) had only 20% bioavailability
*BioAv↝, For example, quickly steaming broccoli sprouts, followed by myrosinase treatment, contains the highest amount SFN, which is approximately 11 and 5 times higher than freeze dried and untreated steamed broccoli sprouts, respectively
*BioAv↝, The peak concentration of SFN metabolites (1.91 ± 0.24 µM) was identified in urine after 1 h of oral dose (200 µmol) of broccoli sprout ITCs to four healthy human volunteers
*BioAv↝, study with 20 participants, providing 200 µmol of SFN in capsule form revealed a peak of SFN equivalence (0.7 ± 0.2 µM) at 3 h
*cardioP↑, FN actives signaling pathways and phosphorylates Nrf2, which further increases the expression and activity of phase 2 enzymes, such as GR, GST, TR, NQO1, to minimize cardiac cell arrest,
*GPx↑, 200 mg of dried broccoli sprouts increased glutathione content, decreased levels of oxidized glutathione, increased the activity of GR and glutathione peroxidase (GPx), which are associated with decreasing oxidative stress in the cardiovascular syst
*SOD↑, SFN treatment activates Nrf2, which translocates into the nucleus to induce production of cellular defense enzymes, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), heme oxygenase (HO) 1, NADPH quinone oxidoreductase
*Catalase↑,
*GPx↑,
*HO-1↑,
*NADPH↑,
*NQO1↑,
*LDH↓, Furthermore, creatinine phosphokinase (CPK) and lactate dehydrogenase (LDH) (two enzymatic markers to assess muscle damage) were significantly lower after SFN treatment compared to a placebo
*hepatoP↑, protects exercise-induced liver damage, evidenced by reducing blood levels of enzymes such as alanine aminotransferase (ALT) and aspartate aminotransferase (AST), via inducing antioxidant defense response
*ALAT↓,
*AST↓,
*IL6↓, fresh broccoli sprouts (30 g/day) daily for 10 weeks. After the intervention period, plasma IL-6 concentrations were significantly lower

1429- SFN,    Preclinical and clinical evaluation of sulforaphane for chemoprevention in the breast
- in-vivo, Nor, NA - Human, Nor, NA
*NADPH↑,
*NQO1↑, x3
*HO-1↑, x4
*Risk↑, strong rationale for evaluating the protective effects of a broccoli sprout preparation in clinical trials of women at risk for breast cancer.

1431- SFN,    Induction of the phase 2 response in mouse and human skin by sulforaphane-containing broccoli sprout extracts
- in-vivo, Nor, NA
*NADPH↑, Topical application of an extract delivering 100 nmol sulforaphane/cm(2)
*NQO1↑,
*GSTA1↑,
*HO-1↑,

3310- SIL,    Silymarin attenuates paraquat-induced lung injury via Nrf2-mediated pathway in vivo and in vitro
- in-vitro, Lung, A549
Inflam↓, silymarin administration abated PQ-induced lung histopathologic changes, decreased inflammatory cell infiltration
MPO↓, suppressed myeloperoxidase (MPO) activity and nitric oxide (NO)/inducible nitric oxide synthases (iNOS) expression,
NO↓,
iNOS↓,
ROS↓, improved oxidative stress (malondialdehyde, MDA; superoxide dismutase, SOD; catalase, CAT; and glutathione peroxidase, GSH-Px) in lung tissue and serum.
MDA↑,
SOD↑,
Catalase↑,
GPx↑,
NRF2↑, silymarin upregulated the levels of nuclear factor-erythroid-2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1) and NAD(P)H:quinone oxidoreductase-1(NQO1).
HO-1↑,
NADPH↑,

2128- TQ,    Thymoquinone inhibits phorbol ester-induced activation of NF-κB and expression of COX-2, and induces expression of cytoprotective enzymes in mouse skin in vivo
- in-vivo, NA, NA
*COX2↓, Pretreatment of female HR-1 hairless mouse skin with TQ attenuated 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced expression of cyclooxygenase-2 (COX-2)
*NF-kB↓, TQ diminished nuclear translocation and the DNA binding of nuclear factor-kappaB (NF-κB) via the blockade of phosphorylation and subsequent degradation of IκBα in TPA-treated mouse skin
*p‑Akt↓, Pretreatment with TQ attenuated the phosphorylation of Akt, c-Jun-N-terminal kinase and p38 mitogen-activated protein kinase,
*p‑cJun↓,
*p‑p38↓,
*HO-1↑, Moreover, topical application of TQ induced the expression of heme oxygenase-1, NAD(P)H-quinoneoxidoreductase-1, glutathione-S-transferase and glutamate cysteine ligase in mouse skin
*NADPH↑,
*GSTA1↑,
*antiOx↑, provide a mechanistic basis of anti-inflammatory and antioxidative effects of TQ in hairless mouse skin.
*Inflam↓,
*NQO1↑, Topical application of TQ (5 lmol) significantly increased the expression of HO-1 (Fig. 4A), NQO1 (Fig. 4B), GCL (Fig. 4C) and GST (Fig. 4D) in mouse epidermal tissue
*GCLC↑,
*GSTA1↑,

4314- VitB1/Thiamine,    Unraveling the molecular mechanisms of vitamin deficiency in Alzheimer's disease pathophysiology
- Review, AD, NA
*Risk↓, Its deficiency disrupts glucose metabolism, impairs neurotransmitter production and DNA synthesis, and increases the risk of AD and neurological deficits
*GlucoseCon↑,
*cognitive↑, Thiamine supplementation, especially benfotiamine, has been shown to improve cognitive function in mild AD, while higher dietary intake supports cognitive impairments
*ATP↑, Low thiamine impairs glucose metabolism, reducing ATP production and increasing ROS, leading to mitochondrial and synaptic dysfunction, key features of AD.
*ROS↓,
*NADPH↑, Thiamine aids in producing ribose-5-phosphate and NADPH, essential for nucleotide synthesis.
*Aβ↓, Low thiamine reduces antioxidant capacity, leading to ROS accumulation and oxidative damage to proteins, lipids, and DNA. This triggers neurodegeneration processes, including development of Aβ plaques
*APP↓, The increase in APP activates beta-site APP cleaving enzymes-1 (BACE1), promoting its cleavage and enhancing the secretion of the Aβ monomers.
*BACE↓,

4031- VitB3,    Nicotinamide Riboside-The Current State of Research and Therapeutic Uses
- Review, NA, NA
*cardioP↑, Accumulating evidence on NRs’ health benefits has validated its efficiency across numerous animal and human studies for the treatment of a number of cardiovascular, neurodegenerative, and metabolic disorders.
*neuroP↑,
*NAD↑, Oral supplementation with NR has been shown to increase NAD+ levels in multiple tissues, along with increased SIRT activity [10,11], improved mitochondrial function [37], and regenerative potential of stem cells
*SIRT1↑,
*NADPH↑, Furthermore, NR is one of the NAD+ intermediates that also serves as a precursor of NADH, as well as hepatic NADP+ and NADPH
*ROS↓, Moreover, SIRT1 inhibits effects of oxidative stress in T2D mice
*IL2↓, NR can similarly decrease IL-2, IL-5, IL-6, and TNFα
*IL5↓,
*IL6↓,
*TNF-α↓,
*Inflam↓, Targeting IL-6 has been recently proposed as a promising treatment to block the inflammatory storm
*BioAv↝, the apparent oral bioavailability of a 1000 mg dose of NR was highly variable among individuals
*BioAv↑, NR was able to increase NAD+ levels in the liver of mice, exhibiting greater oral bioavailability than NAM, which was, in turn, more orally bioavailable than NA

4330- VitB5,    Metabolic changes and inflammation in cultured astrocytes from the 5xFAD mouse model of Alzheimer’s disease: Alleviation by pantethine
- in-vivo, AD, NA
*neuroP↑, Pantethine, the vitamin B5 precursor, known to be neuroprotective and anti-inflammatory, alleviated the pathological pattern in Tg astrocytes
*Inflam↓, pantethine has anti-inflammatory properties,
*ATP↑, Importantly, ATP had its levels increased by 44% in pantethine-treated Tg astrocytes compared to untreated.
*G6PD↑, Pantethine treatment increased both G6PD and PK activity in WT by about 40% and 25%, respectively.
*NADPH↑, in agreement, astrocyte NADPH levels paralleled the changes of G6PD activity described above
*IL1β↓, Pantethine treatment significantly reduced both IL-1β mRNA and protein expression in all conditions where it was applied
*other↝, Administered, at the right time during the disease progression, the pleiotropic action of this natural compound could therefore bring improvement in a complex pathological situation such as AD.


Showing Research Papers: 1 to 21 of 21

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 21

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ATF3↑, 1,   Catalase↓, 2,   Catalase↑, 1,   Fenton↑, 1,   GPx↓, 1,   GPx↑, 1,   GSH↓, 1,   GSR↑, 1,   HO-1↑, 2,   ox-Keap1↓, 1,   rd-Keap1↑, 1,   lipid-P↑, 1,   MDA↑, 1,   MPO↓, 1,   NQO1↑, 1,   NRF2↓, 2,   NRF2↑, 3,   NRF2∅, 1,   ROS↓, 2,   ROS↑, 7,   SIRT3↑, 1,   SOD↓, 2,   SOD↑, 1,   SOD2↓, 1,   Trx↓, 2,  

Mitochondria & Bioenergetics ⓘ

CDC2↓, 1,   mitResp↓, 1,   MMP↓, 2,   MMP↑, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   LDHA↓, 1,   NADPH↑, 8,   PPP↑, 1,   SIRT1↓, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↓, 3,   Akt↑, 1,   Apoptosis↑, 2,   Bax:Bcl2↑, 1,   Bcl-2↓, 1,   Casp12↑, 1,   Casp3↑, 2,   cl‑Casp3↑, 1,   Casp9↑, 2,   cl‑Casp9↑, 1,   Chk2↓, 1,   CK2↓, 1,   Cyt‑c↑, 2,   HEY1↓, 1,   iNOS↓, 1,   JNK↑, 1,   p‑JNK↓, 1,   MAPK↑, 1,   Mcl-1↓, 1,   p27↑, 1,   p38↑, 2,   survivin↓, 1,   Telomerase↓, 1,   TumCD↑, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,   Sp1/3/4↓, 1,  

Transcription & Epigenetics ⓘ

H3↑, 1,   other↓, 1,   other↝, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   ER Stress↑, 1,   HSP90↓, 1,  

DNA Damage & Repair ⓘ

CHK1↓, 1,   P53↑, 2,   PARP↑, 1,   cl‑PARP↑, 2,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK2↓, 3,   CDK4↓, 3,   cycA1/CCNA1↓, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 2,   CycD3↓, 1,   cycE/CCNE↓, 1,   P21↑, 2,   p‑RB1↓, 1,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 3,   EMT↓, 1,   FOXO3↑, 3,   p‑FOXO3↓, 1,   Gli↓, 1,   Gli1↓, 1,   HDAC↓, 1,   HDAC1↓, 1,   HDAC3↓, 1,   HDAC8↓, 1,   IGF-1↓, 1,   NOTCH↓, 1,   PI3K↓, 1,   PI3K↑, 1,   SCF↓, 1,   STAT3↓, 4,   TumCG↓, 1,  

Migration ⓘ

AP-1↓, 1,   Ca+2↑, 1,   E-cadherin↑, 1,   ER-α36↓, 1,   FAK↓, 1,   MMP2↓, 2,   MMP9↓, 3,   MMPs↓, 1,   N-cadherin↓, 1,   Slug↓, 1,   Snail↓, 1,   TIMP1↑, 1,   TIMP2↑, 1,   TumCI↓, 1,   TumMeta↓, 1,   TumMeta↑, 1,   Twist↓, 1,   uPA↓, 2,   uPAR↓, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 3,   ATF4↑, 1,   Hif1a↓, 2,   NO↓, 1,   PDGFR-BB↓, 1,   VEGF↓, 3,  

Barriers & Transport ⓘ

GLUT1↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 3,   CXCR4↓, 1,   IL6↓, 2,   IL8↓, 1,   Inflam↓, 1,   NF-kB↓, 5,   PGE2↓, 1,  

Protein Aggregation ⓘ

NLRP3↓, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

BioEnh↑, 1,   ChemoSen↑, 4,   Dose↓, 1,   Dose↝, 1,   eff↑, 6,   eff↝, 1,   RadioS↑, 3,   selectivity↑, 3,  

Clinical Biomarkers ⓘ

E6↓, 1,   E7↓, 1,   HER2/EBBR2↓, 1,   IL6↓, 2,  

Functional Outcomes ⓘ

AntiCan↑, 2,   chemoP↑, 1,   chemoPv↑, 3,   radioP↑, 3,   RenoP↑, 1,  
Total Targets: 155

Pathway results for Effect on Normal Cells:


NA, unassigned ⓘ

TMAO↑, 1,  

Redox & Oxidative Stress ⓘ

antiOx↑, 4,   Catalase↑, 3,   GCLC↑, 1,   GPx↑, 4,   GSH↑, 6,   GSH/GSSG↑, 1,   GSR↑, 1,   GSTA1↑, 3,   GSTs↑, 3,   HO-1↑, 7,   ox-Keap1↑, 1,   lipid-P↓, 2,   NQO1↑, 5,   NRF2↑, 6,   Prx↑, 1,   ROS↓, 8,   ROS↑, 1,   ROS∅, 1,   SOD↑, 2,   SOD2↑, 1,   Trx1↑, 1,   TrxR1↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 2,   mtDam↓, 1,  

Core Metabolism/Glycolysis ⓘ

ACC↑, 1,   ALAT↓, 1,   AMPK↑, 1,   G6PD↑, 1,   GlucoseCon↑, 2,   LDH↓, 1,   NAD↑, 1,   NADPH↑, 13,   NADPH∅, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↓, 1,   p‑Akt↓, 1,   Casp3?, 1,   iNOS↓, 1,   p‑p38↓, 1,  

Transcription & Epigenetics ⓘ

p‑cJun↓, 1,   other↝, 4,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

p300↓, 1,   STAT3↓, 1,  

Migration ⓘ

AntiAg↓, 1,   APP↓, 1,   Ca+2↑, 1,   CLDN1↓, 1,   TJ↓, 1,   ZO-1↓, 1,  

Barriers & Transport ⓘ

BBB↑, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   IL1β↓, 1,   IL2↓, 1,   IL5↓, 1,   IL6↓, 2,   Inflam↓, 6,   Inflam↑, 1,   NF-kB↓, 4,   TNF-α↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 2,   BACE↓, 1,   NLRP3↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   BioAv↝, 5,   Dose↝, 1,   eff↑, 2,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,   IL6↓, 2,   LDH↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 3,   cognitive↓, 2,   cognitive↑, 2,   hepatoP↑, 1,   memory↑, 1,   neuroP↑, 3,   Risk↓, 1,   Risk↑, 1,   toxicity↓, 2,  
Total Targets: 82

Scientific Paper Hit Count for: NADPH, Nicotinamide adenine dinucleotide phosphate
3 Parthenolide
3 Sulforaphane (mainly Broccoli)
2 Radiotherapy/Radiation
1 Alpha-Lipoic-Acid
1 Apigenin (mainly Parsley)
1 Ashwagandha(Withaferin A)
1 Berbamine
1 Capsaicin
1 Choline
1 Chrysin
1 Curcumin
1 Chemotherapy
1 Honokiol
1 Resveratrol
1 Silymarin (Milk Thistle) silibinin
1 Thymoquinone
1 Vitamin B1/Thiamine
1 Vitamin B3,Niacin
1 Vitamin B5,Pantothenic Acid
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#:2
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