Curcumin Cancer Research Results

CUR, Curcumin: Click to Expand ⟱
Features:
Curcumin is the main active ingredient in Tumeric. Member of the ginger family.Curcumin is a polyphenol extracted from turmeric with anti-inflammatory and antioxidant properties.
- Has iron-chelating, iron-chelating properties. Ferritin. But still known to increase Iron in Cancer cells.
- GSH depletion in cancer cells, exhaustion of the antioxidant defense system. But still raises GSH↑ in normal cells.
- Higher concentrations (5-10 μM) of curcumin induce autophagy and ROS production
- Inhibition of TrxR, shifting the enzyme from an antioxidant to a prooxidant
- Strong inhibitor of Glo-I, , causes depletion of cellular ATP and GSH
- Curcumin has been found to act as an activator of Nrf2, (maybe bad in cancer cells?), hence could be combined with Nrf2 knockdown
-may suppress CSC: suppresses self-renewal and pathways (Wnt/Notch/Hedgehog).
Clinical studies testing curcumin in cancer patients have used a range of dosages, often between 500 mg and 8 g per day; however, many studies note that doses on the lower end may not achieve sufficient plasma concentrations for a therapeutic anticancer effect in humans.
• Formulations designed to improve curcumin absorption (like curcumin combined with piperine, nanoparticle formulations, or liposomal curcumin) are often employed in clinical trials to enhance its bioavailability.

-Note half-life 6 hrs.
BioAv is poor, use piperine or other enhancers
Pathways:
- induce ROS production at high concentration. Lowers ROS at lower concentrations
curcumin can act as a pro-oxidant when blue light is applied
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓
- Lowers AntiOxidant defense in Cancer Cells: GSH↓ Catalase↓ HO1↓ GPx↓
but conversely is known as a NRF2↑ activator in cancer
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, uPA↓, VEGF↓, NF-κB↓, CXCR4↓, SDF1↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, HSP↓, Sp proteins↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, ERK↓, EMT↓, TOP1↓, TET1↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, HK2↓, ECAR↓, OXPHOS↓, GRP78↑, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, ITG">Integrins↓,
- inhibits Cancer Stem Cells : CSC↓, CK2↓, Hh↓, GLi1↓, CD133↓, CD24↓, β-catenin↓, n-myc↓, sox2↓, OCT4↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK↓, ERK↓, JNK, TrxR**,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Rank Pathway / Axis Cancer Cells Normal Cells Label Primary Interpretation Notes
1 NF-κB signaling ↓ NF-κB activation ↓ inflammatory NF-κB tone Driver Suppression of survival and inflammatory transcription NF-κB is a primary, repeatedly validated curcumin target explaining pleiotropic downstream effects
2 STAT3 signaling ↓ STAT3 phosphorylation / activity ↔ or mild suppression Driver Loss of pro-survival and proliferative signaling STAT3 inhibition contributes to growth arrest, apoptosis sensitization, and reduced cytokine signaling in tumors
3 Reactive oxygen species (ROS) ↑ ROS (dose- & context-dependent) ↓ ROS / buffered Conditional Driver Biphasic redox modulation Curcumin can act as a pro-oxidant in cancer cells with high basal stress while acting antioxidant in normal cells
4 Mitochondrial integrity / intrinsic apoptosis ↓ ΔΨm; ↑ caspase activation ↔ preserved Driver Execution of intrinsic apoptosis Mitochondrial dysfunction and caspase activation occur downstream of NF-κB/STAT3 and ROS effects
5 PI3K → AKT → mTOR axis ↓ AKT / ↓ mTOR ↔ or adaptive suppression Secondary Reduced growth and anabolic signaling AKT/mTOR inhibition contributes to growth suppression and autophagy induction in cancer cells
6 Autophagy ↑ autophagy (protective or pro-death) ↑ adaptive autophagy Secondary Stress adaptation vs cell death Autophagy may be cytoprotective or cooperate with apoptosis depending on context and dose
7 HIF-1α / VEGF hypoxia–angiogenesis axis ↓ HIF-1α; ↓ VEGF ↔ minimal effect Secondary Anti-angiogenic pressure Suppression of hypoxia-driven transcription limits angiogenesis and tumor adaptation
8 Cell cycle regulation ↑ G2/M or G1 arrest ↔ largely spared Phenotypic Cytostatic growth control Cell-cycle arrest reflects upstream signaling and epigenetic effects rather than direct CDK inhibition
9 Migration / invasion (EMT, MMP axis) ↓ migration & invasion ↔ Phenotypic Anti-metastatic phenotype Reduced EMT markers and protease activity limit invasive behavior
10 Epigenetic regulation (p300/CBP HAT activity) ↓ histone acetylation ↔ modest Secondary Transcriptional reprogramming Curcumin modulates chromatin via HAT inhibition rather than classic HDAC inhibition


Scientific Papers found: Click to Expand⟱
4415- AgNPs,  SDT,  CUR,    Examining the Impact of Sonodynamic Therapy With Ultrasound Wave in the Presence of Curcumin-Coated Silver Nanoparticles on the Apoptosis of MCF7 Breast Cancer Cells
- in-vitro, BC, MCF-7
tumCV↓, Curcumin-coated silver nanoparticles (Cur@AgNPs) have shown potential as a sensitizer, demonstrating adverse effects on cancer cell survival.
BAX↑, proapoptotic genes, such as Bax and Caspase-3, increased, while the expression of the antiapoptotic gene Bcl-2 decreased in MCF7 cells treated with the SDT.
Casp3↑,
Bcl-2↓,
eff↑, effect of SDT in the presence of Cur@AgNPs decreases cell viability dependence on US mode
ROS↑, Combined treatment increased the amount of ROS induction
sonoS↑, Higher concentrations of AgNPs (100 μg/ml) acted as acoustic sensitizers and enhanced ROS production
eff↑, Using curcumin as a biological coating reduced the toxicity of AgNPs and improved their significant effects with SDT
MMP↓, reduction in mitochondrial membrane potential (MMP) and the opening of mitochondrial permeability transition pores (mPTPs)
Cyt‑c↑, ultimately facilitating the release of cytochrome c from the mitochondria into the cytosol.

3446- ALA,  CUR,    The Potential Protective Effect of Curcumin and α-Lipoic Acid on N-(4-Hydroxyphenyl) Acetamide-induced Hepatotoxicity Through Downregulation of α-SMA and Collagen III Expression
- in-vivo, Nor, NA
*hepatoP↑, Curc and Lip acid can be considered as promising natural therapies against liver injury, induced by NHPA, through their antioxidant and antifibrotic actions.
*α-SMA↓, Curc and Lip acid reduced the expression of alpha-smooth muscle actin and collagen III, upregulated by NHPA intoxication
*COL3A1↓,
*ROS↓, scavenging activity to ROS and a capacity to regenerate endogenous antioxidants such as GSH, and vitamins C and E.
*GSH↑,
*ALAT↓, ALT, AST, and ALP activity levels compared to those of the control group. The use of NACS, Curc, and/or Lip acid significantly reduced the toxic effects of NHPA on those enzymes,
*AST↓,
*ALP↓,
*MDA↓, The combination therapy showed an apparent reduction in MDA level more than other treatments

2635- Api,  CUR,    Synergistic Effect of Apigenin and Curcumin on Apoptosis, Paraptosis and Autophagy-related Cell Death in HeLa Cells
- in-vitro, Cerv, HeLa
TumCD↑, Treatment with a combination of apigenin and curcumin increased the expression levels of genes related to cell death in HeLa cells 1.29- to 27.6-fold.
eff↑, combination of curcumin and apigenin showed a synergistic anti-tumor effect
TumAuto↑, autophagic cell death, as well as ER stress-associated paraptosis
ER Stress↑,
Paraptosis↑,
GRP78/BiP↓, GRP78 expression was down-regulated, and massive cytoplasmic vacuolization was observed in HeLa cells
Dose↝, combined use of 0.09 μg/μl curcumin and 0.06 μg/μl apigenin showed a synergistic anti-tumor effect

1024- Api,  CUR,    Apigenin suppresses PD-L1 expression in melanoma and host dendritic cells to elicit synergistic therapeutic effects
- vitro+vivo, Melanoma, A375 - in-vitro, Melanoma, A2058 - in-vitro, Melanoma, RPMI-7951
TumCG↓,
Apoptosis↑,
PD-L1↓, IFN-γ-induced PD-L1 upregulation was significantly inhibited by flavonoids, especially apigenin
STAT1↓,
tumCV↓,
T-Cell↑, Curcumin and apigenin enhance T cell-mediated melanoma cell killing

147- ATG,  EGCG,  CUR,    Increased chemopreventive effect by combining arctigenin, green tea polyphenol and curcumin in prostate and breast cancer cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, MCF-7
Bax:Bcl2↑, combination treatment significantly increased the ratio of Bax to Bcl-2 proteins, decreased the activation of NFκB, PI3K/Akt and Stat3
NF-kB↓, arctigenin demonstrated the strongest ability to inhibit the activation of both PI3K/Akt and NFκB pathways in both LNCaP and MCF-7 cells.
PI3K/Akt↓,
STAT3↓,
chemoPv↑, combining Arc and EGCG with Cur to enhance chemoprevention in both prostate and breast cancer.
TumCP↓, combining Arc and EGCG with Cur to enhance chemoprevention in both prostate and breast cancer.
TumCCA↑, EGCG significantly increased the effect of curcumin on cell cycle arrest at G0/G1 phase in MCF-7 cells, and the effect was further enhanced by the addition of arctigenin
TumCMig↓, EGCG and arctigenin alone or in combination with curcumin significantly decreased the number of migrated MCF-7 cells compared to control

3754- BBR,  CUR,  EGCG,  Hup,    Traditional Chinese medicinal herbs as potential AChE inhibitors for anti-Alzheimer’s disease: A review
*AChE↓, Berberine (9) has gained considerable attention due to its wide pharmacological potentials and several biological properties, such as acetylcholinesterase and butyrylcholinesterase inhibitory, antioxidant, monoamine oxidase oxidase,
*Aβ↓, amyloid-b peptide level-reducing, cholesterol- lowering and renoprotective activities
*LDL↓,
*RenoP↑,
*BChE↓,
*eff↑, Above all, the berberine-pyrocatechol hybrid (14) showed a strong AChE inhibitor activity (IC50 of 123 ± 3 nM) [34]
*BACE↓, Curcumin: inhibite the rBACE1 activity [42]. In addition, it has made good inhibitory effect on acetylcholinesterase activity
*AChE↓, EGCG promoted brain health, prevented AD progression, and inhibited the AChE activity [52,53].
*eff↑, EGCG could enhance the effect of huperzine A on inhibiting AChE.

2703- BBR,  CUR,  SFN,  UA,  GamB  Naturally occurring anti-cancer agents targeting EZH2
- Review, Var, NA
EZH2↓, In fact, several natural products such as curcumin, triptolide, ursolic acid, sulforaphane, davidiin, tanshindiols, gambogic acid, berberine and Alcea rosea have been shown to serve as EZH2 modulators.

3514- Bor,  CUR,    Effects of Curcumin and Boric Acid Against Neurodegenerative Damage Induced by Amyloid Beta
- in-vivo, AD, NA
*DNAdam↓, Co-administration of BA and curcumin on synaptosomes exposed to Aβ1-42 resulted in a significant decrease in DNA fragmentation values, MDA levels, and AChE activities.
*MDA↓,
*AChE↓,
*neuroP↑, BA and curcumin had protective effects on rat brain synaptosomes against Aβ1-42 exposure.
*ROS↓, BA and curcumin treatment can have abilities to prevent the alterations of the cholinergic system and inhibit oxidative stress in the cerebral cortex synapses of Aβ1-42 exposed.
*NO↓, Synaptosomes treated with BA showed a significant reduction in MDA and NO levels

1426- Bos,  CUR,  Chemo,    Novel evidence for curcumin and boswellic acid induced chemoprevention through regulation of miR-34a and miR-27a in colorectal cancer
- in-vivo, CRC, NA - in-vitro, CRC, HCT116 - in-vitro, CRC, RKO - in-vitro, CRC, SW480 - in-vitro, RCC, SW-620 - in-vitro, RCC, HT-29 - in-vitro, CRC, Caco-2
miR-34a↑, curcumin and AKBA induced upregulation of tumor-suppressive miR-34a and downregulation of miR-27a in CRC cells
miR-27a-3p↓,
TumCG↓,
BAX↑,
Bcl-2↓,
PARP1↓,
TumCCA↑,
Apoptosis↑,
cMyc↓,
CDK4↓,
CDK6↓,
cycD1/CCND1↓,
ChemoSen↑, combined treatment further increased the inhibitory effects
miR-34a↑, miR-34a expression was upregulated by curcumin and further elevated by concurrent treatment with curcumin and AKBA in HCT116 cell
miR-27a-3p↓,

145- CA,  CUR,    The anti-cancer effects of carotenoids and other phytonutrients resides in their combined activity
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3 - in-vitro, PC, DU145
AR↓, Phytonutrients synergistically inhibit androgen signaling
ARE/EpRE↑, x4 the sum of single ingredients
TumCP↓, Phytonutrients inhibit prostate cancer cell proliferation
PSA↓, combination of three compounds such as in the case of curcumin, vitamin E and the tomato extract showed a stronger synergistic effect than each pair of compounds. The inhibition of PSA secretion

2015- CAP,  CUR,  urea,    Anti-cancer Activity of Sustained Release Capsaicin Formulations
- Review, Var, NA
AntiCan↑, Several convergent studies show that capsaicin displays robust cancer activity, suppressing the growth, angiogenesis and metastasis of several human cancers.
TumCG↓,
angioG↓,
TumMeta↓,
BioAv↓, clinical applications of capsaicin as a viable anti-cancer drug have remained problematic due to its poor bioavailability and aqueous solubility properties
BioAv↓, capsaicin is associated with adverse side effects like gastrointestinal cramps, stomach pain, nausea and diarrhea and vomiting
BioAv↑, All these hurdles may be circumvented by encapsulation of capsaicin in sustained release drug delivery systems.
selectivity↑, Most importantly, these long-acting capsaicin formulations selectively kill cancer cells and have minimal growth-suppressive activity on normal cells.
EPR↑, The EPR effect is a mechanism by which high–molecular drug delivery systems (typically prodrugs, liposomes, nanoparticles, and macromolecular drugs) tend to accumulate in tumor tissue much more than they do in normal tissues
eff↓, The efficiency of such extravasation is maximum when the size of the liposomes less than 200 nm The CAP-CUR-GLY-GAL-LIPO were spherical in shape with a narrow range of size distribution ranging from 135–155nm
ChemoSen↑, The chemosensitization and anti-tumor activity of capsaicin involves multiple molecular pathways
Dose∅, oral, Intravenous (IV), and Intraperitoneal (IP) options
Half-Life∅, oral metabolized in 105mins, T1/2in blood=25mins.
eff↑, presence of urea (as a carrier) increased the aqueous solubility of capsaicin by 3.6-fold compared to pure capsaicin

5953- Cela,  CUR,    The Combination of Celastrol and Curcumin Enhances the Antitumor Effect in Nasopharyngeal Carcinoma by Inducing Ferroptosis
- vitro+vivo, NPC, NA
eff↑, The results indicated that low doses of celastrol (0.7 μM) alone do not inhibit proliferation in NPC cells. However, when combined with curcumin, there is a significant enhancement of the antiproliferative effect.
TumCP↓,
GPx4↓, while notably decreasing solute carrier family 7 member 11 and glutathione peroxidase 4,
eff↑, combined treatment exhibited significant antitumor efficacy with low toxic side effects in a xenograft model.
TumAuto↑, Combined Treatment with Curcumin and Low-Dose Celastrol Induced Autophagy in the CNE1 Cell Line
Ferroptosis↑, Ferroptosis Plays a Critical Role in Low-Dose Celastrol Plus Curcumin-Induced Cell Death
Dose↝, more significant decrease observed in cells treated with 0.7 μM celastrol combined with 35 μM curcumin
ACSL4↑, Only the combination of 0.7 μM celastrol and 35 μM curcumin led to a significant increase in ACSL4 levels
toxicity↓, The Combination of Celastrol and Curcumin Demonstrates a Significant Tumor-Suppressive Effect with Low Toxicity

6027- CGA,  CUR,  EGCG,  QC,  RES  Contribution of Non-Coding RNAs to Anticancer Effects of Dietary Polyphenols: Chlorogenic Acid, Curcumin, Epigallocatechin-3-Gallate, Genistein, Quercetin and Resveratrol
- Review, Nor, NA
*ROS↓, polyphenols have similar chemical and biological properties in that they can act as antioxidants and exert the anticancer effects via cell signaling pathways involving their reactive oxygen species (ROS)-scavenging activity.
ROS↑, These polyphenols may also act as pro-oxidants under certain conditions, especially at high concentrations.

5995- Chit,  CUR,    Enhancement of anticancer activity and drug delivery of chitosan-curcumin nanoparticle via molecular docking and simulation analysis
- vitro+vivo, Var, NA
eff↑, Formulated CSCur NPs were assessed for in-vitro release, which exhibited a sustained release pattern and four-fold higher cytotoxic activity in a nanoparticulated system.
EPR↑, Enhanced uptake, apoptotic effect of CSCur NPs were established by morphological changes in cells as observed by fluorescence microscopy and FE-SEM.
DNAdam↑, DNA damage, cell-cycle blockage and elevated ROS levels further confirm the anticancer activity of the CSCur NPs following apoptotic pathways.
TumCCA↑,
ROS↑,
toxicity↓, In-vivo study on Danio rerio, for uptake and toxicity reveal the particle's biocompatibility and nontoxicity

428- Chit,  docx,  CUR,    Chitosan-based nanoparticle co-delivery of docetaxel and curcumin ameliorates anti-tumor chemoimmunotherapy in lung cancer
- vitro+vivo, Lung, H460 - vitro+vivo, Lung, H1299 - vitro+vivo, Lung, A549 - vitro+vivo, Lung, PC9
MDSCs↓,
TregCell↓,
IL10↓,
NK cell↑,

5792- CRMs,  HCA,  CUR,  EGCG,  GAR  Caloric restriction mimetics: natural/physiological pharmacological autophagy inducers
- Review, Nor, NA
*CRM↓, AcCoA depleting agents (e.g., hydroxycitrate),
*Dose?, acetyltransferase inhibitors (e.g., anacardic acid, curcumin, epigallocatechin-3-gallate, garcinol, spermidine)
*AntiAge↑, Another common characteristic of these agents is their capacity to reduce aging-associated diseases and to confer protective responses against ischemia-induced organ damage.
*Acetyl-CoA↓, Altogether, these observations point to the idea that starvation causes autophagy because it results in the early depletion of AcCoA
*SIRT1↑, nduction of the deacetylase activity of sirtuins (as a result of changing NADH/NAD+ ratios and increased SIRT1 expression)
*AMPK↑, activation of AMPK activity (as a result of changing ATP/ADP ratios)
*mTORC1↓, inhibition of MTORC1 (as a result of amino acid depletion).
*AntiAge↑, CR or intermittent fasting are known for their wide life-span-extending
chemoP↑, fasting can reduce the subjective and objective toxicity of cytotoxic anticancer chemotherapies, both in humans and in mouse models, at the same time that it improves treatment outcome in mice

3628- Cro,  VitE,  CUR,    Vitamin E, Turmeric and Saffron in Treatment of Alzheimer’s Disease
- Review, AD, NA
*antiOx↑, Vitamin E is a potent antioxidant that may have beneficial effects in Alzheimer’s in dealing with oxidative stress
*ROS↓,
*lipid-P↓, Alpha-tocopherol was found as protective against lipid peroxidation
*Aβ↓, Researchers found that all forms of tocopherol enhanced the Aβ production and decreased the Aβ degradation. T
*AChE↓, vitamin E treatment significantly restored acetylcholinesterase activity and increased the Na+/K+ ATPase activity.
*cognitive↑, Although high plasma vitamin E is linked to better cognitive performance [
*Inflam↓, curcumin is effective in AD as an antioxidant, anti-inflammatory therapeutic agent that improves the cognitive functions

3861- CUR,    Curcumin as a novel therapeutic candidate for cancer: can this natural compound revolutionize cancer treatment?
- Review, Var, NA
*antiOx↑, fig 1
*Inflam↓,
PI3K↓, By inhibiting pro-survival and pro-inflammatory signaling cascades such as PI3K/Akt/mTOR, MAPK, Wnt/β-catenin, NF-κB, Hedgehog, Notch, and JAK/STAT3, curcumin effectively impedes cancer cell growth and promotes apoptosis.
Akt↓,
mTOR↓,
Wnt↓,
β-catenin/ZEB1↓,
NF-kB↓,
HH↓,
NOTCH↓,
JAK↓,
STAT3↓,
ADAM10↓, Curcumin may inhibit the function of the Notch pathway in cancer by inhibiting Notch pathway activators such as gamma secretases, Notch ligands, or ADAM10.

3797- CUR,    Curcumin reverses cognitive deficits through promoting neurogenesis and synapse plasticity via the upregulation of PSD95 and BDNF in mice
- in-vitro, NA, NA
*cognitive↑, Our results showed that curcumin administration rescued the impaired cognition of mice, shown as enhanced BrdU+ and dendritic spine in hippocampus.
*BDNF↑, At the molecular level, curcumin was found to promote the expression of brain-derived neurotrophic factor (BDNF) and postsynaptic density protein 95 (PSD95).
*PSD95↑,
*memory↑, Studies have shown that curcumin improves the spatial learning and memory abilities of the Alzheimer’s disease model mice

3862- CUR,  RES,    The metalloproteinase ADAM10: A useful therapeutic target?
- Review, AD, NA
*SIRT1↑, Therefore, the Sirt1 activators curcumin and resveratrol are tested for their clinical impact on ADAM10 expression in AD.
*ADAM10↑,

4171- CUR,    Curcumin produces neuroprotective effects via activating brain-derived neurotrophic factor/TrkB-dependent MAPK and PI-3K cascades in rodent cortical neurons
- in-vivo, NA, NA
*BDNF↑, treatment of curcumin increased BDNF and phosphor-TrkB
*TrkB↑,
*CREB↑, curcumin-induced increase in phosphorylated cyclic AMP response element binding protein (CREB), which has been implicated as a possible mediator of antidepressant actions
*Mood↑,
*neuroP↑, Therefore, we hypothesize the neuroprotection of curcumin might be mediated via BDNF/TrkB-MAPK/PI-3K-CREB signaling pathway.

4175- CUR,    Effects of curcumin on learning and memory deficits, BDNF, and ERK protein expression in rats exposed to chronic unpredictable stress
- in-vivo, NA, NA
*BDNF↑, CUS reduced hippocampal BDNF and ERK levels, while curcumin effectively reversed these alterations
*ERK↑, related to its aptitude to promote BDNF and ERK in the hippocampus.

4176- CUR,    Effects of curcumin (Curcuma longa) on learning and spatial memory as well as cell proliferation and neuroblast differentiation in adult and aged mice by upregulating brain-derived neurotrophic factor and CREB signaling
- in-vivo, AD, NA
*BDNF↑, Upregulating Brain-Derived Neurotrophic Factor and CREB Signaling
*CREB↑,

4337- CUR,    Inhibitory effect of curcumin, a food spice from turmeric, on platelet-activating factor- and arachidonic acid-mediated platelet aggregation through inhibition of thromboxane formation and Ca2+ signaling
- in-vitro, NA, NA
*AntiAg↑, We show that curcumin inhibited platelet aggregation mediated by the platelet agonists epinephrine (200 μM), ADP (4 μM), platelet-activating factor (PAF; 800 nM), collagen (20 μg/mL), and arachidonic acid (AA: 0.75 mM).
*TXA2↓, results suggest that the curcumin-mediated preferential inhibition of PAF- and AA-induced platelet aggregation involves inhibitory effects on TXA2 synthesis and Ca2+ signaling, but without the involvement of PKC.

4650- CUR,    Curcumin and cancer stem cells: curcumin has asymmetrical effects on cancer and normal stem cells
- Review, Var, NA
SCD1↓, Curcumin has been shown to have numerous cytotoxic effects on cancer stem cells (CSCs).
IL6↓, This is due to its suppression of the release of cytokines, particularly interleukin (IL)-6, IL-8 and IL-1
IL8↓,
IL1↓,
*selectivity↑, curcumin has little toxicity against normal stem cells (NSCs).
Wnt↝, effects at multiple sites along CSC pathways, such as Wnt, Notch, Hedgehog and FAK.
NOTCH↝,
HH↝,
FAK↝,

4651- CUR,    Targeting cancer stem cells by curcumin and clinical applications
- Review, Var, NA
CSCs↓, recent research has shown that curcumin can target cancer stem cells (CSCs)
*toxicity↓, safety and tolerability of curcumin have been well-established by numerous clinical studies
*BioAv↝, Importantly, the low bioavailability of curcumin has been dramatically improved through the use of structural analogues or special formulations.
chemoP↑, promising agent in cancer chemoprevention and therapy

3860- CUR,    Curcumin Ameliorates Memory Decline via Inhibiting BACE1 Expression and β-Amyloid Pathology in 5×FAD Transgenic Mice
- in-vivo, AD, NA
*Aβ↓, Our results showed that curcumin administration (150 or 300 mg/kg/day, intragastrically, for 60 days) dramatically reduced Aβ production by downregulating BACE1 expression
*BACE↓,
*memory↑, Curcumin Ameliorates Memory Decline

3857- CUR,    Alpha-Secretase ADAM10 Regulation: Insights into Alzheimer’s Disease Treatment
- Review, AD, NA
*Inflam↓, curcumin, a natural component extracted from the plant Curcuma longa that presents anti-inflammatory, antioxidant, and copper and iron chelation properties
*antiOx↑,
*IronCh↑,
*BBB↑, can easily penetrate the blood–brain barrier (BBB), and was suggested as a promising therapy for AD
*ADAM10↝, Curcumin conjugated with isoleucine, phenylalanine or valine at both extremities—but not curcumin alone or its metabolite tetrahydro-curcumin—was able to enhance ADAM10 protein expression

3856- CUR,    Curcumin induces IL-6 receptor shedding via the ADAM10 proteinase
- in-vitro, AD, NA
*ADAM10↑, Herein, we report that membrane-modulating agents including curcumin, enhance IL-6R shedding in human monocytes via a mechanism involving a disintegrin and metalloprotease 10 (ADAM10).
*Inflam↓, therapeutic intervention using membrane-active compounds, such as curcuminoids, for diseases such as inflammation and cancer.

3831- CUR,    Traditional Chinese Medicine: Role in Reducing β-Amyloid, Apoptosis, Autophagy, Neuroinflammation, Oxidative Stress, and Mitochondrial Dysfunction of Alzheimer’s Disease
- Review, AD, NA
*neuroP↑, Several studies have shown that C. longa is a potential neuroprotective drug
*ROS↓, Curcumin inhibited Aβ-induced DNA damage by reducing of ROS generation through p38 MAPK and AKT pathways
*Ca+2↓, attenuate apoptosis by regulating intracellular Ca2+ release, ROS, and mitochondrial membrane potential depolarization level in SH-SY5Y cells
*MMP↑,

4655- CUR,    Inhibition of Cancer Stem-like Cells by Curcumin and Other Polyphenol Derivatives in MDA-MB-231 TNBC Cells
- in-vitro, BC, NA
CSCs↓, Curcumin, a polyphenol derived from turmeric (Curcuma longa), exhibits anticancer effects against breast cancer cells and BCSCs.
*BioAv↓, curcumin derivatives has been suggested as an approach to overcome the bioavailability and solubility problems of curcumin in humans, thereby increasing its anticancer effects

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.

3794- CUR,    Curcumin hybrid molecules for the treatment of Alzheimer's disease: Structure and pharmacological activities
- Review, AD, NA
*GSK‐3β↓, Firstly, curcumin can inhibit kinases, such as GSK-3β and Cyclin-Dependent Kinase 5 (Cdk5), that excessively phosphorylate Tau protein
*CDK5↓,
*p‑tau↓,
*IronCh↑, curcumin's metal ion chelating capability contributes to the reduction of free radicals
*ROS↓,
*HO-1↑, upregulating antioxidant enzymes including heme oxygenase 1 (HO-1), superoxide dismutase (SOD), catalase, and enzymes involved in the synthesis of endogenous antioxidants, specifically glutathione (GSH)
*SOD↑,
*Catalase↑,
*GSH↑,
*TNF-α↓, inhibiting the expression of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-12,
*IL6↓,
*IL12↓,
*NRF2↑, inducing the production of anti-inflammatory mediators including HO-1/NRF-2, PPARα-γ, and IL-4
*PPARγ↑,
*IL4↑,
*AChE↓, researchers have observed that curcumin can suppress AChE mRNA expression levels, effectively preventing the Cd-induced rise in AChE activity
*Dose↝, While curcumin directly interacts with AChE, its inhibitory activity remains weak (IC50 = 67.69 μM)
*GutMicro↑, curcumin's interaction with gut microbiota exhibits potential anti-AD properties.

3793- CUR,    Curcumin Downregulates GSK3 and Cdk5 in Scopolamine-Induced Alzheimer’s Disease Rats Abrogating Aβ40/42 and Tau Hyperphosphorylation
- in-vivo, AD, NA
*Aβ↓, We found that curcumin-treated AD rats markedly reduced the levels of Aβ40 and Aβ42 in the brain and in the plasma in comparison to untreated AD rats
*p‑tau↓, Moreover, the levels of phosphorylated tau at Ser396 (PHF13), Ser202/Thr205 (AT8), and Aβ40/42 (MOAB2) were decreased significantly in AD rats treated with curcumin.
*GSK‐3β↓, Phospho-GSK3β (Tyr216), the active form of GSK3β, and total GSK3β were significantly decreased in AD rats treated with curcumin.
*CDK5↓, Cdk5 and its activators p35 and p25 were significantly decreased in curcumin-treated AD rats.
*memory↑, Impaired spatial memory and locomotor activity in AD rats were partially reversed by curcumin.

3760- CUR,  GI,  CAP,  RosA,  PI  Extending the lore of curcumin as dipteran Butyrylcholine esterase (BChE) inhibitor: A holistic molecular interplay assessment
*AChE↓, Previously we have reported curcumin to induce mortality in Cx. pipiens by inhibiting AChE.
*other↓, The next hit, gingerol, is also reported to be an AChE inhibitor [61].
*other↓, Capsaicin, a phytochemical is reported to be AChE inhibitor [62].
*other↓, Rosmarinic acid is a polyphenol found in multiple aromatic plants and is reported to inhibit glutathione S-transferase, lactoperoxidase, AChE, BChE and carbonic anhydrase isoenzymes
*other↓, The next hit, piperine is known to inhibit ChEs, moreover curcumin and piperine are reported to synergically inhibit AChE and BChE in humans
*other↓, Sesamin is a phytochemical found in Cortex Acanthopanacis radicis, is reported to inhibit AChE, and known to improve memory impairment in mouse [65]
*other↓, Lastly as represented earlier, ursolic and oleanolic acid from the leaves of C. talcana are reported to inhibit AChE [14]

3753- CUR,  Gala,    A Novel Galantamine–Curcumin Hybrid Inhibits Butyrylcholinesterase: A Molecular Dynamics Study
- Study, AD, NA
*BChE↓, newly designed hybrid of galantamine (GAL) and curcumin (CCN) (compound 4b) decreases the activity of BChE in murine brain homogenates.
*AChE↓, Galantamine (GAL) is a natural alkaloid : It functions as an AChE inhibitor, enhancing the levels of acetylcholine in the brain, which are important for memory and cognitio
*Ach↑,
*cognitive↑,
*memory↑,
*ROS↓, CCN is its ability to neutralize free radicals and reduce oxidative stress
*Inflam↓, CCN inhibits key enzymes and signaling pathways involved in inflammation, such as NF-kB and COX-2, making it valuable in managing inflammatory conditions like arthritis
*NF-kB↓,
*COX2?,

3752- CUR,    Revealing the molecular interplay of curcumin as Culex pipiens Acetylcholine esterase 1 (AChE1) inhibitor
- in-vivo, AD, NA
*AChE↓, curcumin induces mortality in Cx. pipiens at an early stage of its life cycle by AChE inhibition.

3751- CUR,  Gala,    A Novel Galantamine-Curcumin Hybrid as a Potential Multi-Target Agent against Neurodegenerative Disorders
- in-vivo, AD, NA
*AChE↓, AChE inhibitor galantamine (GAL) and the antioxidant polyphenol curcumin (CU) showed high AChE inhibition in vitro.
*MDA↑, 25% reduction in AChE activity, as well as a 28% and 73% increase in the levels of MDA and GSH, respectively
*GSH↑,
*BBB↑, Accordingly, GAL and CU have intermediate BBB permeability

4708- CUR,    Molecular mechanisms underlying curcumin-mediated microRNA regulation in carcinogenesis; Focused on gastrointestinal cancers
- Review, GC, NA
chemoPv↑, Curcumin is well known for its chemopreventive and anti-cancer properties.
AntiCan↑,
*antiOx↑, Mechanistically, curcumin exerts its biological impacts via antioxidant and anti-inflammatory effects through the interaction with various transcription factors and signaling molecules.
*Inflam↓,
miR-21↓, Table 1
miR-34a↑,
miR-200b↑,
miR-27a-3p↓,

6050- CUR,  SeNPs,    Efficacy of curcumin-selenium nanoemulsion in alleviating oxidative damage induced by aluminum chloride in a rat model of Alzheimer's disease
- in-vivo, AD, NA
*cognitive↑, Treatment with a curcumin-selenium nanoemulsion has been shown to enhance behavioural performance and mitigate degenerative changes induced by aluminium chloride (AlCl3)
*AChE↓, This nanoemulsion also reduced the activity of acetylcholinesterase (AChE) and lowered levels of key proteins, including Aβ, p53, tau, nuclear factor erythroid 2-related factor 2 (Nrf2), and tumour necrosis factor-alpha (TNF-α).
*Aβ↓,
*P53↓,
*tau↓,
*NRF2↓,
*TNF-α↓,
*NO↑, it significantly decreased nitric oxide (NO) levels in the brain while enhancing the activity of catalase (CAT) and superoxide dismutase (SOD).
*Catalase↑,
*antiOx↑, The study highlights the antioxidant and anti-inflammatory properties of the curcumin-selenium nanoemulsion, suggesting its potential as a therapeutic option for alleviating AD induced by AlCl3.
*Inflam↓,

5783- CUR,  EGCG,    The effects of tetrahydrocurcumin and green tea polyphenol on the survival of male C57BL/6 mice
- in-vivo, Nor, NA
*OS↑, Mice that started to receive diets containing TC (0.2%) at the age of 13 months had significantly longer average life spans (days, mean +/- SD) than control mice (797.6 +/- 151.2 vs.882 +/- 154.6, both n = 50, controls vs.

5397- CUR,  SFN,  RES,  EGCG,  Ash  Targeting Cancer Stem Cells with Phytochemicals: Molecular Mechanisms and Therapeutic Potential
- Review, Var, NA
CSCs↓, curcumin, sulforaphane, resveratrol, EGCG, genistein, quercetin, parthenolide, berberine, and withaferin A. Collectively, these compounds suppress CSC self-renewal,

5229- CUR,    Activation of Transcription Factor NF-κB Is Suppressed by Curcumin (Diferuloylmethane)
- in-vitro, Melanoma, NA
NF-kB↓, Besides TNF, curcumin also blocked phorbol ester- and hydrogen peroxide-mediated activation of NF-κB.

4881- CUR,  SFN,  RES,  EGCG,  Lyco  An update of Nrf2 activators and inhibitors in cancer prevention/promotion
- Review, Var, NA
*NRF2↑, natural Nrf2 activators include curcumin, sulforaphane (SF), kahweol, resveratrol, garlic oganosulfur compounds, zerumbone, epigallocatechin-3-gallate, carnosol, cinnamonyl-based compounds, lycopene, and cafestol
*antiOx↑, these chemopreventive agents can activate the antioxidants, phase II detoxification factors, and transducers, and protect the cells from carcinogenic exposure

4831- CUR,    The dual role of curcumin and ferulic acid in counteracting chemoresistance and cisplatin-induced ototoxicity
- in-vitro, NA, NA
*NRF2↑, We reported that both polyphenols show antioxidant and oto-protective activity in the cochlea by up-regulating Nrf-2/HO-1 pathway and downregulating p53 phosphorylation.
*P53↓,
*NF-kB↓, only curcumin is able to influence inflammatory pathways counteracting NF-κB activation
ROS↑, In human cancer cells, curcumin converts the anti-oxidant effect into a pro-oxidant and anti-inflammatory one
Inflam↓,
ChemoSen↑, Curcumin exerts permissive and chemosensitive properties by targeting the cisplatin chemoresistant factors Nrf-2, NF-κB and STAT-3 phosphorylation.

4830- CUR,    Curcumin and Its Derivatives Induce Apoptosis in Human Cancer Cells by Mobilizing and Redox Cycling Genomic Copper Ions
- in-vitro, Var, NA
eff↑, intracellular copper reacts with curcuminoids in cancer cells to cause DNA damage via ROS generation.
ROS↑, Apoptosis of Cancer Cells Induced by Curcumin Is Mediated by ROS
DNAdam↑,
TumCG↓, Curcumin Inhibits Growth and Induces Apoptosis in Different Types of Cancer Cells
Apoptosis↑,
eff↓, Curcumin-Induced Antiproliferation and Apoptosis in Cancer Cells Are Inhibited by a Cuprous Chelator but Not by Iron and Zinc Chelators
Fenton↑, Generation of superoxide anions may spontaneously result in the synthesis of H2O2, which in turn results in the formation of hydroxyl radicals via oxidation of reduced copper (Fenton reaction)
eff↑, Copper Supplementation Increases the Sensitivity of Normal Breast Epithelial Cells to the Antiproliferative Effects of Curcumin

4829- CUR,    Dual Action of Curcumin as an Anti- and Pro-Oxidant from a Biophysical Perspective
- Review, Var, NA
*antiOx↑, therapeutic effects against different disorders, mostly due to its anti-oxidant properties.
ROS↑, However, curcumin can act as a pro-oxidant when blue light is applied, since upon illumination it can generate singlet oxygen
*lipid-P↓, In addition to inhibiting lipid peroxidation, curcumin appears to reduce induciblenitric oxide (NO) synthase (iNOS) activity.
*iNOS↓,
*BioAv↓, poor bioavailability is the key to curcumin’s health-promoting effects,

4828- CUR,    Role of pro-oxidants and antioxidants in the anti-inflammatory and apoptotic effects of curcumin (diferuloylmethane)
- Review, Var, NA
*NF-kB↓, TNF-mediated NF-κB activation was inhibited by curcumin
ROS↑, curcumin induced the production of reactive oxygen species and modulated intracellular GSH levels.

4826- CUR,    The Bright Side of Curcumin: A Narrative Review of Its Therapeutic Potential in Cancer Management
- Review, Var, NA
*antiOx↑, Curcumin demonstrates strong antioxidant and anti-inflammatory properties, contributing to its ability to neutralize free radicals and inhibit inflammatory mediators
*Inflam↑,
*ROS↓,
Apoptosis↑, Its anticancer effects are mediated by inducing apoptosis, inhibiting cell proliferation, and interfering with tumor growth pathways in various colon, pancreatic, and breast cancers
TumCP↓,
BioAv↓, application is limited by its poor bioavailability due to its rapid metabolism and low absorption.
Half-Life↓,
eff↑, curcumin-loaded hydrogels and nanoparticles, have shown promise in improving curcumin bioavailability and therapeutic efficacy.
TumCCA↑, Studies have demonstrated that curcumin can suppress the proliferation of cancer cells by interfering with the cell cycle [21,22]
BAX↑, Curcumin enhances the expression of pro-apoptotic proteins such as Bax, Bak, PUMA, Bim, and Noxa and death receptors such as TRAIL-R1/DR4 and TRAIL-R2/DR5
Bak↑,
PUMA↑,
BIM↑,
NOXA↑,
TRAIL↑,
Bcl-2↓, curcumin decreases the levels of anti-apoptotic proteins like Bcl-2, Bcl-XL, survin, and XIAP
Bcl-xL↓,
survivin↓,
XIAP↓,
cMyc↓, This shift in the balance of apoptotic regulators facilitates the release of cytochrome c from mitochondria [33,35] and activates caspases
Casp↑,
NF-kB↓, Curcumin suppresses the activity of key transcription factors like NF-κB, STAT3, and AP-1 and interferes with critical signal transduction pathways such as PI3K/Akt/mTOR and MAPK/ERK.
STAT3↓,
AP-1↓,
angioG↓, curcumin inhibits angiogenesis and metastasis by downregulating VEGF, VEGFR2, and matrix metalloproteinases (MMPs).
TumMeta↑,
VEGF↓,
MMPs↓,
DNMTs↓, Epigenetic modifications through the inhibition of DNA methyltransferases (DNMTs) and histone deacetylases (HDACs) further contribute to its anticancer properties.
HDAC↓,
ROS↑, curcumin-loaded nanoparticles showed significant cytotoxicity in the SCC25, MDA-MB-231, and A549 cell lines, with a decrease in tumor cell proliferation, an increase in ROS, and an increase in apoptosis.

4710- CUR,    Curcumin inhibits migration and invasion of non-small cell lung cancer cells through up-regulation of miR-206 and suppression of PI3K/AKT/mTOR signaling pathway
- in-vitro, Lung, A549
TumCMig↓, Curcumin significantly inhibited migration and invasion in A549 cells, accompanied by significantly elevated miR-206 expression.
TumCI↓,
miR-206↑, Overexpression of miR-206 could inhibit migration and invasion of A549 cells, but it could also significantly decrease the phosphorylation levels of mTOR and AKT.
p‑mTOR↓,
p‑Akt↓,


Showing Research Papers: 1 to 50 of 301
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 301

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ARE/EpRE↑, 1,   Fenton↑, 1,   Ferroptosis↑, 1,   GPx4↓, 1,   ROS↑, 8,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

ACSL4↑, 1,   cMyc↓, 2,   PI3K/Akt↓, 1,   SCD1↓, 1,  

Cell Death ⓘ

Akt↓, 1,   p‑Akt↓, 1,   Apoptosis↑, 4,   Bak↑, 1,   BAX↑, 3,   Bax:Bcl2↑, 1,   Bcl-2↓, 3,   Bcl-xL↓, 1,   BIM↑, 1,   Casp↑, 1,   Casp3↑, 1,   Cyt‑c↑, 1,   Ferroptosis↑, 1,   NOXA↑, 1,   Paraptosis↑, 1,   PUMA↑, 1,   survivin↓, 1,   TRAIL↑, 1,   TumCD↑, 1,  

Transcription & Epigenetics ⓘ

EZH2↓, 1,   miR-21↓, 1,   miR-27a-3p↓, 3,   sonoS↑, 1,   tumCV↓, 2,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,   GRP78/BiP↓, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 2,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,   DNMTs↓, 1,   PARP1↓, 1,  

Cell Cycle & Senescence ⓘ

CDK4↓, 1,   cycD1/CCND1↓, 1,   TumCCA↑, 4,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 3,   HDAC↓, 1,   HH↓, 1,   HH↝, 1,   miR-34a↑, 3,   mTOR↓, 1,   p‑mTOR↓, 1,   NOTCH↓, 1,   NOTCH↝, 1,   PI3K↓, 1,   STAT1↓, 1,   STAT3↓, 3,   TumCG↓, 4,   Wnt↓, 1,   Wnt↝, 1,  

Migration ⓘ

AP-1↓, 1,   FAK↝, 1,   miR-200b↑, 1,   miR-206↑, 1,   MMPs↓, 1,   TregCell↓, 1,   TumCI↓, 1,   TumCMig↓, 2,   TumCP↓, 4,   TumMeta↓, 1,   TumMeta↑, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   EPR↑, 2,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

IL1↓, 1,   IL10↓, 1,   IL6↓, 1,   IL8↓, 1,   Inflam↓, 1,   JAK↓, 1,   MDSCs↓, 1,   NF-kB↓, 4,   NK cell↑, 1,   PD-L1↓, 1,   PSA↓, 1,   T-Cell↑, 1,  

Synaptic & Neurotransmission ⓘ

ADAM10↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,   CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 3,   BioAv↑, 1,   ChemoSen↑, 3,   Dose↝, 2,   Dose∅, 1,   eff↓, 2,   eff↑, 10,   Half-Life↓, 1,   Half-Life∅, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 1,   EZH2↓, 1,   IL6↓, 1,   PD-L1↓, 1,   PSA↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 2,   chemoP↑, 2,   chemoPv↑, 2,   toxicity↓, 2,  
Total Targets: 108

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 9,   Catalase↑, 2,   GSH↑, 3,   HO-1↑, 2,   lipid-P↓, 3,   MDA↓, 2,   MDA↑, 1,   MPO↓, 1,   NQO1↑, 1,   NRF2↓, 1,   NRF2↑, 4,   ROS↓, 9,   SOD↑, 2,  

Metal & Cofactor Biology ⓘ

IronCh↑, 2,  

Mitochondria & Bioenergetics ⓘ

MMP↑, 1,  

Core Metabolism/Glycolysis ⓘ

Acetyl-CoA↓, 1,   ALAT↓, 1,   AMPK↑, 2,   CREB↑, 2,   CRM↓, 1,   LDL↓, 2,   NADPH↓, 1,   PPARγ↑, 1,   SIRT1↑, 3,  

Cell Death ⓘ

iNOS↓, 1,  

Transcription & Epigenetics ⓘ

Ach↑, 1,   other↓, 6,  

DNA Damage & Repair ⓘ

DNAdam↓, 1,   P53↓, 2,  

Proliferation, Differentiation & Cell State ⓘ

ERK↑, 1,   GSK‐3β↓, 3,   mTOR↓, 1,   mTORC1↓, 1,  

Migration ⓘ

AntiAg↑, 1,   Ca+2↓, 1,   CDK5↓, 3,   COL3A1↓, 1,   TXNIP↓, 1,   α-SMA↓, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,   NO↑, 1,   TXA2↓, 1,  

Barriers & Transport ⓘ

BBB↑, 2,  

Immune & Inflammatory Signaling ⓘ

COX2?, 1,   COX2↓, 1,   IL10↑, 1,   IL12↓, 1,   IL17↓, 1,   IL1β↓, 1,   IL23↓, 1,   IL4↑, 1,   IL6↓, 1,   Inflam↓, 8,   Inflam↑, 1,   MCP1↓, 1,   NF-kB↓, 4,   TNF-α↓, 3,  

Synaptic & Neurotransmission ⓘ

AChE↓, 11,   ADAM10↑, 2,   ADAM10↝, 1,   BChE↓, 2,   BDNF↑, 5,   PSD95↑, 1,   tau↓, 1,   p‑tau↓, 3,   TrkB↑, 1,  

Protein Aggregation ⓘ

Aβ↓, 6,   BACE↓, 3,   NLRP3↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↝, 1,   Dose?, 1,   Dose↝, 1,   eff↑, 2,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   ALP↓, 1,   AST↓, 1,   GutMicro↑, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

AntiAge↑, 3,   cognitive↑, 4,   hepatoP↑, 1,   memory↑, 5,   Mood↑, 1,   neuroP↑, 4,   OS↑, 2,   RenoP↑, 1,   toxicity↓, 1,  
Total Targets: 89

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

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