Formononetin / ROS Cancer Research Results

Form, Formononetin: Click to Expand ⟱
Features:
Formononetin is an O-methylated isoflavone.
-Ononin is formononetin-7-O-β-D-glucoside, meaning formononetin with a glucose attached at the 7-position.
Found in several plant sources, including:

Red Clover (Trifolium pratense):
Astragalus membranaceus:
Other Leguminous Plants:
-Various plants in the legume family (Fabaceae) may also contain formononetin, although the levels and bioavailability can differ depending on the plant species and extraction methods.

Pathways:
PI3K/Akt Pathway: formononetin may inhibit the phosphorylation of Akt
(MAPK) Pathway: may modulate components of the MAPK pathway
STAT3 Signaling Pathway: formononetin can downregulate STAT3 activity
NF-κB Pathway: modulating NF-κB activation
Apoptotic Pathways: via mitochondrial-dependent pathways, enhancing caspase activation
Induce cell cycle arrest at different checkpoints (e.g., G1 or G2/M phases)

Formononetin, a naturally occurring isoflavone found in red clover, Astragalus membranaceus, and other leguminous plants, shows promise as an anticancer agent. Its ability to modulate key signaling pathways—including PI3K/Akt, MAPK, STAT3, NF-κB, and apoptotic and cell cycle regulatory mechanisms—suggests a multifaceted potential in cancer prevention and therapy.

Formononetin — Formononetin is a naturally occurring O-methylated isoflavone and phytoestrogen found primarily in red clover, Astragalus membranaceus, licorice, kudzu, and other Fabaceae plants. It is classified as a plant-derived isoflavonoid small molecule and is commonly abbreviated FMN, FNT, FT, or Form. Formononetin is also produced from its glycoside ononin and is extensively converted in vivo to daidzein and phase-II conjugates. Its anticancer activity remains experimental and is complicated by concentration-dependent estrogen-receptor signaling, limited aqueous solubility, rapid metabolism, and comparatively low systemic exposure to unconjugated parent compound.

Primary mechanisms (ranked):

  1. Suppression of receptor tyrosine kinase and survival signaling, particularly IGF1R, EGFR, PI3K, AKT, and mTOR pathways.
  2. Induction of mitochondrial apoptosis through ↑ Bax/Bcl-2 ratio, caspase activation, PARP cleavage, and suppression of MCL-1 and other survival proteins.
  3. Inhibition of JAK1/JAK2–STAT3/STAT5 signaling, including reduced STAT nuclear translocation, transcriptional activity, and downstream proliferative and anti-apoptotic proteins.
  4. Cell-cycle arrest through ↓ cyclin D1 and related cell-cycle regulators, commonly producing G0/G1 arrest, although the phase is model-dependent.
  5. Context-dependent oxidative stress induction, with ↑ ROS and glutathione imbalance contributing to STAT inhibition, apoptosis, ferroptotic signaling, and reversal of multidrug resistance.
  6. Suppression of invasion and metastasis through modulation of MMP2/9, EMT-related signaling, EphB3, ERK, NF-κB, AP-1, and regulatory non-coding RNAs.
  7. Immune-checkpoint modulation through ↓ MYC–STAT3-dependent PD-L1 synthesis and increased lysosomal PD-L1 degradation.
  8. Chemosensitization through inhibition of drug-efflux transporters, autophagy or mitophagy modulation, and suppression of survival pathways.
  9. Estrogen-receptor modulation, including ERα agonism and ERβ-associated effects; biological direction is concentration-, tissue-, and receptor-context-dependent.

Bioavailability / PK relevance: Native formononetin has poor water solubility, substantial intestinal and hepatic first-pass metabolism, rapid glucuronidation and sulfation, and extensive O-demethylation to daidzein. Rat oral bioavailability has been reported at approximately 22%, but this does not establish comparable human exposure. Free parent formononetin generally represents only a small fraction of circulating total isoflavones. Phospholipid, nanoparticle, lipid, and bioenhancer formulations can increase exposure in animals but are not validated cancer treatments.

In-vitro vs systemic exposure relevance: Many anticancer studies use approximately 20–100 µM formononetin, whereas exposure to unconjugated parent compound after ordinary oral red-clover or dietary-isoflavone intake is generally much lower. Consequently, many direct cytotoxic, ROS-generating, STAT-inhibitory, and apoptosis-inducing findings occur at concentrations unlikely to be achieved systemically with conventional oral preparations. Lower concentrations may instead produce estrogenic or proliferative effects in ERα-positive cells, creating a clinically important biphasic-response concern.

Clinical evidence status: Preclinical. Evidence includes cancer-cell experiments and multiple murine xenograft or carcinogenesis models. No established formononetin monotherapy or adjunctive cancer regimen is supported by completed randomized clinical trials, and formononetin is not an approved anticancer drug. Human trials involving red-clover isoflavone mixtures address menopausal, vascular, or bone outcomes rather than cancer treatment and cannot be attributed specifically to formononetin.

Safety considerations: Human safety data for purified formononetin are limited. Its ERα agonist and phytoestrogen properties warrant caution in estrogen-sensitive malignancies and in patients using endocrine therapies. Experimental studies demonstrate concentration-dependent stimulation of ERα-positive breast-cancer cells at low micromolar concentrations and inhibition at higher concentrations. Potential interactions may also arise through drug-efflux transporters, CYP enzymes, glucuronidation pathways, anticoagulant drugs, or combination chemotherapy. Long-term reproductive, endocrine, hepatic, and oncologic safety of pharmacological-dose purified formononetin remains unresolved.



Formononetin Mechanistic Profile

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 IGF1R EGFR PI3K AKT mTOR IGF1R↓ EGFR↓ PI3K↓ AKT↓ mTOR↓ Context-dependent R G Reduced survival and proliferation One of the most consistently reported anticancer axes; upstream receptor affected varies by cancer model.
2 Mitochondrial apoptosis Bax↑ Bcl-2↓ MCL-1↓ caspase-3/9↑ PARP cleavage↑ Usually protective or mixed (context-dependent) G Apoptotic cell death Observed in breast, cervical, ovarian, prostate, lung, osteosarcoma, gastric, colorectal, and myeloma models.
3 JAK STAT signaling JAK1↓ JAK2↓ STAT3↓ STAT5↓ JAK STAT↓ during inflammatory stress R G Reduced transcription of survival and inflammatory genes Includes reduced STAT phosphorylation, DNA binding, and nuclear translocation.
4 Cell-cycle regulation Cyclin D1↓ CDK activity↓ G0/G1 arrest↑ Mixed G Proliferation arrest Checkpoint is model-dependent; G0/G1 arrest is best characterized in breast and colorectal models.
5 Oxidative stress and glutathione ROS↑ GSH/GSSG ratio↓ ROS↓ or antioxidant defenses↑ (context-dependent) P R Redox-mediated apoptosis and signal inhibition Pro-oxidant activity is prominent in myeloma and multidrug-resistant cancer models but is dose-dependent.
6 Ferroptosis and lipid redox metabolism Lipid peroxidation↑ GPX4-related defense↓ ferroptosis↑ Ferroptosis↓ in some tissue-injury models R G Iron-dependent oxidative cell death Emerging mechanism with opposite effects possible in cancer versus normal-tissue injury models.
7 Ras MAPK ERK p38 ERK1/2↓ or p38↑ Context-dependent R G Apoptosis and growth suppression Direction differs by MAPK branch and cancer type; p38 activation can be pro-apoptotic while ERK suppression reduces survival.
8 NF-κB and AP-1 NF-κB↓ AP-1↓ NF-κB↓ during inflammatory activation R G Reduced inflammation, survival, and invasion Particularly documented in myeloma and neuroinflammatory or vascular stress models.
9 PD-L1 immune checkpoint MYC↓ STAT3↓ PD-L1↓ lysosomal degradation↑ Not established G Enhanced cytotoxic T-cell activity Demonstrated in cervical-cancer co-culture and xenograft systems; clinical immunotherapy relevance is unproven.
10 Invasion EMT and matrix remodeling MMP2↓ MMP9↓ migration↓ invasion↓ EMT↓ Endothelial migration↑ in some models G Reduced metastatic phenotype Cancer-cell inhibition conflicts with pro-migratory and pro-angiogenic ERα effects reported in normal endothelial cells.
11 Estrogen receptor signaling ERα agonism↑ or ERβ-associated suppression↑ (dose-dependent) ERα↑ ERβ↑ (tissue-dependent) R G Biphasic estrogenic modulation Low micromolar exposure may stimulate ERα-positive breast-cancer proliferation, whereas higher concentrations may inhibit proliferation and induce apoptosis.
12 Angiogenesis Angiogenesis↓ secondary to STAT3 PD-L1 or tumor suppression ERα ROCK-II MMP2/9↑ angiogenesis↑ G Strongly context-dependent vascular effect Formononetin can promote endothelial migration and vascular sprouting; it should not be categorized as a uniformly anti-angiogenic compound.
13 Autophagy and mitophagy Autophagy↓ or mitophagy altered (model-dependent) Frequently protective autophagy↑ G Chemosensitization or stress adaptation Taxane-resistant and triple-negative breast-cancer studies report reversal of resistance through autophagy or BACH1-associated mitophagy regulation.
14 Drug efflux and multidrug resistance P-glycoprotein↓ ABCC2↓ intracellular chemotherapy↑ Drug-disposition effects possible R G Chemosensitization Synergy has been reported with bortezomib, paclitaxel, vincristine, doxorubicin, and 5-fluorouracil in preclinical systems.
15 Clinical Translation Constraint High experimental concentrations; heterogeneous and biphasic responses Estrogenic and pro-angiogenic activity possible G Limits direct clinical extrapolation Poor solubility, extensive metabolism, low free-parent exposure, formulation dependence, absent cancer trials, and unresolved safety in hormone-sensitive disease.

P: 0–30 min    R: 30 min–3 hr    G: >3 hr
ROS, Reactive Oxygen Species: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
Reactive oxygen species (ROS) are highly reactive molecules that contain oxygen and can lead to oxidative stress in cells. They play a dual role in cancer biology, acting as both promoters and suppressors of cancer.
ROS can cause oxidative damage to DNA, leading to mutations that may contribute to cancer initiation and progression. So normally you want to inhibit ROS to prevent cell mutations.
However excessive ROS can induce apoptosis (programmed cell death) in cancer cells, potentially limiting tumor growth. Chemotherapy typically raises ROS.
-mitochondria is the main source of reactive oxygen species (ROS) (and the ETC is heavily related)
ROS Homeostasis in Cancer Cells and Its Potential as a Therapeutic Target

"Reactive oxygen species (ROS) are two electron reduction products of oxygen, including superoxide anion, hydrogen peroxide, hydroxyl radical, lipid peroxides, protein peroxides and peroxides formed in nucleic acids 1. They are maintained in a dynamic balance by a series of reduction-oxidation (redox) reactions in biological systems and act as signaling molecules to drive cellular regulatory pathways."
"During different stages of cancer formation, abnormal ROS levels play paradoxical roles in cell growth and death 8. A physiological concentration of ROS that maintained in equilibrium is necessary for normal cell survival. Ectopic ROS accumulation promotes cell proliferation and consequently induces malignant transformation of normal cells by initiating pathological conversion of physiological signaling networks. Excessive ROS levels lead to cell death by damaging cellular components, including proteins, lipid bilayers, and chromosomes. Therefore, both scavenging abnormally elevated ROS to prevent early neoplasia and facilitating ROS production to specifically kill cancer cells are promising anticancer therapeutic strategies, in spite of their contradictoriness and complexity."
"ROS are the collection of derivatives of molecular oxygen that occur in biology, which can be categorized into two types, free radicals and non-radical species. The non-radical species are hydrogen peroxide (H 2O 2 ), organic hydroperoxides (ROOH), singlet molecular oxygen ( 1 O 2 ), electronically excited carbonyl, ozone (O3 ), hypochlorous acid (HOCl, and hypobromous acid HOBr). Free radical species are super-oxide anion radical (O 2•−), hydroxyl radical (•OH), peroxyl radical (ROO•) and alkoxyl radical (RO•) [130]. Any imbalance of ROS can lead to adverse effects. H2 O 2 and O 2 •− are the main redox signalling agents. The cellular concentration of H2 O 2 is about 10−8 M, which is almost a thousand times more than that of O2 •−".
"Radicals are molecules with an odd number of electrons in the outer shell [393,394]. A pair of radicals can be formed by breaking a chemical bond or electron transfer between two molecules."

Recent investigations have documented that polyphenols with good antioxidant activity may exhibit pro-oxidant activity in the presence of copper ions, which can induce apoptosis in various cancer cell lines but not in normal cells. "We have shown that such cell growth inhibition by polyphenols in cancer cells is reversed by copper-specific sequestering agent neocuproine to a significant extent whereas iron and zinc chelators are relatively ineffective, thus confirming the role of endogenous copper in the cytotoxic action of polyphenols against cancer cells. Therefore, this mechanism of mobilization of endogenous copper." > Ions could be one of the important mechanisms for the cytotoxic action of plant polyphenols against cancer cells and is possibly a common mechanism for all plant polyphenols. In fact, similar results obtained with four different polyphenolic compounds in this study, namely apigenin, luteolin, EGCG, and resveratrol, strengthen this idea.
Interestingly, the normal breast epithelial MCF10A cells have earlier been shown to possess no detectable copper as opposed to breast cancer cells [24], which may explain their resistance to polyphenols apigenin- and luteolin-induced growth inhibition as observed here (Fig. 1). We have earlier proposed [25] that this preferential cytotoxicity of plant polyphenols toward cancer cells is explained by the observation made several years earlier, which showed that copper levels in cancer cells are significantly elevated in various malignancies. Thus, because of higher intracellular copper levels in cancer cells, it may be predicted that the cytotoxic concentrations of polyphenols required would be lower in these cells as compared to normal cells."

Majority of ROS are produced as a by-product of oxidative phosphorylation, high levels of ROS are detected in almost all cancers.
-It is well established that during ER stress, cytosolic calcium released from the ER is taken up by the mitochondrion to stimulate ROS overgeneration and the release of cytochrome c, both of which lead to apoptosis.

Note: Products that may raise ROS can be found using this database, by:
Filtering on the target of ROS, and selecting the Effect Direction of ↑

Targets to raise ROS (to kill cancer cells):
• NADPH oxidases (NOX): NOX enzymes are involved in the production of ROS.
    -Targeting NOX enzymes can increase ROS levels and induce cancer cell death.
    -eNOX2 inhibition leads to a high NADH/NAD⁺ ratio which can lead to increased ROS
• Mitochondrial complex I: Inhibiting can increase ROS production
• P53: Activating p53 can increase ROS levels(by inducing the expression of pro-oxidant genes)
• Nrf2 inhibition: regulates the expression of antioxidant genes. Inhibiting Nrf2 can increase ROS levels
• Glutathione (GSH): an antioxidant. Depleting GSH can increase ROS levels
• Catalase: Catalase converts H2O2 into H2O+O. Inhibiting catalase can increase ROS levels
• SOD1: converts superoxide into hydrogen peroxide. Inhibiting SOD1 can increase ROS levels
• PI3K/AKT pathway: regulates cell survival and metabolism. Inhibiting can increase ROS levels
• HIF-1α inhibition: regulates genes involved in metabolism and angiogenesis. Inhibiting HIF-1α can increase ROS
• Glycolysis: Inhibiting glycolysis can increase ROS levels • Fatty acid oxidation: Cancer cells often rely on fatty acid oxidation for energy production.
-Inhibiting fatty acid oxidation can increase ROS levels
• ER stress: Endoplasmic reticulum (ER) stress can increase ROS levels
• Autophagy: process by which cells recycle damaged organelles and proteins.
-Inhibiting autophagy can increase ROS levels and induce cancer cell death.
• KEAP1/Nrf2 pathway: regulates the expression of antioxidant genes.
    -Inhibiting KEAP1 or activating Nrf2 can increase ROS levels and induce cancer cell death.
• DJ-1: regulates the expression of antioxidant genes. Inhibiting DJ-1 can increase ROS levels
• PARK2: regulates the expression of antioxidant genes. Inhibiting PARK2 can increase ROS levels
• SIRT1 inhibition:regulates the expression of antioxidant genes. Inhibiting SIRT1 can increase ROS levels
• AMPK activation: regulates energy metabolism and can increase ROS levels when activated.
• mTOR inhibition: regulates cell growth and metabolism. Inhibiting mTOR can increase ROS levels
• HSP90 inhibition: regulates protein folding and can increase ROS levels when inhibited.
• Proteasome: degrades damaged proteins. Inhibiting the proteasome can increase ROS levels
• Lipid peroxidation: a process by which lipids are oxidized, leading to the production of ROS.
    -Increasing lipid peroxidation can increase ROS levels
• Ferroptosis: form of cell death that is regulated by iron and lipid peroxidation.
    -Increasing ferroptosis can increase ROS levels
• Mitochondrial permeability transition pore (mPTP): regulates mitochondrial permeability.
    -Opening the mPTP can increase ROS levels
• BCL-2 family proteins: regulate apoptosis and can increase ROS levels when inhibited.
• Caspase-independent cell death: a form of cell death that is regulated by ROS.
    -Increasing caspase-independent cell death can increase ROS levels
• DNA damage response: regulates the repair of DNA damage. Increasing DNA damage can increase ROS
• Epigenetic regulation: process by which gene expression is regulated.
    -Increasing epigenetic regulation can increase ROS levels

-PKM2, but not PKM1, can be inhibited by direct oxidation of cysteine 358 as an adaptive response to increased intracellular reactive oxygen species (ROS)

ProOxidant Strategy:(inhibit the Mevalonate Pathway (likely will also inhibit GPx)
-HydroxyCitrate (HCA) found as supplement online and typically used in a dose of about 1.5g/day or more
-Atorvastatin typically 40-80mg/day, -Dipyridamole typically 200mg 2x/day Combined effect research
-Lycopene typically 100mg/day range (note debatable as it mainly lowers NRF2)

Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy 
ROS-Inducing Interventions in Cancer — Canonical + Mechanistic Reference
-generated from AI and Cancer database
ROS rating:  +++ strong | ++ moderate | + weak | ± mixed | 0 none
NRF2:        ↓ suppressed | ↑ activated | ± mixed | 0 none
Conditions:  [D] dose  [Fe] metal  [M] metabolic  [O₂] oxygen
             [L] light [F] formulation [T] tumor-type [C] combination




Item ROS↑ NRF2 Condition Mechanism Class Remarks 



ROS">Piperlongumine
+++ ↓ [D][T] ROS-dominant






ROS">Shikonin
+++↓/±[D][T]ROS-dominant






ROS">Vitamin K3 (menadione)
+++↓[D]ROS-dominant






ROS">Copper (ionic / nano)
+++↓[Fe][F]ROS-dominant






ROS">Sodium Selenite
+++↓[D]ROS-dominant






ROS">Juglone
+++↓[D]ROS-dominant






ROS">Auranofin
+++↓[D]ROS-dominant






ROS">Photodynamic Therapy (PDT)
+++0[L][O₂]ROS-dominant






ROS">Radiotherapy / Radiation
+++0[O₂]ROS-dominant






ROS">Doxorubicin
+++↓[D]ROS-dominant






ROS">Cisplatin
++↓[D][T]ROS-dominant






ROS">Salinomycin
++↓[D][T]ROS-dominant






ROS">Artemisinin / DHA
++↓[Fe][T]ROS-dominant






ROS">Sulfasalazine
++↓[C][T]ROS-dominant






ROS">FMD / fasting
++↓[M][C][O₂]ROS-dominant






ROS">Vitamin C (pharmacologic)
++↓[Fe][D]ROS-dominant






ROS">Silver nanoparticles
++±[F][D]ROS-dominant






ROS">Gambogic acid
++↓[D][T]ROS-dominant






ROS">Parthenolide
++↓[D][T]ROS-dominant






ROS">Plumbagin
++↓[D]ROS-dominant






ROS">Allicin
++↓[D]ROS-dominant






ROS">Ashwagandha (Withaferin A)
++↓[D][T]ROS-dominant






ROS">Berberine
++↓[D][M]ROS-dominant






ROS">PEITC
++↓[D][C]ROS-dominant






ROS">Methionine restriction
+↓[M][C][T]ROS-secondary






ROS">DCA
+±[M][T]ROS-secondary






ROS">Capsaicin
+±[D][T]ROS-secondary






ROS">Galloflavin
+0[D]ROS-secondary






ROS">Piperine
+±[D][F]ROS-secondary






ROS">Propyl gallate
+↓[D]ROS-secondary






ROS">Scoulerine
+?[D][T]ROS-secondary






ROS">Thymoquinone
±±[D][T]Dual redox






ROS">Emodin
±±[D][T]Dual redox






ROS">Alpha-lipoic acid (ALA)
±↑[D][M]NRF2-dominant






ROS">Curcumin
±↑/↓[D][F]NRF2-dominant






ROS">EGCG
±↑/↓[D][O₂]NRF2-dominant






ROS">Quercetin
±↑/↓[D][Fe]NRF2-dominant






ROS">Resveratrol
±↑[D][M]NRF2-dominant






ROS">Sulforaphane
±↑↑[D]NRF2-dominant






ROS">Lycopene
0↑—Antioxidant






ROS">Rosmarinic acid
0↑—Antioxidant






ROS">Citrate
00—Neutral


Scientific Papers found: Click to Expand⟱
6981- Form,    Formononetin: a review of its source, pharmacology, drug combination, toxicity, derivatives, and drug delivery systems
- Review, Var, NA - Review, AD, NA - Review, PSA, NA
BioAv↝, *memory↑, *ROS↓, *AChE↓, *NF-kB↓, *Keap1↝, *NRF2↑, *Inflam↓, *PGC-1α↝, *HO-1↓, *p‑tau↓, *cognitive↑, *BDNF↑, *5HT↑, *Stroke↓, *PARP1↓, *AIF↓, *Casp3↓, NP/CIPN↓, *neuroP↑, *NGF↑, *TNF-α↓, *IL1β↓, *IL18↓, *IL6↓, *VCAM-1↓, *pol-M2 MC↑, *hepatoP↑, *AST↓, *ALAT↓, *LC3II↑, *Beclin-1↑, *p62↑, *COX2↑, *MMP↑, *ATP↑, *GSH↑, *Catalase↑, *GPx↑, *MDA↓, *antiPs↑, *AntiDiabetic↑, *glucose↓, *Insulin↑, *GutMicro↑, *Obesity↓, COX2↓, cycD1/CCND1↓, TumCCA↑, EGFR↓, GSK‐3β↑, Mcl-1↓, *toxicity↓, TumCP↓, Hif1a↓, VEGF↓, ERK↓, LAMs↓, Cyt‑c↑, Casp9↑, Casp3↑, PARP↑, TumCD↑, mitA↑, BACH1↓, P53↓, ROS↑, PD-1↓, NF-kB↓, *Bacteria↓, *AntiViral↑, *mt-ROS?, *PI3K↓, *chemoP↑, ChemoSen↑, eff↑, *toxicity↓, *BioAv↑, *BioAv↑, *eff↑,
6983- Form,    Formononetin enhances angiogenesis in diabetic wounds by inhibiting ferroptosis through suppression of mtROS-mediated xCT/GPX4 upregulation
- vitro+vivo, Nor, HUVECs - vitro+vivo, Diabetic, NA
*BloodF↑, *Ferroptosis↓, *eff↓, *mtDam↓, *xCT↑, *GPx4↑, *Wound Healing↑, *CD31↑, *mt-ROS↓,

Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 1,  

Cell Death(tgid=5) ⓘ

Casp3↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   Mcl-1↓, 1,   TumCD↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↓, 1,   PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

cycD1/CCND1↓, 1,   mitA↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

ERK↓, 1,   GSK‐3β↑, 1,  

Migration(tgid=13) ⓘ

BACH1↓, 1,   LAMs↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

EGFR↓, 1,   Hif1a↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↓, 1,   NF-kB↓, 1,   PD-1↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↝, 1,   ChemoSen↑, 1,   eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

EGFR↓, 1,  

Functional Outcomes(tgid=23) ⓘ

NP/CIPN↓, 1,  
Total Targets: 27

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

Stroke↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↑, 1,   Ferroptosis↓, 1,   GPx↑, 1,   GPx4↑, 1,   GSH↑, 1,   HO-1↓, 1,   Keap1↝, 1,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 1,   mt-ROS?, 1,   mt-ROS↓, 1,   xCT↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

AIF↓, 1,   ATP↑, 1,   Insulin↑, 1,   MMP↑, 1,   mtDam↓, 1,   PGC-1α↝, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   glucose↓, 1,  

Cell Death(tgid=5) ⓘ

Casp3↓, 1,   Ferroptosis↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↑, 1,   LC3II↑, 1,   p62↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

PARP1↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

PI3K↓, 1,  

Migration(tgid=13) ⓘ

CD31↑, 1,   VCAM-1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↑, 1,   IL18↓, 1,   IL1β↓, 1,   IL6↓, 1,   Inflam↓, 1,   pol-M2 MC↑, 1,   NF-kB↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↑, 1,   AChE↓, 1,   BDNF↑, 1,   NGF↑, 1,   p‑tau↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 2,   eff↓, 1,   eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

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

Functional Outcomes(tgid=23) ⓘ

AntiDiabetic↑, 1,   antiPs↑, 1,   chemoP↑, 1,   cognitive↑, 1,   hepatoP↑, 1,   memory↑, 1,   neuroP↑, 1,   Obesity↓, 1,   toxicity↓, 2,   Wound Healing↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiViral↑, 1,   Bacteria↓, 1,  
Total Targets: 64

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
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#:274  Target#:275  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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