Biochanin A / ROS Cancer Research Results

BCA, Biochanin A: Click to Expand ⟱

Features:

Biochanin A is a O-methylated isoflavone.
Found in soy, alfalfa sprouts, peanuts, chickpeas and other legumes.
Inhibits fatty acid amide hydrolase.
-gut/metabolic precursor to genistein

Biochanin A — Biochanin A is a naturally occurring O-methylated isoflavone phytochemical and phytoestrogen found mainly in red clover and other legumes including chickpea, soybean, peanut, and alfalfa. It is best classified as a small-molecule dietary isoflavone / nutraceutical lead rather than an approved oncology drug. Standard abbreviations include BCA and Bio-A. In biological systems it can act both as the parent compound and as a metabolic precursor to genistein and related conjugates, which is important when interpreting systemic effects. In cancer research, Biochanin A is primarily a multi-target preclinical antitumor candidate with anti-proliferative, pro-apoptotic, anti-EMT, and immune-evasion-limiting effects, but translation is constrained by low oral bioavailability, extensive metabolism, estrogenic context dependence, and limited human efficacy data.

main ingredients in many types of supplements used to alleviate postmenopausal symptoms in women

Primary mechanisms (ranked):

EMT suppression centered on ZEB1 downregulation, with associated E-cadherin increase, N-cadherin decrease, reduced invasion/migration, and lower metastatic competence.
Immune-evasion attenuation via ZEB1-linked PD-L1 downregulation in colorectal cancer models.
Mitochondria-associated intrinsic apoptosis with caspase activation, PARP cleavage, Bax/Bcl-2 shift, and cell-cycle arrest in multiple tumor models.
Mitogenic signaling suppression, variably involving PI3K/Akt, ERK/MAPK, NF-κB, and related growth/survival pathways depending on model.
Chemosensitization / resistance modulation, especially in ZEB1-high settings and selected combination regimens.
Redox modulation is context-dependent rather than uniformly antioxidant; some cancer models show ROS increase contributing to apoptosis, while in other settings anti-inflammatory / antioxidant signaling predominates.
FAAH inhibition is a recognized biochemical activity of Biochanin A but is not currently a core cancer mechanism.

Bioavailability / PK relevance: Oral translation is limited by poor solubility, poor oral absorption, extensive intestinal/hepatic phase I–II metabolism, high clearance, enterohepatic cycling, and rapid conversion to conjugates and downstream isoflavone metabolites including genistein. As a result, formulation strategy is often mechanistically relevant to outcome.

In-vitro vs systemic exposure relevance: Many anticancer in-vitro studies use tens of micromolar concentrations, often around 20–100 μM, which likely exceed routine free systemic exposure achievable from ordinary oral intake of unformulated Biochanin A. Therefore, direct concentration-driven antitumor claims should be interpreted cautiously unless supported by formulation, tissue-delivery, or metabolite data.

Clinical evidence status: Preclinical. There is substantial in-vitro and animal antitumor literature, but human oncology evidence remains very limited, with no established role as a standard anticancer therapy. Human deployment is mainly as part of dietary / red-clover isoflavone supplement use rather than cancer-directed drug treatment.

Mechanistic table

Rank	Pathway / Axis	Cancer Cells	Normal Cells	TSF	Primary Effect	Notes / Interpretation
1	ZEB1 EMT axis	↓ ZEB1, ↓ EMT, ↓ migration, ↓ invasion	↔ / not well defined	G	Anti-metastatic state shift	Most coherent cancer-specific axis across current evidence; especially relevant in colorectal and lung adenocarcinoma models.
2	PD-L1 immune-evasion signaling	↓ PD-L1	↔	G	Reduced immune escape potential	Best supported in CRC through ZEB1-linked regulation; mechanistically meaningful but not yet clinically validated as an immunotherapy adjunct.
3	Intrinsic apoptosis program	↑ caspases, ↑ PARP cleavage, ↑ Bax/Bcl-2 ratio, ↑ apoptosis	↔ / selective in some models	R/G	Cytotoxic / cytostatic tumor control	Common downstream output across multiple cancer models; likely integrates mitochondrial stress and growth-signal suppression.
4	Mitochondria / redox stress	↑ ROS (context-dependent), ↑ oxidative stress, ↓ mitochondrial fitness	↔ / potential protection in non-cancer inflammatory settings	R/G	Facilitates apoptosis in susceptible tumors	ROS is not uniformly directional across all literature; in cancer it can rise enough to support death signaling, whereas outside cancer Biochanin A is often described as antioxidant.
5	PI3K Akt survival signaling	↓ PI3K/Akt (model-dependent)	↔	R/G	Reduced survival / proliferation	Frequently reported in breast and other tumor models, but less specific than the ZEB1-centered mechanism.
6	ERK MAPK proliferation signaling	↓ ERK (model-dependent)	↔	R/G	Anti-proliferative effect	Consistent with Nestronics indexing and broader preclinical literature, but not universal across tumor types.
7	Cell-cycle machinery	↓ cyclins / CDKs, arrest ↑	↔	G	Cytostasis preceding apoptosis	Phase specificity varies by model; contributes to lower clonogenicity and slower tumor expansion.
8	Chemosensitization	↑ cisplatin sensitivity, ↓ resistance traits	↔	G	Adjunct leverage	Best-supported adjunct signal is ZEB1-linked sensitization in lung adenocarcinoma; combination effects are promising but still preclinical.
9	FAAH and non-oncology biochemical activity	↔ / indirect	↔	R/G	Not a core cancer effect	Real biochemical property, but currently peripheral to anticancer ranking.
10	Clinical Translation Constraint	Low free exposure, extensive metabolism, estrogenic context, interaction risk	Potential endocrine / PK relevance	G	Limits direct monotherapy translation	Common in-vitro doses likely exceed achievable free systemic exposure of unformulated oral Biochanin A; formulation or metabolite-aware development is likely required.

P: 0–30 min
R: 30 min–3 hr
G: >3 hr

For Alzheimer’s

Biochanin A — Biochanin A is a naturally occurring O-methylated isoflavone phytoestrogen found mainly in red clover and other legumes. It is best classified in the AD context as a preclinical neuroprotective small molecule / nutraceutical lead rather than an approved CNS drug. Standard abbreviations include BCA and Bio-A. Current Alzheimer’s relevance is based on cell, mouse, and review-level evidence suggesting anti-amyloid, anti-apoptotic, anti-neuroinflammatory, antioxidant-response, mitochondrial-protective, and cholinergic-supportive actions. Its translational interpretation is limited by sparse brain PK data, likely extensive metabolism, and the fact that many mechanistic studies use concentrations above typical dietary exposure.

Primary mechanisms (ranked):

Mitochondrial protection with suppression of Aβ-triggered intrinsic apoptosis, including preservation of mitochondrial membrane potential and improvement of Bcl-2/Bax balance.
Neuroinflammation reduction through suppression of pro-inflammatory mediators and downregulation of NF-κB-linked signaling.
Antioxidant-response support, including Nrf2-linked cytoprotection and reduction of oxidative stress markers in preclinical CNS models.
Cholinergic support, with reduced whole-brain acetylcholinesterase activity and improved behavioral performance in scopolamine and aged-mouse models.
Anti-amyloid effect, reported mainly as reduced Aβ-associated injury and, in reviews, reduced Aβ burden in experimental systems.
Blood-brain barrier support is plausible and preclinically supported in ischemia-reperfusion models, but this is not yet AD-specific proof.

Bioavailability / PK relevance: CNS translation remains uncertain because Biochanin A has generally poor oral bioavailability and substantial metabolism; whether parent Biochanin A, its conjugates, or downstream metabolites mediate brain effects remains incompletely resolved.

In-vitro vs systemic exposure relevance: Many neuroprotection studies use approximately 10–100 μM in vitro, including Aβ-PC12 work up to 100 μM, which likely exceeds routine free brain exposure from ordinary oral intake. Therefore, direct concentration-driven neuroprotective claims should be interpreted cautiously.

Clinical evidence status: Preclinical. I did not locate established AD clinical trials showing therapeutic efficacy of Biochanin A itself. Current support comes from mechanistic reviews, cell systems, and animal models rather than human efficacy studies.

AD mechanistic table

Rank	Pathway / Axis	Modulation	TSF	Primary Effect	Notes / Interpretation
1	Mitochondrial apoptosis control	↓ cytochrome c, ↓ Puma, ↑ Bcl-2/Bax, ↑ Bcl-xL/Bax, ↓ caspase-9, ↓ caspase-3	R/G	Neuronal survival support	Best direct AD-relevant mechanistic evidence comes from Aβ25–35-treated PC12 cells, where Biochanin A preserved mitochondrial function and reduced apoptosis.
2	Mitochondrial membrane potential	↑ MMP stability	R	Limits Aβ-linked mitochondrial collapse	A central proximal mechanism in the PC12 amyloid-toxicity model.
3	Neuroinflammation and NF-κB-linked signaling	↓ TNF-α, ↓ IL-1β, ↓ NO, ↓ inflammatory tone	G	Reduces inflammatory neuronal stress	Supported mainly by reviews and broader neuroprotection literature; likely important but less directly demonstrated in AD-specific human systems.
4	Nrf2 antioxidant-response axis	↑ Nrf2 signaling, ↑ GSH/SOD/CAT, ↓ oxidative stress	G	Cytoprotective redox buffering	Mechanistically plausible and supported in CNS disease models; AD relevance is still preclinical and partly inferential.
5	Aβ-associated neuronal injury	↓ Aβ toxicity, ↓ LDH leakage, ↑ viability	R/G	Attenuates amyloid-linked cell damage	Strongly supported in the Aβ25–35 PC12 model; evidence for lowering in vivo plaque burden is review-level rather than established clinical fact.
6	Cholinergic axis	↓ acetylcholinesterase	G	Supports memory-related neurotransmission	Observed in scopolamine-treated and aged mice together with behavioral improvement, but this is not equivalent to approved ChE inhibitor efficacy.
7	Behavioral and memory phenotype	↑ cognitive performance	G	Functional preclinical improvement	Behavioral benefit is reported in mouse dementia-like models, which strengthens relevance but remains model-dependent.
8	Blood-brain barrier support	↑ BBB integrity	G	Potential vascular-neuroprotective support	Supported in ischemia-reperfusion studies, not yet a core AD mechanism but potentially relevant to mixed neurovascular pathology.
9	Clinical Translation Constraint	↓ direct translatability	G	Limits therapeutic certainty	Key constraints are low oral bioavailability, uncertain brain exposure of parent compound, likely metabolite contribution, estrogenic context, and lack of convincing human AD efficacy data.

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)

"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
Selective <span class="wphighlight">ROS</span> stressor, Prevents compensatory upregulation of NRF2, ie GSH↓



ROS">Shikonin
+++ ↓/± [D][T] ROS-dominant
<span class="wphighlight">ROS</span> + glycolysis + GPX4 inhibition



ROS">Vitamin K3 (menadione)
+++ ↓ [D] ROS-dominant
Quinone redox cycler; toxicity limits use



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



ROS">Sodium Selenite
+++ ↓ [D] ROS-dominant
Pro-oxidant, depletes GSH



ROS">Juglone
+++ ↓ [D] ROS-dominant
Strong quinone <span class="wphighlight">ROS</span> chemistry



ROS">Auranofin
+++ ↓ [D] ROS-dominant
TrxR inhibition → redox collapse



ROS">Photodynamic Therapy (PDT)
+++ 0 [L][O₂] ROS-dominant
Singlet oxygen is core cytotoxic mechanism



ROS">Radiotherapy / Radiation
+++ 0 [O₂] ROS-dominant
DNA damage largely via <span class="wphighlight">ROS</span>



ROS">Doxorubicin
+++ ↓ [D] ROS-dominant
Chemo; redox cycling + mitochondrial <span class="wphighlight">ROS</span>



ROS">Cisplatin
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span> contributes to DNA/protein damage



ROS">Salinomycin
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated CSC toxicity



ROS">Artemisinin / DHA
++ ↓ [Fe][T] ROS-dominant
Iron-activated radical generation



ROS">Sulfasalazine
++ ↓ [C][T] ROS-dominant
Ferroptosis; xCT inhibition → lipid <span class="wphighlight">ROS</span>



ROS">FMD / fasting
++ ↓ [M][C][O₂] ROS-dominant
Metabolic stress → mitochondrial <span class="wphighlight">ROS</span>



ROS">Vitamin C (pharmacologic)
++ ↓ [Fe][D] ROS-dominant
Extracellular H₂O₂ at high dose



ROS">Silver nanoparticles
++ ± [F][D] ROS-dominant
<span class="wphighlight">ROS</span> common; selectivity unreliable



ROS">Gambogic acid
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated apoptosis



ROS">Parthenolide
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span> + NF-κB suppression



ROS">Plumbagin
++ ↓ [D] ROS-dominant
Quinone <span class="wphighlight">ROS</span> driver



ROS">Allicin
++ ↓ [D] ROS-dominant
Thiol-reactive oxidative stress



ROS">Ashwagandha (Withaferin A)
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated apoptosis



ROS">Berberine
++ ↓ [D][M] ROS-dominant
Mitochondrial <span class="wphighlight">ROS</span> induction



ROS">PEITC
++ ↓ [D][C] ROS-dominant
GSH depletion + <span class="wphighlight">ROS</span>



ROS">Methionine restriction
+ ↓ [M][C][T] ROS-secondary
Redox vulnerability increased; <span class="wphighlight">ROS</span> indirect



ROS">DCA
+ ± [M][T] ROS-secondary
<span class="wphighlight">ROS</span> via forced OXPHOS



ROS">Capsaicin
+ ± [D][T] ROS-secondary
Ca²⁺ stress → <span class="wphighlight">ROS</span>



ROS">Galloflavin
+ 0 [D] ROS-secondary
<span class="wphighlight">ROS</span> not primary driver



ROS">Piperine
+ ± [D][F] ROS-secondary
Weak <span class="wphighlight">ROS</span> induction



ROS">Propyl gallate
+ ↓ [D] ROS-secondary
Pro-oxidant at high dose



ROS">Scoulerine
+ ? [D][T] ROS-secondary
Sparse <span class="wphighlight">ROS</span> data



ROS">Thymoquinone
± ± [D][T] Dual redox
Antioxidant ↔ pro-oxidant switch



ROS">Emodin
± ± [D][T] Dual redox
Not cancer-exclusive



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



ROS">Curcumin
± ↑/↓ [D][F] NRF2-dominant
Hormetic redox behavior



ROS">EGCG
± ↑/↓ [D][O₂] NRF2-dominant
Auto-oxidation artifacts common



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



ROS">Resveratrol
± ↑ [D][M] NRF2-dominant
<span class="wphighlight">ROS</span> only at high dose



ROS">Sulforaphane
± ↑↑ [D] NRF2-dominant
Strong NRF2 activator



ROS">Lycopene
0 ↑ — Antioxidant
Consistently antioxidant



ROS">Rosmarinic acid
0 ↑ — Antioxidant
Primarily antioxidant



ROS">Citrate
0 0 — Neutral
Metabolic; not a <span class="wphighlight">ROS</span> agent

Scientific Papers found: Click to Expand⟱

5631-

BCA,

Perspectives Regarding the Role of Biochanin A in Humans

Review,

Var,

Review,

AD,

*BioAv↓, *Inflam↓, AntiCan↑, *neuroP↑, chemoPv↑, Dose↝, *SOD↑, *MDA↓, *BAX↓, *HSP70/HSPA5↑, *AntiDiabetic↑, *Insulin↑, *TNF-α↓, *IL1β↓, *IL6↓, *iNOS↓, *COX2↓, *MMP9↓, *ROS↓, *PGE2↓, *BACE↓, *BioAv↑, P-gp⇅,

5633-

BCA,

Mechanisms Behind the Pharmacological Application of Biochanin-A: A review

Review,

Var,

Review,

AD,

*AntiDiabetic↑, *neuroP↑, *toxicity↓, *CYP19↓, p‑Akt↓, mTOR↓, TumCCA↑, P21↑, Casp3↑, Bcl-2↑, Apoptosis↑, E-cadherin↓, TumMeta↓, eff↑, GSK‐3β↓, β-catenin/ZEB1↓, RadioS↑, ROS↑, Casp1↑, MMP2↓, MMP9↓, EGFR↓, ChemoSen↑, PI3K↓, MMPs↓, Hif1a↓, VEGF↓, *ROS↓, *Obesity↓, *cardioP↑, *NRF2↑, *NF-kB↓, *Inflam↓, *lipid-P↓, *hepatoP↑, *AST↓, *ALP↓, *Bacteria↓, *neuroP↑, *SOD↑, *GPx↑, *AChE↓, *BACE↓, *memory↑, *BioAv↓,

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:

Functional Outcomes ⓘ

AntiCan↑, 1, chemoPv↑, 1,
Total Targets: 28

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

GPx↑, 1, lipid-P↓, 1, MDA↓, 1, NRF2↑, 1, ROS↓, 2, SOD↑, 2,

Mitochondria & Bioenergetics ⓘ

Insulin↑, 1,

Cell Death ⓘ

BAX↓, 1, iNOS↓, 1,

Protein Folding & ER Stress ⓘ

HSP70/HSPA5↑, 1,

Migration ⓘ

MMP9↓, 1,

Immune & Inflammatory Signaling ⓘ

COX2↓, 1, IL1β↓, 1, IL6↓, 1, Inflam↓, 2, NF-kB↓, 1, PGE2↓, 1, TNF-α↓, 1,

Synaptic & Neurotransmission ⓘ

AChE↓, 1,

Protein Aggregation ⓘ

BACE↓, 2,

Hormonal & Nuclear Receptors ⓘ

CYP19↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 2, BioAv↑, 1,

Clinical Biomarkers ⓘ

ALP↓, 1, AST↓, 1, IL6↓, 1,

Functional Outcomes ⓘ

AntiDiabetic↑, 2, cardioP↑, 1, hepatoP↑, 1, memory↑, 1, neuroP↑, 3, Obesity↓, 1, toxicity↓, 1,

Infection & Microbiome ⓘ

Bacteria↓, 1,
Total Targets: 34

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#:45  Target#:275  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

Biochanin A / ROS Cancer Research Results

Mechanistic table

For Alzheimer’s

AD mechanistic table

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Cell Death ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Cell Death ⓘ

Protein Folding & ER Stress ⓘ

Migration ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

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