Ginkgetin / ROS Cancer Research Results

Gink, Ginkgetin: Click to Expand ⟱

Features:

Ginkgetin — a naturally occurring biflavonoid, specifically a dimethylated derivative of amentoflavone, found in Ginkgo biloba and several other plants. It is chemically and pharmacologically distinct from generic Ginkgo biloba extract, EGb 761, ginkgolides, bilobalide, and ginkgolic acids. Ginkgetin has predominantly preclinical anticancer evidence, with reported effects on ferroptosis, apoptosis, cell-cycle arrest, proliferation, invasion, angiogenesis, and chemotherapy sensitivity. Major signaling systems reported to be modulated include NRF2/HO-1, JAK/STAT, PI3K/AKT/GSK-3β, MAPK, Wnt/β-catenin, and TFEB-associated ferroptotic signaling. It should be treated as an isolated natural-product constituent rather than as evidence for the pharmacological effects of ordinary Ginkgo supplementation.

Ginkgetin — a naturally occurring biflavonoid, specifically a 3′→8″-linked biflavone and dimethylated derivative of amentoflavone, with the synonym 7,4′-dimethylamentoflavone. It is a small-molecule plant polyphenol rather than a Ginkgo extract and is commonly abbreviated GK. Ginkgetin occurs in Ginkgo biloba leaves and several other plant species. It is chemically and pharmacologically distinct from generic Ginkgo biloba extract, EGb 761, ginkgolides, bilobalide, and ginkgolic acids. Current evidence is predominantly preclinical and supports treating Ginkgetin as a separate isolated natural-product constituent rather than extrapolating its effects to ordinary Ginkgo supplementation.

Primary mechanisms (ranked):

Induction of Ferroptosis through TFEB activation and TFEB–TRIM25-dependent GPX4 ubiquitination and lysosomal degradation, producing loss of GPX4-mediated lipid-peroxide defense.
Disruption of NRF2/HO-1 antioxidant signaling with SLC7A11/GPX4 suppression, GSH depletion, Fe²⁺ accumulation, lipid peroxidation, and increased oxidative stress, particularly during cisplatin treatment.
Suppression of oncogenic JAK2/STAT3 signaling, including SHP-1/PTEN-associated inhibition of STAT3 phosphorylation, proliferation, survival, and tumorigenic signaling.
Suppression of metastatic EMT through AKT/GSK-3β/Snail and Wnt/β-catenin signaling, reducing migration and invasion in experimental lung-cancer models.
Induction of apoptotic signaling through mitochondrial dysfunction, Bax/Bcl-2 modulation, caspase activation, PARP cleavage, and context-dependent MAPK activation.
ROS/H₂O₂-mediated cytotoxicity, with rapid oxidative stress contributing to caspase-dependent apoptosis in susceptible cancer cells.
Cell-cycle inhibition, including G2/M arrest and suppression of proliferative Wnt target genes such as cyclin D1 and survivin.
Anti-angiogenic activity through inhibition of VEGF/VEGFR2-associated AKT, eNOS, ERK, MMP-2, and MMP-9 signaling in experimental vascular models.
Chemosensitization, particularly increased cisplatin responsiveness in experimental lung and cisplatin-resistant cervical cancer through ferroptotic and redox mechanisms.

Bioavailability / PK relevance: Ginkgetin is highly lipophilic and poorly water-soluble, creating an important oral-delivery limitation. Human pharmacokinetic data for isolated Ginkgetin are essentially absent, and no validated human anticancer plasma target or therapeutic dose has been established. Experimental formulation work, including nanomicelles, is being investigated specifically to improve its systemic exposure. Ginkgetin is also a potent in-vitro inhibitor of UGT1A1, creating a potential drug-interaction concern if pharmacologically relevant systemic concentrations can be achieved.

In-vitro vs systemic exposure relevance: Most anticancer studies use isolated Ginkgetin at micromolar concentrations, commonly over prolonged exposures. These concentrations cannot presently be assumed achievable through oral Ginkgo products or conventional Ginkgetin administration because human Cmax data are unavailable and oral bioavailability is poorly characterized. Thus, direct translation of micromolar cell-culture effects to dietary or supplemental Ginkgo exposure is weak.

Clinical evidence status: Preclinical only. Evidence includes cancer-cell studies and multiple mouse xenograft or metastasis models, including lung, breast, prostate, medulloblastoma, and cervical-cancer systems. No established human anticancer trials, approved anticancer indication, validated clinical dose, or demonstrated human therapeutic efficacy was identified. FDA substance registration provides a chemical identifier but does not constitute regulatory approval.

Ginkgetin Cancer-Relevant Mechanisms

Rank	Pathway / Axis	Cancer Cells	Normal Cells	TSF	Primary Effect	Notes / Interpretation
1	STAT3 survival signaling	STAT3 phosphorylation ↓; nuclear STAT3 ↓; STAT3-dependent survival signaling ↓	Not established	R, G	Proliferation ↓; apoptosis ↑	Among the best independently replicated Ginkgetin mechanisms. South Korean studies support inhibition of constitutive and inducible STAT3 signaling in prostate cancer and hematologic cancer models.
2	Caspase and mitochondrial apoptosis	Caspase-3 ↑; caspase-8 ↑; caspase-9 ↑; Bax ↑; Bcl-2 ↓; Bcl-xL ↓; survivin ↓; apoptosis ↑	Apoptosis effects context-dependent	R, G	Programmed cell death	Supported across multiple cancer models and geographically independent laboratories. ROS-dependent caspase activation was demonstrated in an early Taiwanese ovarian-cancer study.
3	Cell-cycle regulation	G2 arrest ↑; cyclin D1 ↓; proliferation ↓	Not established	G	Cytostatic growth inhibition	Independent South Korean colorectal-cancer work demonstrated dose-dependent growth inhibition and G2-phase arrest. Other tumor models also report cell-cycle suppression.
4	ROS and hydrogen peroxide stress	ROS ↑; H₂O₂ ↑; oxidative DNA damage ↑	ROS may ↓ (context-dependent)	P, R	Oxidative stress-mediated apoptosis	In ovarian adenocarcinoma cells, intracellular H₂O₂ increased within approximately 30 minutes; catalase and antioxidant pretreatment partially reduced DNA damage and cytotoxicity. This provides geographically independent evidence predating recent ferroptosis studies.
5	NRF2 HO-1 SLC7A11 GPX4 ferroptosis	NRF2 ↓; HO-1 ↓; SLC7A11 ↓; GPX4 ↓; GSH ↓; Fe²⁺ ↑; lipid peroxidation ↑; ferroptosis ↑	NRF2 may ↑ in nonmalignant injury models (context-dependent)	R, G	Ferroptotic cell death and chemosensitization	Strong mechanistic evidence exists in lung and cervical-cancer models, particularly with cisplatin, but this evidence is presently concentrated in mainland Chinese research groups and has limited geographically independent replication.
6	TFEB TRIM25 GPX4 lysosomal degradation	TFEB activation ↑; TRIM25-mediated GPX4 ubiquitination ↑; GPX4 lysosomal degradation ↑; ferroptosis ↑	Not established	R, G	Ferroptosis	Recent mechanistically detailed pathway in EGFR wild-type lung adenocarcinoma. Potentially important, but independent replication is currently limited; therefore ranked below the more broadly replicated STAT3, apoptosis, cell-cycle, and ROS mechanisms.
7	Wnt β-catenin and EMT signaling	Wnt β-catenin signaling ↓; Snail ↓; EMT ↓; migration ↓; invasion ↓	Not established	R, G	Metastatic phenotype suppression	Supported in medulloblastoma and lung-cancer models. Evidence is biologically coherent but remains more geographically concentrated than the higher-ranked mechanisms.
8	AKT GSK-3β Snail signaling	AKT signaling ↓; GSK-3β-associated EMT signaling ↓; Snail ↓; migration ↓; invasion ↓	Not established	R, G	Migration and invasion ↓	Primarily supported by lung adenocarcinoma studies. Closely overlaps with Wnt and EMT modulation and should be interpreted as a context-dependent metastatic signaling mechanism.
9	Estrogen receptor and PFKFB3 signaling	ERα signaling ↓; PFKFB3-associated survival signaling ↓; viability ↓	Not established	G	ER-positive breast-cancer growth inhibition	Supported by an independent South Korean study in MCF-7 and T-47D breast-cancer cells. Likely tumor-subtype specific rather than a universal Ginkgetin mechanism.
10	VEGF VEGFR2 angiogenic signaling	Angiogenesis ↓	VEGFR2 signaling ↓; AKT ↓; eNOS ↓; ERK ↓; MMP-2 ↓; MMP-9 ↓	R, G	Anti-angiogenic activity	Experimental endothelial and tumor models support anti-angiogenic activity, but independent geographic replication is limited and some evidence involves combination treatment.
11	Cisplatin chemosensitization	Cisplatin sensitivity ↑; ferroptosis ↑; apoptosis ↑	Normal-tissue selectivity not established	G	Drug-response enhancement	Preclinical lung and cervical-cancer studies indicate increased cisplatin responsiveness, principally through ferroptotic and redox pathways. No human clinical validation has been established.
12	Clinical Translation Constraint	Effective experimental exposure generally micromolar; human therapeutic exposure unknown	Potential metabolic drug interactions; normal-tissue exposure insufficiently characterized	G	Limits clinical extrapolation	Poor aqueous solubility, uncertain human bioavailability, absence of validated human pharmacokinetic targets, geographic concentration of several newer mechanistic findings, and lack of clinical cancer trials substantially limit translation.

TSF: 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
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⟱

7267-

Gink,

Neuroprotective Potential of Biflavone Ginkgetin: A Review

Review,

AD,

Review,

Park,

Review,

Stroke,

*neuroP↑, *ROS↓, *Aβ↓, *Inflam↓, *Dose↝, *cardioP↑, TumCCA↑, Apoptosis↑, TumAuto↑, STAT↓, *Stroke↓,

7263-

Gink,

Ginkgetin delays the progression of osteoarthritis by inhibiting the NF-κB and MAPK signaling pathways

in-vitro,

ostP,

SW1353

*ROS↓, *MMP13↓, *Cartilage↑,

7260-

Gink,

Ginkgetin: A natural biflavone with versatile pharmacological activities

Review,

Var,

Review,

Stroke,

Review,

AD,

*AntiCan↑, *Inflam↓, *AntiBio↑, *neuroP↑, *TumCCA↑, Apoptosis↑, TumAuto↑, iNOS↓, COX2/PTGS2↓, PGE2↓, NF-kB↓, PLA2↓, *neuroP↑, *Stroke↓, *AntiFungal↓, *Bacteria↓, Bcl-xL↓, Bcl-2↓, Casp9↑, Casp3↑, cl‑PARP↑, IL6↓, STAT3↓, JAK1↓, survivin↓, COX2/PTGS2↓, IAP1↓, MMP2↓, MMP9↓, PTEN↑, SHP1↑, eff↑, TumVol↓, TumW↓, *toxicity↓, *ROS↓,

7242-

Gink,

Cisplatin,

Ginkgetin reverses cisplatin resistance in cervical cancer by regulating the Nrf2/HO-1 signaling pathway to induce ferroptosis

in-vitro,

Cerv,

HeLa

TumCP↓, NRF2↓, ROS↑, i-Iron↑, GSH↓, SOD↓, Catalase↓, lipid-P↑, ACSL4↑, NO↓, GPx4↓, Ferroptosis↑,

7251-

Gink,

Ginkgetin: A Promising Multitarget Agent for Diverse Diseases

Review,

Var,

*Inflam↓, *antiOx↓, AntiCan↑, *neuroP↑, *cardioP↑, *Bacteria↓, *ROS↓, *lipid-P↓, *NRF2↓, *Keap1↓, *NF-kB↓, *MAPK↓, MMP2↓, M2 MC↓, JAK2↓, STAT3↓, TumCP↓, Casp↑, ChemoSen↑, *BMD↑, *Aβ↓, *Stroke↓, *BioAv↓,

7250-

Gink,

Ginkgetin from Ginkgo biloba: mechanistic insights into anticancer efficacy

Review,

Var,

AntiCan↑, toxicity↓, ChemoSen↑, chemoP↑, TumCCA↑, TumCD↑, TumCI↓, angioG↓, Ferroptosis↑, Imm↑, MOMP↑, Cyt‑c↑, Casp↑, cl‑Casp3↑, cl‑Casp9↑, cl‑PARP↑, Apoptosis↑, ROS↑, TumAuto↑, GPx4↓, xCT/SLC7A11↓, RadioS↑, NRF2↓, HO-1↓, HSP90↓, Dose↝, Dose↝, BioAv↓, BioAv↝, CYP3A4↓, *toxicity↑, *toxicity↝,

7248-

Gink,

Studies on the cytotoxic mechanisms of ginkgetin in a human ovarian adenocarcinoma cell line

in-vitro,

Ovarian,

OVCAR-3

in-vitro,

Cerv,

HeLa

NA,

OV1369

Dose↝, TumCD↑, eff↓, Casp↑, H2O2↑, i-ROS↑,

Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

AntiBio↑, 1, Stroke↓, 3,

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↓, 1, Keap1↓, 1, lipid-P↓, 1, NRF2↓, 1, ROS↓, 4,

Cell Death(tgid=5) ⓘ

MAPK↓, 1,

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,

Migration(tgid=13) ⓘ

Cartilage↑, 1, MMP13↓, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 3, NF-kB↓, 1,

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 2,

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1, Dose↝, 1,

Clinical Biomarkers(tgid=22) ⓘ

BMD↑, 1,

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1, cardioP↑, 2, neuroP↑, 4, toxicity↓, 1, toxicity↑, 1, toxicity↝, 1,

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↓, 1, Bacteria↓, 2,
Total Targets: 25

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species

7 Ginkgetin
1 Cisplatin

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

Ginkgetin / ROS Cancer Research Results

Ginkgetin Cancer-Relevant Mechanisms

Pathway results for Effect on Cancer / Diseased Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

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

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Cell Death(tgid=5) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

Migration(tgid=13) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Protein Aggregation(tgid=19) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

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