Ginkgolide B / ROS Cancer Research Results

GGB, Ginkgolide B: Click to Expand ⟱

Features:

Ginkgolide B — a naturally occurring diterpene trilactone and one of the principal terpene lactones of Ginkgo biloba. It is a chemically defined small molecule, commonly abbreviated GB, GGB, GKB, and historically BN 52021. Its best-established pharmacological identity is as a potent competitive antagonist of the platelet-activating factor receptor (PAFR). Ginkgolide B is present in standardized Ginkgo extracts such as EGb 761 but is pharmacologically distinct from whole Ginkgo extract, ginkgetin, other biflavonoids, bilobalide, and ginkgolic acids. Its cancer evidence remains preclinical, with the strongest recurring theme being interference with PAF/PAFR-dependent tumor signaling and chemotherapy resistance.

Primary mechanisms (ranked):

PAF receptor antagonism, suppressing PAF/PAFR-dependent inflammatory, survival, stemness, metastatic, and chemotherapy-resistance signaling.
PAFR/NF-κB suppression, reducing pro-survival signaling and increasing chemotherapy sensitivity, particularly to gemcitabine and cisplatin in experimental cancer models.
Antiproliferative and cell-cycle effects, including p21/p27 induction, cyclin D1 suppression, and G0/G1-S or related cell-cycle blockade in susceptible tumor cells.
Apoptosis induction through caspase activation, BAX/Bcl-2-family modulation, and loss of tumor-cell survival signaling.
Suppression of EMT, migration, and invasion through context-dependent regulation of ZEB1, miR-223-3p, PI3K/AKT/mTOR, and epithelial/mesenchymal markers.
Suppression of cancer-stem-cell phenotypes through blockade of PAF/PAFR signaling, demonstrated particularly in ovarian-cancer models.
Pyroptosis induction with GSDMD activation in gastric-cancer models, associated with inhibition of PI3K/AKT/mTOR signaling; currently a recent and less independently replicated mechanism.
TSPO/PBR suppression in aggressive breast-cancer models, associated with cytostatic effects and reduced xenograft growth.
Immune-microenvironment modulation through PAFR-dependent pathways, including emerging SREBP1/KLK8/CCL22-related effects in oral squamous-cell carcinoma.

Bioavailability / PK relevance: Ginkgolide B is systemically bioavailable in humans after oral standardized Ginkgo preparations, and human pharmacokinetic studies confirm measurable circulating Ginkgolide B. Its circulating lactone undergoes reversible hydrolysis to carboxylated forms, which have lower PAF-antagonist potency than the parent trilactone. Renal elimination is important. Direct intravenous studies of isolated Ginkgolide B in healthy subjects have used approximately 20–60 mg doses and demonstrate dose-related systemic exposure. Therefore, unlike many poorly characterized phytochemicals, Ginkgolide B has genuine human PK data; however, the exposure required for anticancer activity has not been clinically established.

In-vitro vs systemic exposure relevance: Cancer experiments commonly use isolated Ginkgolide B in the tens to hundreds of micromolar range, with some studies using approximately 100 µM or higher. These exposures should not be assumed achievable from ordinary oral Ginkgo supplements. Intravenous Ginkgolide B can produce substantially greater systemic exposure than oral extract, but no human anticancer exposure-response relationship has been established. Human PK therefore supports systemic availability but does not validate the concentrations used in cancer-cell experiments.

Clinical evidence status: Preclinical for cancer. Evidence includes cell culture, xenograft, chemotherapy-resistance, cancer-stem-cell, migration/invasion, and tumor-microenvironment studies. No established human anticancer trial or approved anticancer indication for isolated Ginkgolide B was identified. Direct Ginkgolide B injection is undergoing human pharmacokinetic and tolerability investigation for non-cancer indications, while standardized Ginkgo preparations provide extensive human exposure data. PAF antagonism may affect platelet biology, so concomitant anticoagulant or antiplatelet therapy remains an important clinical safety consideration even though bleeding effects cannot be extrapolated quantitatively from isolated Ginkgolide B experiments.

Ginkgolide B Cancer-Relevant Mechanisms

Rank	Pathway / Axis	Cancer Cells	Normal Cells	TSF	Primary Effect	Notes / Interpretation
1	PAF PAFR signaling	PAFR signaling ↓; tumor survival ↓; stemness ↓; migration ↓; chemoresistance ↓	PAFR signaling ↓; platelet activation ↓; inflammatory activation ↓	P, R, G	Central pharmacological mechanism	PAFR antagonism is the best-established direct molecular action of Ginkgolide B and provides a biologically coherent link between inflammation, tumor progression, cancer stemness, and treatment resistance.
2	PAFR NF-κB survival signaling	NF-κB activation ↓; survival signaling ↓; chemotherapy sensitivity ↑	NF-κB inflammatory signaling ↓ (context-dependent)	R, G	Chemosensitization and survival suppression	PAFR blockade increases gemcitabine sensitivity in pancreatic-cancer cells and modifies cisplatin resistance in oral-cancer models. Mechanistically stronger than many downstream pathways because it derives from the established pharmacological target of Ginkgolide B.
3	Cell-cycle and proliferative signaling	p21 ↑; p27 ↑; cyclin D1 ↓; proliferation ↓; cell-cycle arrest ↑	Generally less cytotoxic in tested normal cells	G	Cytostatic growth inhibition	Ovarian-cancer studies demonstrate substantial proliferation inhibition at high micromolar exposure. Earlier ovarian studies also indicate G0/G1-to-S cell-cycle blockade.
4	Caspase and mitochondrial apoptosis	Cleaved caspase-3 ↑; cleaved caspase-8 ↑; BAX ↑; Bcl-2 ↓; apoptosis ↑	Apoptosis generally ↓ in stressed neural and cardiovascular cells	R, G	Programmed tumor-cell death	Direction is strongly context-dependent. Ginkgolide B may promote apoptosis in tumor cells while protecting stressed normal neural or cardiovascular cells from apoptotic injury.
5	Cancer stemness	CSC phenotype ↓; spheroid formation ↓; tumor initiation ↓	Not established	G	Cancer stem-cell suppression	PAF promotes ovarian-cancer stemness, while Ginkgolide B antagonism of PAFR suppresses CSC properties and reduces tumor growth in experimental models.
6	EMT and ZEB1 signaling	EMT ↓; migration ↓; invasion ↓; ZEB1 ↓ (model-dependent); E-cadherin ↑; N-cadherin ↓	Not established	G	Metastatic phenotype suppression	Supported in bladder and gastric-cancer models. The bladder-cancer literature implicates miR-223-3p-associated regulation of ZEB1; directionality reported within that paper should be interpreted at the protein-regulation level rather than generalized to all cancers.
7	PI3K AKT mTOR signaling	PI3K ↓; AKT ↓; mTOR ↓	AKT ↑ in some stressed normal cells (context-dependent)	R, G	Survival and EMT suppression	Reported prominently in recent gastric-cancer work. In normal endothelial, cardiac, or neural injury models Ginkgolide B can instead activate AKT-mediated survival pathways, making this strongly cell-context dependent.
8	Pyroptosis and GSDMD	GSDMD ↑; pyroptosis ↑	Pyroptotic inflammation generally ↓ in neuroinflammatory models (context-dependent)	G	Inflammatory tumor-cell death	Recent gastric-cancer evidence links Ginkgolide B to increased pyroptosis alongside PI3K/AKT/mTOR suppression. Independent replication remains limited.
9	TSPO peripheral benzodiazepine receptor	TSPO expression ↓; proliferation ↓	Not established	G	Cytostatic tumor suppression	An independent U.S. study demonstrated reduced TSPO expression and growth of aggressive MDA-MB-231 breast-cancer cells and xenografts. Historically TSPO was termed the peripheral-type benzodiazepine receptor.
10	Tumor immune microenvironment	SREBP1 KLK8 CCL22 signaling ↓ (model-dependent); immunosuppressive recruitment ↓	Not established	G	Immune-microenvironment modulation	Emerging oral-cancer evidence suggests Ginkgolide B can modify tumor-associated immune signaling. This is promising but considerably less replicated than PAFR antagonism.
11	Chemosensitization	Gemcitabine sensitivity ↑; cisplatin sensitivity ↑	Normal-tissue selectivity incompletely established	G	Reduction of drug resistance	Experimental pancreatic, ovarian, and oral-cancer studies support chemotherapy sensitization. No human oncology trial has established a clinically useful combination dose.
12	Clinical Translation Constraint	Effective experimental concentrations often high; clinical anticancer exposure unknown	PAF-dependent platelet function ↓; systemic PK established	G	Exposure and clinical-validation constraint	Human oral and intravenous PK is documented, but cancer-active concentrations and therapeutic windows are unknown. Antiplatelet pharmacology and treatment interactions require consideration. No established clinical anticancer efficacy exists.

TSF: P: 0–30 min R: 30 min–3 hr G: >3 hr

Alzheimer’s disease relevance: Ginkgolide B has meaningful preclinical evidence for neuroprotection in Alzheimer’s disease models. Reported actions include suppression of Aβ-induced microglial activation and neurotoxicity, inhibition and autophagic degradation of the NLRP3 inflammasome, reduced inflammatory caspase-1 signaling, enhancement of autophagic clearance of phosphorylated tau, increased BDNF-associated neuronal survival, and improvement of learning and memory in animal models. These effects contrast with several cancer mechanisms: AKT and cytoprotective signaling may increase in stressed neural cells, while apoptosis, oxidative stress, and inflammatory signaling decrease. No clinical efficacy of isolated Ginkgolide B for Alzheimer’s disease has been established.

Clinical evidence status: Preclinical for isolated Ginkgolide B. Human studies of Ginkgo extracts cannot be treated as direct clinical evidence for purified Ginkgolide B because extracts contain multiple terpene lactones and flavonoids.

Ginkgolide B Alzheimer’s-Relevant Mechanisms

Rank	Pathway / Axis	AD Modulation	TSF	Primary Effect	Notes / Interpretation
1	Amyloid beta neurotoxicity	Aβ-induced neurotoxicity ↓; neuronal survival ↑	R, G	Neuroprotection	Direct protection from Aβ-mediated neuronal and microglial toxicity has been demonstrated experimentally.
2	NLRP3 inflammasome	NLRP3 activation ↓; caspase-1 ↓; neuroinflammation ↓	R, G	Inflammasome suppression	Multiple experimental studies support inhibition of Aβ-associated NLRP3 signaling. Autophagic degradation of NLRP3 has also been reported.
3	Microglial activation	Microglial activation ↓; inflammatory cytokines ↓	R, G	Reduced neuroinflammation	PAFR antagonism and downstream inflammatory suppression are mechanistically consistent with reduced microglia-mediated neuronal injury.
4	Tau autophagic clearance	Autophagy ↑; phosphorylated tau degradation ↑; p-Tau ↓	G	Proteostasis improvement	Experimental studies comparing EGb 761 constituents identify Ginkgolide B as capable of increasing autophagic degradation of phosphorylated tau.
5	BDNF neuronal survival	BDNF ↑; neuronal survival ↑; apoptosis ↓	G	Synaptic and neuronal protection	Ginkgolide B protects hippocampal neurons from Aβ-associated apoptosis partly through increased BDNF signaling.
6	Oxidative and mitochondrial stress	ROS ↓; mitochondrial dysfunction ↓; Cyt-c release ↓; apoptosis ↓	R, G	Cellular stress protection	Common neuroprotective pattern across Aβ and other neural-injury models; contrasts with pro-death effects observed in some cancer cells.
7	Cognitive function	Learning ↑; memory ↑	G	Functional improvement	Reported in animal neurodegeneration models; no validated clinical cognitive benefit can presently be attributed specifically to isolated Ginkgolide B.
8	Clinical Translation Constraint	Human exposure established; isolated Ginkgolide B efficacy unproven	G	Clinical-evidence limitation	Human Ginkgo-extract studies cannot establish efficacy of purified Ginkgolide B. Brain exposure, optimal dose, and long-term therapeutic window remain incompletely defined.

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⟱

7279-

GGB,

Rad,

Radioprotective effect of Ginkgolide B on brain: the mediating role of DCC/MST1 signaling

in-vivo,

Nor,

 C57BL/6 mice were stimulated with an X-ray (20 Gy) to establish an RBI model.

*cognitive↑, *radioP↑, *ROS↓, *p‑Akt↑, *Bcl-2↑, *Mst1↓, *p‑p38↓, *JNK↓, *cl‑Casp3↓, *BAX↓,

7217-

GGB,

Role of Ginkgolides in the Inflammatory Immune Response of Neurological Diseases: A Review of Current Literatures

Review,

AD,

*eff↑, *AntiAg↑, *Apoptosis↓, *antiOx↑, *Inflam↓, *MAPK↓, *NF-kB↓, *PAF↓, *TLR1↓, *MyD88↓, *BDNF↑, *ROS↓, *PARP↓, *Cyt‑c↓,

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:

Total Targets: 0

Pathway results for Effect on Normal Cells:

Functional Outcomes(tgid=23) ⓘ

cognitive↑, 1, radioP↑, 1,
Total Targets: 23

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

Ginkgolide B / ROS Cancer Research Results

Ginkgolide B Cancer-Relevant Mechanisms

Ginkgolide B Alzheimer’s-Relevant Mechanisms

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Cell Death(tgid=5) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

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

Migration(tgid=13) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Synaptic & Neurotransmission(tgid=18) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Functional Outcomes(tgid=23) ⓘ

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