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| 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):
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
TSF: P: 0–30 min R: 30 min–3 hr G: >3 hr |
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| SHP1 is a non-receptor protein tyrosine phosphatase primarily encoded by the gene PTPN6. Immune Checkpoint Brake, Tumor Suppressor Signaling, and Immune Evasion – In blood cancers such as leukemia and lymphoma, altered SHP1 expression (often downregulation) is frequently observed. – Downregulation or loss of SHP1 is often associated with more aggressive disease phenotypes and poorer prognosis. Direction of Regulation in Cancer Two distinct, context-specific directions: A. Tumor Cells (especially hematologic malignancies): DOWNREGULATED -Frequently silenced epigenetically (promoter methylation) -Rarely mutated; loss is regulatory -Results in unchecked growth and survival signaling B. Immune Cells within the Tumor Microenvironment: FUNCTIONALLY UPREGULATED -Actively recruited by inhibitory receptors -Suppresses T-cell, NK-cell, and myeloid anti-tumor responses -Promotes immune evasion This duality is critical to interpret SHP1 correctly. When SHP1 is lost in tumor cells: -JAK–STAT signaling becomes hyperactive -Growth and survival pathways escape negative feedback -Cells gain a proliferative and survival advantage |
| 7260- | Gink, | Ginkgetin: A natural biflavone with versatile pharmacological activities |
| - | Review, | Var, | NA | - | Review, | Stroke, | NA | - | Review, | AD, | NA |
| 7244- | Gink, | Ginkgetin Blocks Constitutive STAT3 Activation and Induces Apoptosis through Induction of SHP-1 and PTEN Tyrosine Phosphatases |
| - | in-vitro, | Lung, | A549 | - | in-vitro, | Laryn, | FaDu |
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#:1331 State#:% Dir#:2
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