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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 |
| Source: CGL-CS |
| Type: |
| Mitogen-activated protein kinases (MAPKs) are a group of proteins involved in transmitting signals from the cell surface to the nucleus, playing a crucial role in various cellular processes, including growth, differentiation, and apoptosis (programmed cell death). MAPK Pathways: The MAPK family includes several pathways, the most notable being: 1.ERK (Extracellular signal-Regulated Kinase): Often associated with cell proliferation and survival. 2.JNK (c-Jun N-terminal Kinase): Typically involved in stress responses and apoptosis. 3.p38 MAPK: Associated with inflammatory responses and apoptosis. Inhibitors: Targeting the MAPK pathway has become a strategy in cancer therapy. For example, BRAF inhibitors (like vemurafenib) are used in treating melanoma with BRAF mutations. Altered Expression Levels: Overexpression: Many cancers exhibit overexpression of MAPK pathway components, such as RAS, BRAF, and MEK. This overexpression can lead to increased signaling activity, promoting cell proliferation and survival. Downregulation: In some cases, negative regulators of the MAPK pathway (e.g., MAPK phosphatases) may be downregulated, leading to enhanced MAPK signaling. The expression levels of MAPK pathway components can serve as biomarkers for cancer diagnosis, prognosis, and treatment response. For example, high levels of phosphorylated ERK (p-ERK) may indicate active MAPK signaling and poor prognosis in certain cancers. Numerous reports indicate that the MAPK pathway plays a major role in tumor progression and invasion, while inhibition of MAPK signaling reduces invasion. |
| 7251- | Gink, | Ginkgetin: A Promising Multitarget Agent for Diverse Diseases |
| - | Review, | Var, | NA |
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#:181 State#:% Dir#:1
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