Ginsenoside CK is a white crystalline powder, soluble in methanol, ethanol, DMSO and other organic solvents, derived from ginseng rhizome, Gynostemma pentaphyllum.
Ginsenoside CK is the main metabolite of protopanaxadiol saponins in human intestinal tract. Studies have shown that the pharmacological activities of ginsenosides are mainly mediated through its metabolic component CK, and CK has a variety of pharmacological activities, such as anti-inflammatory, anti-tumor, anti-allergic, anti-diabetic, hepatoprotective, neuroprotective, and cardiovascular protection.
Ginsenoside CK (CK) is a promising clinical antitumor drug that effectively inhibits the proliferation of liver and lung cancer and metastasis of human osteosarcoma and liver cancer in vitro and in vivo. CK exerts a greater antitumor effect against hormone-independent breast cancer cells than the other 16 ginsenosides[2].
Ginsenoside compound K (C-K) is a metabolite of the protopanaxadiol-type saponins of Panax ginseng C.A. Meyer, has long been used to treat against the development of cancer, inflammation, allergies, and diabetes; C-K acts as a unique HUVEC migration inhibitor by regulating MMP expression, as well as the activity of SPHK1 and its related sphingolipid metabolites. C-K exhibits anti-inflammatory effects by reducing iNOS and COX-2, C-K exhibits an inhibition against the activity of CYP2C9 and CYP2A6 in human liver microsomes with IC50s of 32.0±3.6 μM and 63.6±4.2 μM, respectively. C-K promotes Aβ clearance by enhancing autophagy via the mTOR signaling pathway in primary astrocytes.
White crystalline powder, soluble in organic solvents such as methanol, ethanol, and DMSO, derived from ginseng rhizomes and Gynostemma pentaphyllum.
Ginsenoside C-K is reported to exhibit anti-wrinkle effects. Also, it potentiates tumor necrosis factor (TNF)-related apotosis-inducing ligand (TRAIL)-induced apotosis in HCT116 colon cancer.
ChEBI: Ginsenoside C-K is a ginsenoside found in Panax species that is dammarane which is substituted by hydroxy groups at the 3beta, 12beta and 20 pro-S positions, in which the hydroxy group at position 20 has been converted to the corresponding beta-D-glucopyranoside, and in which a double bond has been introduced at the 24-25 position. It has a role as a plant metabolite, an antineoplastic agent, a hepatoprotective agent, an anti-allergic agent and an anti-inflammatory agent. It is a beta-D-glucoside, a 12beta-hydroxy steroid, a ginsenoside, a tetracyclic triterpenoid, a 3beta-hydroxy steroid and a 3beta-hydroxy-4,4-dimethylsteroid. It derives from a hydride of a dammarane.
This substance is a primary reference substance with assigned absolute purity (considering chromatographic purity, water, residual solvents, inorganic impurities). The exact value can be found on the certificate.
Ginsenoside compound K (GCK, 20-O-beta-D-glucopyranosyl-20(S)-protopanaxadiol, C36H62O8, also known as M1, IH-901, Ginsenoside CK), belonging to tetracyclic dammarane-type triterpenoid saponins. Ginsenosides are poorly absorbed from the gut by oral administration. Still, their major intestinal bacterial metabolite GCK is absorbed, indicating that the in vivo action of ginsenosides oral administration is mediated by their intestinal bacterial metabolic component GCK. The various processes used for GCK synthesis include enzymatic use, microbial conversion, heating, mycelial fermentation, and metabolic engineering[1-3].
Mechanistically, Ginsenoside CK (CK) was found to inhibit hormone-independent breast cancer growth by decreasing cyclin D1 expression to induce G1 cycle arrest and induce apoptosis in MCF-7 human breast cancer cells by activating adenosine 5′-monophosphate (AMP)-activated protein kinase (AMPK) through the production of reactive oxygen species (ROS). High glutamine-addicted TNBC cells were particularly sensitive to CK treatment. Ginsenoside CK exerted antitumor activity against TNBC by suppressing glutamine consumption and glutamate production via downregulation of glutaminase 1 (GLS1) expression. CK treatment further decreased cellular ATP production, reduced the utilisation of amino acids associated with glutamine metabolism, and induced glutathione (GSH) depletion and reactive oxygen species (ROS) accumulation, consequently triggering apoptosis in TNBC. Furthermore, CK decreased GLS1 expression in SUM159 xenograft mouse mammary tumors and significantly inhibited tumor growth with few side effects[2].
[1] Anshul Sharma, Hae-Jeung Lee. “Ginsenoside Compound K: Insights into Recent Studies on Pharmacokinetics and Health-Promoting Activities.” Biomolecules (2020).
[2] Bo Zhang. “Ginsenoside CK induces apoptosis in triple-negative breast cancer cells by targeting glutamine metabolism.” Biochemical pharmacology 1 1 (2022): 115101.
[3] Mengshi Tang . “Ginsenoside compound K- a potential drug for rheumatoid arthritis.” Pharmacological research 166 (2021): Article 105498.
