Ginsenoside CK

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.

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.

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].