Ginsenoside Compound K

Catalogue number C108812
Chemical nameGinsenoside Compound K
CAS Number39262-14-1
Synonyms20(S)-Protopanaxadiol 20-O-D-glucopyranoside
Molecular WeightC36H62O8
Physical DescriptionWhite powder
SolventChloroform, Dichloromethane,DMSO
StorageStored at 2-8°C, Protected from air and light, refrigerate or freeze

Ginsenoside compound K (C-K) is an intestinal microbiota metabolite of ginsenoside Rb1, a major constituent in American ginseng. The effects of Rb1 and C-K on the proliferation of HCT-116 and SW-480 human colorectal cancer cells were compared using an MTS assay. Cell cycle and cell apoptosis were assayed using flow cytometry. Enzymatic activities of caspases were determined by colorimetric assay, and interactions of C-K and caspases were explored by docking analysis. C-K showed significant anti-proliferative effects in HCT-116 and SW-480 cells at concentrations of 30-50 µM. At the same concentrations, Rb1 did not show any effects, while C-K arrested the cells in the G1 phase, and significantly induced cell apoptosis. Compared to HCT-116 (p53 wild-type), the p53 mutant cell line SW-480 was more sensitive to C-K as assessed by cell cycle regulation and apoptosis induction. C-K activated expression of caspases 8 and 9, consistent with docking analysis. The docking data suggested that C-K forms hydrogen bonds with Lys253, Thr904 and Gly362 in caspase 8, and with Thr62, Ser63 and Arg207 in caspase 9. C-K, but not its parent ginsenoside Rb1, showed significant anti-proliferative and pro-apoptotic effects in human colorectal cancer cells. These results suggest that C-K could be a potentially effective anti-colorectal cancer agent.

Pediatric acute myeloid leukemia (AML) is a heterogeneous disease and remains clinically challenging. Currently chemotherapies are frequently associated with treatment-related death and long-term side effects. Therefore, alternative approaches with lower toxicity are highly desired. C-K inhibited the growth of the clinically relevant pediatric AML cell lines in a time- and dose-dependent manner. This growth inhibitory effect was attributable to suppression of DNA synthesis during cell proliferation. Furthermore, we observed significant G1 cell cycle arrest and apoptosis induced by C-K. The induction of apoptosis was accompanied by DNA double strand breaks. Our findings suggest that as a low toxic natural reagent, C-K could be a potential drug for pediatric AML intervention and to improve the outcome of pediatric AML treatment.

CK is a bioactive compound with poor oral bioavailability due to its high polarity, while its novel ester prodrugs, the butyl and octyl ester (CK-B and CK-O), are more lipophilic than the original drug and have an excellent bioavailability. The aim of this study was to examine the transport mechanisms of CK, CK-B, and CK-O using human Caco-2 cells. Results showed that CK had a low permeability coefficient (8.65 × 10–7 cm/s) for apical-to-basolated (AP-BL) transport at 10–50 μM, while the transport rate for AP to BL flux of CK-B (2.97 × 10–6 cm/s) and CK-O (2.84 × 10–6 cm/s) was significantly greater than that of CK. Furthermore, the major transport mechanism of CK was found as passive transcellular diffusion with active efflux mediated by P-glycoprotein (P-gp). In addition, it was found that CK-B and CK-O were not the substrate of efflux transporter since the selective inhibitors (verapamil and MK-571) of efflux transporter had little effects on the transport of CK-B and CK-O in the Caco-2 cells. These results suggest that improving the lipophilicity of CK by acylation can significantly improve the transport across Caco-2 cells.

CK potently inhibited the production of NO and prostaglandin E2 in LPS-induced RAW 264.7 cells, with IC(50) values of 0.012 and 0.004 mM, respectively. CK also reduced the expression levels of the inducible NO synthase (iNOS) and COX-2 proteins and inhibited the activation of NF-kB, a nuclear transcription factor. CK inhibited the NO level produced by iNOS enzyme activity in a cell-free system, but did not inhibit COX-1 and 2 activities. When ginsenoside Rb1 was orally administered to rats, CK, but not ginsenoside Rb1, were excreted in their urine. These findings suggest that ginsenoside Rb1 can be transformed to CK by intestinal bacteria, and CK may be effective against inflammation.

References1. Int. J. Oncol., 2012, 40(6), 1970-1976.
2. Cancer Cell International, 2013, 13, 24.
3. J. Agric. Food Chem., 2012, 60(41), 10278-10284.
4. Biological & Pharmaceutical Bulletin, 2005, 28(4), 652-656.
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20mg$126.005% OFF
50mg$290.008% OFF
100mg$493.0015% OFF
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