|Source:||The roots of Panax ginseng C.A.Mey.|
|Biological Activity or Inhibitors:||1. 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.
2. Ginsenoside compound K has various chemopreventive and chemotherapeutic activities, including anti-tumor activity; C-K suppresses the activation of the NF-κB pathway, may become a potential cytotoxic drug in the prevention and treatment of hepatocellular carcinoma( HCC).
3. Ginsenoside compound K shows significant anti-proliferative effects and pro-apoptotic effects in HCT-116 and SW-480 cells at concentrations of 30-50 uM, suggests that C-K could be potentially effective anti-colorectal cancer agent.
4. Ginsenoside compound K promotes Aβ clearance by enhancing autophagy via the mTOR signaling pathway in primary astrocytes.
|Solvent:||Pyridine, Methanol, Ethanol, etc.|
|Storage:||Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: email@example.com
|After receiving:||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||1.6054 mL||8.0272 mL||16.0545 mL||32.1089 mL||40.1361 mL|
|5 mM||0.3211 mL||1.6054 mL||3.2109 mL||6.4218 mL||8.0272 mL|
|10 mM||0.1605 mL||0.8027 mL||1.6054 mL||3.2109 mL||4.0136 mL|
|50 mM||0.0321 mL||0.1605 mL||0.3211 mL||0.6422 mL||0.8027 mL|
|100 mM||0.0161 mL||0.0803 mL||0.1605 mL||0.3211 mL||0.4014 mL|
Fitoterapia. 2015 Jan;100:208-20.
|A review of biotransformation and pharmacology of ginsenoside compound K.[Pubmed: 25449425]|
|As an intestinal bacterial metabolite of ginseng protopanaxadiol saponins, Ginsenoside Compound K (20-O-beta-d-glucopyranosyl-20(S)-protopanaxadiol, CK) is a major deglycosylated metabolite form of ginsenosides which is absorbed into the systemic circulation. And it has demonstrated such diverse intriguing biological properties as anticarcinogenic, anti-inflammation, antiallergic, anti-diabetic, anti-angiogenesis, anti-aging, neuroprotective and hepatoprotective effects. The present review shall summarize recent studies on various biotransformation and pharmacological activities of Ginsenoside Compound K.|
Carbohydr Polym. 2014 Nov 4;112:359-66.
|Ginsenoside compound K-bearing glycol chitosan conjugates: synthesis, physicochemical characterization, and in vitro biological studies.[Pubmed: 25129755]|
|Ginsenosides are triterpenoids found in Panax ginseng and have a numerous structural, functional, and pharmacological properties. The purpose of this study was to develop hydrophilic polymer functionalized ginsenoside conjugates to enhance water solubility and targeted delivery. To this end, hydrophobic Ginsenoside Compound K (CK) was covalently conjugated to the backbone of hydrophilic glycol chitosan (GC) through an acid-labile linkage. The resulting GC-Ginsenoside Compound K conjugates formed self-assembled spherical nanoparticles in an aqueous solution, and their particles sizes were (296 nm and 255 nm) dependent on the degree of Ginsenoside Compound K substitution. The nanoparticles were stable in the physiological buffer (pH 7.4) over a period of 8 days, whereas they were readily degraded under acidic conditions (pH 5.0) mimicking the intracellular pH-conditions. From in vitro release experiment, it was found that Ginsenoside Compound K released slowly from the self-assembled nanoparticles in the physiological buffer (pH 7.4). On the other hand, the release rate of Ginsenoside Compound K was rapidly increased under the acidic condition (pH 5.0). In vitro cytotoxicity assays revealed that GC-Ginsenoside Compound K conjugates exhibited higher cytotoxicity than Ginsenoside Compound K in HT29, and similar cytotoxicity in HepG2, and HT22 cell lines. Moreover, RAW264.7 cells treated with GC-Ginsenoside Compound K maintained good cell viability and exhibited decreased lipopolysaccharide-induced NO production. Taken together, these results suggest that the GC-Ginsenoside Compound K conjugate may be potentially useful as a tumor-specific delivery vehicle.|
Arch Pharm Res. 2014 Sep;37(9):1183-92.
|Ginsenoside compound K inhibits angiogenesis via regulation of sphingosine kinase-1 in human umbilical vein endothelial cells.[Pubmed: 24687256]|
|Ginsenoside Compound K (CK) is a metabolite of the protopanaxadiol-type saponins of Panax ginseng C.A. Meyer (Araliaceae), has long been used to treat against the development of cancer, inflammation, allergies, and diabetes. This study examined the anti-angiogenic properties of Ginsenoside Compound K against sphingosine 1-phosphate (S1P)-induced cell migration via regulation of sphingosine kinase 1 (SPHK1) in human umbilical vein endothelial cells (HUVEC). Studies on S1P-induced cell migration, expression of SPHK1 and MMPs and analysis of sphingolipid metabolites by LC-MS/MS were examined after the treatment of Ginsenoside Compound K (2.5, 5, 10 μg/mL) in HUVEC. S1P produced by SPHK1 is also involved in cell growth, migration, and protection of apoptosis; therefore, we sought to investigate whether ginsenosides are able to regulate SPHK1. For this purpose, we developed an inhibitory assay of SPHK1 activity and an analytical method for detection of S1P and other sphingolipid metabolites in HUVEC. Ginsenoside Ginsenoside Compound K inhibited 100 nM S1P-induced cell migrations in a dose-dependent manner. Among tested ginsenosides, Ginsenoside Compound K exclusively inhibited S1P production, SPHK1 activity and SPHK1 expression in HUVEC, whereas expression of the pro-apoptotic sphingolipids, sphingosine and ceramide, was increased in response to Ginsenoside Compound K. The major subspecies of the increased ceramide was C24:0-ceramide. Ginsenoside Compound K also disrupted the sphingolipid rheostat, which ultimately influences cell fate, and dose-dependently inhibited HUVEC migration by reducing expression of metalloproteinases (MMPs). Ginsenoside Ginsenoside Compound K acts as a unique HUVEC migration inhibitor by regulating MMP expression, as well as the activity of SPHK1 and its related sphingolipid metabolites.|
Exp Ther Med. 2014 Oct;8(4):1271-1274.
|Ginsenoside compound K promotes β-amyloid peptide clearance in primary astrocytes via autophagy enhancement.[Pubmed: 25187838]|
|The aim of the present study was to investigate the effect of Ginsenoside Compound K on β-amyloid (Aβ) peptide clearance in primary astrocytes. Aβ degradation in primary astrocytes was determined using an intracellular Aβ clearance assay. Aggregated LC3 in astrocyte cells, which is a marker for the level of autophagy, was detected using laser scanning confocal microscope. The effect of compound K on the mammalian target of rapamycin (mTOR)/autophagy pathway was determined using western blot analysis, and an enzyme-linked immunosorbent assay was used for Aβ detection. The results demonstrated that compound K promoted the clearance of Aβ and enhanced autophagy in primary astrocytes. In addition, it was found that phosphorylation of mTOR was inhibited by compound K, which may have contributed to the enhanced autophagy. In conclusion, compound K promotes Aβ clearance by enhancing autophagy via the mTOR signaling pathway in primary astrocytes.|
Planta Med. 2011 Mar;77(5):428-33.
|Ginsenoside compound K attenuates metastatic growth of hepatocellular carcinoma, which is associated with the translocation of nuclear factor-κB p65 and reduction of matrix metalloproteinase-2/9.[Pubmed: 20979019 ]|
|The intestinal metabolite of ginseng saponin, compound K (CK), has various chemopreventive and chemotherapeutic activities, including anti-tumor activity. However, the functional mechanisms through which CK attenuates metastatic growth in hepatocellular carcinoma (HCC) remain unclear. Here, using multiple IN VITRO and IN VIVO models, we reported that CK strongly attenuated colony formation, adhesion, and invasion of HCC cells IN VITRO and dramatically inhibited spontaneous HCC metastatic growth IN VIVO. At the molecular level, immunofluorescence and Western blotting analysis confirmed that inhibition of metastatic growth of HCC induced by CK treatment caused a time-dependent decrease in nuclear NF- κB p65 and a concomitant increase in cytosolic NF- κB p65, indicating that CK suppressed the activation of the NF- κB pathway. Meanwhile, our study showed that the inhibition of matrix metalloproteinase2/9 (MMP2/9) expression caused by CK treatment was associated with NF- κB p65 nuclear export. Taken together, our results not only revealed that NF- κB p65 nuclear export and the reduction of MMP2/9 expression were associated with the metastatic inhibition induced by CK, but also suggested that CK may become a potential cytotoxic drug in the prevention and treatment of HCC.|
Int J Oncol.,2012 Jun; 40(6): 1970-6.
|Ginsenoside compound K, not Rb1, possesses potential chemopreventive activities in human colorectal cancer[Pubmed: 22426808]|
|Ginsenoside Compound K (C-K) is an intestinal microbiota metabolite of ginsenoside Rb1, a major constituent in American ginseng. However, previous ginseng anticancer observations were largely focused on ginseng parent compounds but not metabolites, and anti-colorectal cancer studies on C-K were limited. This study investigated the antiproliferative effects of C-K when compared to those of Rb1, and the related mechanisms of action, in HCT-116 and SW-480 colorectal cancer cells. 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 antiproliferative 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 Lys-253, Thr-904 and Gly-362 in caspase 8, and with Thr-62, Ser-63 and Arg-207 in caspase 9. C-K, but not its parent ginsenoside Rb1, showed significant antiproliferative and pro-apoptotic effects in human colorectal cancer cells. These results suggest that C-K could be a potentially effective anti-colorectal cancer agent.|