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    Natural Products
    Ginsenoside Compound K
    CAS No. 39262-14-1 Price $100 / 20mg
    Catalog No.CFN99756Purity>=98%
    Molecular Weight622.88Type of CompoundTriterpenoids
    FormulaC36H62O8Physical DescriptionWhite powder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    According to end customer requirements, ChemFaces provide solvent format. This solvent format of product intended use: Signaling Inhibitors, Biological activities or Pharmacological activities.
    Size /Price /Stock 10 mM * 1 mL in DMSO / $51.4 / In-stock
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  • Biological Activity
    Description: 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.
    Targets: NO | MMP(e.g.TIMP) | mTOR | Beta Amyloid | NF-kB | p65 | Caspase | CYP2C9 | CYP2A6 | NOS | COX
    In vitro:
    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 CK.
    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, Ginsenoside 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.
    J Ginseng Res . 2017 Oct;41(4):435-443.
    Role of ginsenosides, the main active components of Panax ginseng, in inflammatory responses and diseases[Pubmed: 29021688]
    Panax ginseng is one of the most universally used herbal medicines in Asian and Western countries. Most of the biological activities of ginseng are derived from its main constituents, ginsenosides. Interestingly, a number of studies have reported that ginsenosides and their metabolites/derivatives-including ginsenoside (G)-Rb1, compound K, G-Rb2, G-Rd, G-Re, G-Rg1, G-Rg3, G-Rg5, G-Rh1, G-Rh2, and G-Rp1-exert anti-inflammatory activities in inflammatory responses by suppressing the production of proinflammatory cytokines and regulating the activities of inflammatory signaling pathways, such as nuclear factor-κB and activator protein-1. This review discusses recent studies regarding molecular mechanisms by which ginsenosides play critical roles in inflammatory responses and diseases, and provides evidence showing their potential to prevent and treat inflammatory diseases.
    Acta Pharmacol Sin . 2014 May;35(5):599-612.
    Ginsenoside compound K suppresses the abnormal activation of T lymphocytes in mice with collagen-induced arthritis[Pubmed: 24727939]
    Aim: To investigate the anti-arthritis and immunomodulatory activities of Ginsenoside Compound K (C-K) in mice with collagen-induced arthritis (CIA). Methods: DBA/1 mice with CIA were treated with C-K (28, 56 or 112 mg·kg(-1)·d(-1), ig) or the positive control methotrexate (2 mg/kg, ig, every 3 d) for 34 d. Splenic T and B lymphocytes were positively isolated using anti-CD3-coated magnetic beads or a pan B cell isolation kit. T lymphocyte subsets, and CD28, T cell receptor (TCR), cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) and programmed death-1 (PD-1) expression in purified splenic T lymphocytes were analyzed using flow cytometry, Western blotting and laser confocal microscopy. Results: C-K treatment significantly ameliorated the pathologic manifestations of CIA mice, remarkably inhibited T lymphocyte proliferation, and marginally inhibited the proliferation of B lymphocytes. C-K treatment significantly suppressed TNF-α and anti-CII antibody levels, and increased IFN-γ level in the joints of CIA mice, but did not alter IL-4 production. Treatment of CIA mice with C-K significantly decreased the percentages of activated T cells, co-stimulatory molecule-expressing T cells and effector memory T cells, and increased the frequencies of naive T cells and regulatory T cells. Furthermore, C-K treatment significantly decreased the expression of CD28 and TCR, whereas it increased the expression of CTLA-4 and PD-1 on T lymphocytes of CIA mice. Methotrexate treatment exerted comparable effects in all these experiments.
    Ginsenoside Compound K Description
    Source: The roots of Panax ginseng C.A.Mey.
    Solvent: DMSO, 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:

    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.
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    Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

    Cell. 2018 Jan 11;172(1-2):249-261.e12.
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    Calculate Dilution Ratios(Only for Reference)
    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
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Kinase Assay:
    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]
    There is still an argument about ginseng-prescription drug interactions.
    To evaluate the influence on cytochrome P450 (P450) activities of ginseng in the present study, the influence on P450 activities of naturally occurring ginsenosides and their degradation products in human gut lumen was assayed by using human liver microsomes and cDNA-expressed CYP3A4. The results showed that the naturally occurring ginsenosides exhibited no inhibition or weak inhibition against human CYP3A4, CYP2D6, CYP2C9, CYP2A6, or CYP1A2 activities; however, their main intestinal metabolites demonstrated a wide range of inhibition of the P450-mediated metabolism. There was no mechanism-based inhibition found on these P450 isoforms. It is noteworthy that Ginsenoside Compound K, protopanaxadiol (Ppd), and protopanaxatriol (Ppt) all exhibited moderate inhibition against CYP2C9 activity, and Ppd and Ppt also exhibited potent competitive inhibition against CYP3A4 activity.
    We suggest that after oral administration, naturally occurring ginsenosides might influence hepatic P450 activity in vivo via their intestinal 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.
    Cell Research:
    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.