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39262-14-1

Compound K

CAS: 39262-14-1

Molecular Formula: C36H62O8

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39262-14-1 - Names and Identifiers

Name Compound K
Synonyms IH-901
Compound K
Ginsenoside CK
GINSENOSIDE COMPOUND K(P)
20(S)-Protopanaxadiol 20-O-D-glucopyranoside
(20S)-20-O-β-D-Glucopyranosylprotopanaxadiol
20-(β-D-Glucopyranosyloxy)dammar-24-ene-3β,12β-diol
20-(β-D-Glucopyranosyloxy)-5α-dammara-24-ene-3β,12β-diol
(20S)-20-(β-D-Glucopyranosyloxy)dammara-24-ene-3β,12β-diol
b-D-Glucopyranoside, (3b,12b)-3,12-dihydroxydaMMar-24-en-20-yl
CAS 39262-14-1

39262-14-1 - Physico-chemical Properties

Molecular FormulaC36H62O8
Molar Mass622.88
Density1.19
Melting Point181~183℃
Boling Point723.1±60.0 °C(Predicted)
Specific Rotation(α)(c, 1 in MeOH)+39
Solubility Soluble in DMSO, pyridine, insoluble in petroleum ether, chloroform and other organic solvents.
AppearanceWhite powder
pKa12.94±0.70(Predicted)
Storage Condition2-8℃
MDLMFCD07772261
Physical and Chemical PropertiesWhite crystalline powder, soluble in methanol, ethanol, DMSO and other organic solvents, derived from ginseng rhizome, Gynostemma pentaphyllum.
In vitro study Ginsenoside C-K, a bacterial metabolite of G-Rb1, exhibits anti-inflammatory effects mainly by reducing inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, and proinflammatory cytokines. Ginsenoside C-K suppresses the expression of proinflammatory cytokines by downregulating the activities of IRAK-1, MAPKs, IKK-α, and NF-κB in LPS-treated murine peritoneal macrophages. Ginsenoside C-K also suppresses the expression of iNOS and COX-2 by inhibiting NF-κB signaling in LPS-stimulated RAW264.7 cells. In zymosan-treated bone-marrow-derived macrophages (BMDMs) and RAW264.7 cells, Ginsenoside C-K inhibits inflammatory responses by negatively regulating the secretion of proinflammatory cytokines, the activation of MAPKs, and the generation of ROS. In addition, anti-inflammatory activity of Ginsenoside C-K has been observed in LPS-stimulated microglial cells. Ginsenoside C-K hinders inflammatory responses by controlling both the generation of ROS and the activities of MAPKs, NF-κB, and AP-1. Ginsenoside C-K, a major metabolite of ginsenosides in the gastrointestinal tract, inhibits NF-κB signaling in a PXR-dependent manner. Ginsenoside C-K is shown to promote recovery of dextran sulfate sodium (DSS) -induced colitis by suppressing NF-κB activation. Ginsenoside C-K significantly reduces TNF-α-induced upregulation of IL-1β and iNOS mRNA levels, and restores the mRNA levels of PXR and CYP3A4 in LS174T cells. Ginsenoside C-K, one of the intestinal metabolites of 20(S)-protopanaxadiol derivatives, exhibits an inhibition against the activity of CYP2C9 in human liver microsomes with an IC 50 value of 32.0±3.6 μM, a weak inhibition against the activity of CYP2A6 in human liver microsomes with an IC 50 value of 63.6±4.2 μM, and an even weaker inhibition against the activity of CYP2D6 in human liver microsomes with an IC 50 value of more than 100 μM.
In vivo study The weight of the collagen-induced arthritis (CIA) mice increases slowly and is significantly less than that of the normal DBA/1 mice beginning on d 3 after injection of the emulsion. Ginsenoside C-K (28, 56, and 112 mg/kg) mice recover their weight by d 32 after the emulsion injection. Ginsenoside C-K (56 and 112 mg/kg) and Methotrexate (MTX)-treated (2 mg/kg) mice show significantly increased body weight on d 50 as compared with CIA mice. Hind paw-swelling began on d 24 post-immunization. CIA mice are treated from d 28 to d 50. Arthritis scores are measured every 4 d beginning on d 24. Ginsenoside C-K (56 and 112 mg/kg) significantly reduces the arthritis scores of the mice on d 51.
39262-14-1
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View History
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