Lithocholic acid - 10mM in DMSO, high purity , CAS No.434-13-9(DMSO), Agonist of Farnesoid X receptor;Agonist of GPBA receptor;Agonist of Pregnane X receptor;Agonist of Vitamin D receptor
Lithocholic acid - 10mM in DMSO, high purity , CAS No.434-13-9(DMSO), Agonist of Farnesoid X receptor;Agonist of GPBA receptor;Agonist of Pregnane X receptor;Agonist of Vitamin D receptor
Lithocholic acid is a toxic secondary bile acid, causes intrahepatic cholestasis, has tumor-promoting activity, its toxic effect can be protected after it activates the vitamin D receptor, PXR and FXR.
Storage Temp
Store at -80°C
Shipped In
Dry ice packs + Cold packs
This product requires cold chain shipping. Ground and other economy services are not available.
Grade
Moligand™
Action Type
AGONIST
Mechanism of action
Agonist of Farnesoid X receptor;Agonist of GPBA receptor;Agonist of Pregnane X receptor;Agonist of Vitamin D receptor
Product Description
Information
Lithocholic acid Lithocholic acid is a toxic secondary bile acid, causes intrahepatic cholestasis, has tumor-promoting activity, its toxic effect can be protected after it activates the vitamin D receptor , PXR and FXR . In vitro
Lithocholic acid (LCA) is a hydrophobic secondary bile acid that is primarily formed in the intestine by the bacterial 7α-dehydroxylation of chenodeoxycholic acid. LCA causes intrahepatic cholestasis (cessation or impairment of bile flow). LCA activates PXR (pregnane X receptor), and the LCA-induced severe liver damage can be protected by the activation of PXR. LCA is a ligand for farnesoid X receptor (FXR) with EC50 of 3.8 μM. LCA directly binds VDR (vitamin D receptor) with Ki of 29μM, activates VDR (vitamin D receptor) 30 μM, with much more sensitivity than the other nuclear receptors (eg. PXR, FXR), and its toxic effect is thus protected. LCA has tumor-promoting activity, inhibits mammalian DNA Polymerase β with IC50 of 15 μM.
In vivo
Administration of LCA and its conjugates to rodents causes intrahepatic cholestasis,a pathogenic state characterized by decreased bile flow and the accumulation of bile constituents in the liver and blood. In DMH (dimethyldydrazine)-induced murine carcinogenesis model, LCA suppresses apoptosis almost completely in premalignant colon. LCA activates VDR, induces expression in vivo of CYP3A, a cytochrome P450 enzyme that detoxifies LCA in the liver and intestine. Cell Data
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