25696-60-0
Chemical Structure
Tauro-β-muricholic acid
Synonym(s): TβMCA
- CAS No.: 25696-60-0
- Formula:C26H45NO7S
- Molecular Weight:515.70
IUPAC Name: 2-((R)-4-((3R,5R,6S,7R,8S,9S,10R,13R,14S,17R)-3,6,7-trihydroxy-10,13-dimethylhexadecahydro-1H-cyclopenta[a]phenanthren-17-yl)pentanamido)ethane-1-sulfonic acid
InChIKey: XSOLDPYUICCHJX-UZUDEGBHSA-N
SMILES: C[C@@]12[C@]3([H])[C@]([C@H]([C@H]([C@]1([H])C[C@@H](CC2)O)O)O)([H])[C@@]4([H])[C@](CC3)([C@@](CC4)([H])[C@H](C)CCC(NCCS(=O)(O)=O)=O)C
Biological Activity: Tauro-β-muricholic acid (TβMCA) is an orally active trihydroxylated bile acid and a competitive, reversible FXR antagonist (IC50=40 μM). Tauro-β-muricholic acid inhibits bile acid-induced hepatocyte apoptosis by maintaining mitochondrial membrane potential, while simultaneously inhibiting intestinal FXR signaling, affecting bile acid synthesis, hepatic lipid metabolism, and insulin sensitivity. Accumulation of tauro-β-muricholic acid disrupts metabolic homeostasis, promoting cancer stem cell proliferation and tumor progression. The mechanisms of tauro-β-muricholic acid involve two aspects: first, inhibiting the translocation of the pro-apoptotic protein Bax to mitochondria and maintaining mitochondrial membrane potential (MMP); and second, blocking the FXR signaling pathway to regulate bile acid metabolism, reduce serum ceramide production, and downregulate the hepatic SREBP1C/CIDEA pathway. Tauro-β-muricholic acid possesses anti-hepatocyte apoptosis, bile acid homeostasis regulation, and liver fat accumulation reduction properties, and also functions as a biomarker, making it useful in the study of diseases such as bile acid metabolism disorders, non-alcoholic fatty liver disease, colorectal cancer, and liver fibrosis[1][2][3][4].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
|
|
Tauro-β-muricholic acid | 99.91% | Tauro-β-muricholic acid (TβMCA) is an orally active trihydroxylated bile acid and a competitive, reversible FXR antagonist (IC50=40 μM). Tauro-β-muricholic acid inhibits bile acid-induced hepatocyte apoptosis by maintaining mitochondrial membrane potential, while simultaneously inhibiting intestinal FXR signaling, affecting bile acid synthesis, hepatic lipid metabolism, and insulin sensitivity. Accumulation of tauro-β-muricholic acid disrupts metabolic homeostasis, promoting cancer stem cell proliferation and tumor progression. The mechanisms of tauro-β-muricholic acid involve two aspects: first, inhibiting the translocation of the pro-apoptotic protein Bax to mitochondria and maintaining mitochondrial membrane potential (MMP); and second, blocking the FXR signaling pathway to regulate bile acid metabolism, reduce serum ceramide production, and downregulate the hepatic SREBP1C/CIDEA pathway. Tauro-β-muricholic acid possesses anti-hepatocyte apoptosis, bile acid homeostasis regulation, and liver fat accumulation reduction properties, and also functions as a biomarker, making it useful in the study of diseases such as bile acid metabolism disorders, non-alcoholic fatty liver disease, colorectal cancer, and liver fibrosis. | ||||||||||||||||||||
|
loading...
/
|
|||||||||||||||||||||||
|
|
Tauro-β-muricholic acid-d4-1 sodium | Tauro-β-muricholic acid-d4-1 (T-βMCA-d4-1) sodium is the deuterium labeled Tauro-β-muricholic acid (HY-N9933). | |||||||||||||||||||||
|
loading...
/
|
|||||||||||||||||||||||
- [1]. Denk GU, et al. Tauro-β-muricholic acid restricts bile acid-induced hepatocellular apoptosis by preserving the mitochondrial membrane potential. Biochem Biophys Res Commun. 2012 Aug 10;424(4):758-64. [Content Brief]
- [2]. Sayin SI, et al. Gut microbiota regulates bile acid metabolism by reducing the levels of tauro-beta-muricholic acid, a naturally occurring FXR antagonist. Cell Metab. 2013 Feb 5;17(2):225-35. [Content Brief]
- [3]. Zhao DS, et al. Identification of urine tauro-β-muricholic acid as a promising biomarker in Polygoni Multiflori Radix-induced hepatotoxicity by targeted metabolomics of bile acids. Food Chem Toxicol. 2017 Oct;108(Pt B):532-542. [Content Brief]
- [4]. Jiang C, et al. Intestinal farnesoid X receptor signaling promotes nonalcoholic fatty liver disease. J Clin Invest. 2015 Jan;125(1):386-402. [Content Brief]