1. Metabolic Enzyme/Protease Apoptosis
  2. FXR Apoptosis
  3. Tauro-β-muricholic acid

Tauro-β-muricholic acid  (Synonyms: TβMCA)

Cat. No.: HY-N9933 Purity: 99.91%
Handling Instructions Technical Support

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.

For research use only. We do not sell to patients.

Tauro-β-muricholic acid

Tauro-β-muricholic acid Chemical Structure

CAS No. : 25696-60-0

Size Price Stock Quantity
Solid + Solvent (Highly Recommended)
10 mM * 1 mL in DMSO
ready for reconstitution
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10 mM * 1 mL in DMSO In-stock
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Based on 4 publication(s) in Google Scholar

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Description

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].

IC50 & Target

40 μM (FXR)[1]

In Vitro

Co-incubation of tauro-β-muricholic acid (25 μM; 4 h) with GCDCA reduced apoptosis in human Ntcp-HepG2 cells, and co-incubation with palmitic acid restored the GCDCA-induced disruption of mitochondrial membrane potential (MMP). Both treatments also inhibited the translocation of the pro-apoptotic protein Bax to the mitochondria[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Apoptosis Analysis[1]

Cell Line: Human Ntcp-transfected HepG2 cells, Primary rat hepatocytes, Primary mouse hepatocytes
Concentration: 25 μmol/L (Ntcp-HepG2 cells, primary rat hepatocytes), 100 μmol/L (primary mouse hepatocytes)
Incubation Time: 24 h
Result: When co-incubated with glycochenodeoxycholic acid (GCDCA), Tauro-β-muricholic acid reduced GCDCA-induced hepatocellular apoptosis to 49% in Ntcp-HepG2 cells, and significantly decreased apoptosis in primary rat and mouse hepatocytes after 4 hours of treatment; nuclear fragmentation induced by GCDCA was also inhibited as visualized by Hoechst 33342 staining.
In Vivo

Tauro-β-muricholic acid (400 mg/kg, in combination with TCA; gavage; twice, 12 hours apart; single dose) inhibited TCA-induced ileal Fgf15 and Shp gene expression, exerting an FXR antagonistic effect, and simultaneously inhibited intestinal FXR signaling, reduced serum ceramides, and improved hepatic steatosis in high-fat diet-induced non-alcoholic fatty liver disease (NAFLD) model mice [2][4]. Tauro-β-muricholic acid (oral antibiotic, 200 mg/kg/day; once daily; 3 days) increased TbMCA levels in the gallbladder of mice, inhibited ileal Fgf15 expression, upregulated hepatic Cyp7a1 expression, and altered bile acid composition [2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Swiss Webster mice (male, 9-16 weeks old), conventional raised (CONV-R) and germ-free (GF) mice; C57BL/6 mice (male, 9-16 weeks old), Fxr-deficient mice (backcrossed 8 generations on C57BL/6 background), CONV-R and GF mice [2]
Dosage: Combined with TCA, 400 mg/kg, 200 mg/kg/day
Administration: Oral administration
Result: Significantly reduced the TCA-induced expression of Fgf15 and Shp in the ileum of GF C57BL/6 mice. Antibiotic treatment increased the levels of TbMCA in the gallbladder of CONV-R C57BL/6 mice, suppressed ileal Fgf15 expression, and increased hepatic Cyp7a1 expression. GF mice had higher levels of TbMCA and a larger bile acid pool compared with CONV-R mice, and TbMCA functioned as a natural FXR antagonist to inhibit bile acid synthesis.
Molecular Weight

515.70

Formula

C26H45NO7S

CAS No.
Appearance

Solid

Color

White to off-white

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

Structure Classification
Initial Source
Shipping

Room temperature in continental US; may vary elsewhere.

Storage

-20°C, sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

Solvent & Solubility
In Vitro: 

DMSO : 25 mg/mL (48.48 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 1.9391 mL 9.6956 mL 19.3911 mL
5 mM 0.3878 mL 1.9391 mL 3.8782 mL
View the Complete Stock Solution Preparation Table

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

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Purity & Documentation
References

Complete Stock Solution Preparation Table

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Optional Solvent Concentration Solvent Mass 1 mg 5 mg 10 mg 25 mg
DMSO 1 mM 1.9391 mL 9.6956 mL 19.3911 mL 48.4778 mL
5 mM 0.3878 mL 1.9391 mL 3.8782 mL 9.6956 mL
10 mM 0.1939 mL 0.9696 mL 1.9391 mL 4.8478 mL
15 mM 0.1293 mL 0.6464 mL 1.2927 mL 3.2319 mL
20 mM 0.0970 mL 0.4848 mL 0.9696 mL 2.4239 mL
25 mM 0.0776 mL 0.3878 mL 0.7756 mL 1.9391 mL
30 mM 0.0646 mL 0.3232 mL 0.6464 mL 1.6159 mL
40 mM 0.0485 mL 0.2424 mL 0.4848 mL 1.2119 mL
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