Tauro-β-muricholic acid sodium

Tauro-β-muricholic Acid sodium (T-βMCA sodium), a endogenous metabolite, is a competitive and reversible farnesoid X receptor (FXR) antagonist, with an IC50 of 40 μM[1][2][3].

Research Areas >> Cancer

Signaling Pathways >> Metabolic Enzyme/Protease >> FXR

IC50: 40 μM (FXR)[1]

T-βMCA sodium inhibits FXR reporter activity in the CRC cell line HT29 (EC50 ~10 μM)[3]. T-βMCA sodium dose-dependently increases WNT signaling in HT29 and HCT116 cells[3]. T-βMCA sodium induces proliferation and DNA damage in Lgr5+ cells[3].

T-βMCA sodium (400 mg/kg; i.g.; twice a week; for 6 weeks) can effectively recapitulate the ability of HFD to promote CRC progression[3]. T-βMCA sodium treatment also significantly increases levels of serum cytokines, including IFN-γ, IL-6, and IL-17[3]. Animal Model: APCmin/+ mice[3] Dosage: 400 mg/kg Administration: Oral gavage; twice a week; for 6 weeks Result: Markedly decreased intestinal integrity and accelerated tumor growth in the intestine and colon.

[1]. 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.

[2]. Wahlström A, et al. Induction of farnesoid X receptor signaling in germ-free mice colonized with a human microbiota. J Lipid Res. 2017 Feb;58(2):412-419.

[3]. Fu T, et al. FXR Regulates Intestinal Cancer Stem Cell Proliferation. Cell. 2019 Feb 21;176(5):1098-1112.e18.