Hyodeoxycholic acid sodium  (Synonyms: HDCA sodium)

Hyodeoxycholic acid sodium is a secondary bile acid formed in the small intestine by the gut flora, and acts as a TGR5 (GPCR19) agonist, with an EC₅₀ of 31.6 µM in CHO cells^[1][2].

Hyodeoxycholic acid sodium is a secondary hydrophilic bile acid formed in the small intestine by the gut flora, and acts as an agonist of TGR5, with an EC₅₀ of 31.6 μM in CHO cells^[1].
Hyodeoxycholic acid (50, 100 μM) sodium increases the expression of genes (Abca1, Abcg1, and Apoe) involved in cholesterol efflux in RAW 264.7 cells^[2].

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

Hyodeoxycholic acid (HDCA; 1.25% (wt/wt)) sodium obviously decreases fat mass and increases lean mass but does not raise the serum levels of any organ toxicity markers in LDLRKO mice. Hyodeoxycholic acid inhibits atherosclerotic lesion formation in LDLRKO at multiple sites, improves plasma lipoprotein profiles, decreases plasma glucose level and intestinal cholesterol absorption efficiency and increases daily cholesterol excretion through fecal output. Hyodeoxycholic acid sodium also improves HDL function as measured by a cholesterol efflux assay^[2].

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

414.55

C₂₄H₃₉NaO₄

10421-49-5

C[C@@H]([C@H]1CC[C@]2([C@@]3(C[C@@H]([C@@]4(C[C@@H](CC[C@@]4([C@]3(CC[C@]12C)[H])C)O)[H])O)[H])[H])CCC(O[Na])=O

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Sato H, et al. Novel potent and selective bile acid derivatives as TGR5 agonists: biological screening, structure-activity relationships, and molecular modeling studies. J Med Chem. 2008 Mar 27;51(6):1831-41.  [Content Brief]

  [2]. Shih DM, et al. Hyodeoxycholic acid improves HDL function and inhibits atherosclerotic lesion formation in LDLR-knockout mice. FASEB J. 2013 Sep;27(9):3805-17.  [Content Brief]