RG-239 

RG-239 is an orally active TGR5 agonist with an EC₅₀ of 120 nM, significantly outperforming Betulinic acid (HY-10529) (EC₅₀ = 1.04 μM). RG-239 demonstrates higher selectivity for TGR5 compared to the FXRα. RG-239 increases mitochondrial activity in adipocytes and promotes neurite outgrowth at higher concentrations. RG-239 inhibits LPS-induced iNOS expression and nitrite production in Raw264.7 and microglia cells. RG-239 can be used for the study of type 2 diabetes^{[1][2][3][4][5]}.

RG-239 (Compound 18 dia 2) (10 μM) increases mitochondrial activity in adipocytes as demonstrated by the increase in cytochrome c oxidase activity in 3T3L1 adipocyte cells^[2].

RG-239 (1-10 μM) induces a neurite length of 9.5 μm at 1 μM significantly lower than induced by Retinoic acid (RA) (HY-14649), but the median neurite length is 37.0 μm at 10 μM, almost identical to that induced by Deoxycholic acid (DCA) (HY-N0593) in NSC-34 cells^[3].

RG-239 (2 μM, 24 h) inhibits LPS-induced iNOS expression and nitrite production in Raw264.7 and microglia cells^[4].

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

RG-239 (Compound 18 dia 2) (30 mg/kg/day, p.o., 3 weeks) decreases the plasma glucose level in obese mice induced by a 10-week high-fat (HF) diet (60% kcal from fat)^[2].

RG-239 (10 mg/kg/day, p.o., 2 weeks) decreases the expression of the inflammatory genes Tnfα, IL-6 and IL-1β in the livers of B6J mice induced by a 10-week high-fat (HF) diet (60% kcal from fat)^[5].

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

496.76

C₃₃H₅₂O₃

1199222-56-4

OC([C@]12[C@@]([C@@H](CC2)C(C)=C)([H])[C@]3([H])[C@@](CC1)([C@]4([C@]([C@@]5([C@@](C(C)([C@](O)(CC=C)CC5)C)([H])CC4)C)([H])CC3)C)C)=O

Room temperature in continental US; may vary elsewhere.

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

• [1]. Genet C, et al. Redefining the TGR5 triterpenoid binding pocket at the C-3 position. ChemMedChem. 2010 Dec 3;5(12):1983-8.  [Content Brief]

  [2]. Genet C, et al. Structure-activity relationship study of betulinic acid, a novel and selective TGR5 agonist, and its synthetic derivatives: potential impact in diabetes. J Med Chem. 2010 Jan 14;53(1):178-90.  [Content Brief]

  [3]. Ackerman HD, et al. Bile Acids Induce Neurite Outgrowth in Nsc-34 Cells via TGR5 and a Distinct Transcriptional Profile. Pharmaceuticals (Basel). 2023 Jan 24;16(2):174.  [Content Brief]

  [4]. Romero-Ramírez L, et al. Bile acids attenuate PKM2 pathway activation in proinflammatory microglia. Sci Rep. 2022 Jan 27;12(1):1459.  [Content Brief]

  [5]. Fujisaka S, et al. Antibiotic effects on gut microbiota and metabolism are host dependent. J Clin Invest. 2016 Dec 1;126(12):4430-4443.  [Content Brief]