FXR antagonist 1 (化合物 F6) 是一种口服有效的、选择性的肠道FXR拮抗剂 (IC50=2.1 μM)。FXR antagonist 1 通过拮抗肠道FXR和反馈激活肝脏FXR来选择性地抑制肠道FXR信号，改善 NASH (非酒精性脂肪性肝炎) 模型中的肝脏脂肪变性、炎症和纤维化。FXR antagonist 1 可用于 NASH 的研究。

FXR antagonist 1 (compound F6) is an orally active and selective intestinal FXR antagonist ( IC 50 =2.1 μM). FXR antagonist 1 selectively inhibits intestinal FXR signalling through antagonism of intestinal FXR and feedback activation of hepatic FXR to improve hepatic steatosis, inflammation and fibrosis in NASH (nonalcoholic steatohepatitis) models. FXR antagonist 1 can be used in NASH studies [1].

FXR antagonist 1 (0-100 μM; 24 h) shows FXR antagonistic activities in HEK293T cells [1]. Cell Viability Assay [1] Cell Line: HEK293T cells (co-transfected with pCMV-Script-hFXR and pGL4.11-hSHP-Luciferase) Concentration: 0-100 μM Incubation Time: 24 h Result: Exhibited FXR antagonistic activities with an IC 50 value of 2.1 μM.

FXR antagonist 1 (10 mg/kg; p.o.; single daily for 12 weeks) reduces adiposity and improves glucose sensitivity and ameliorates the progress of NASH in GAN-diet-induced NASH mice [1]. FXR antagonist 1 (10 mg/kg; p.o.; single daily for 12 weeks) inhibits intestinal FXR Signaling but indirectly activates hepatic FXR signaling in GAN-diet-induced mice [1]. FXR antagonist 1 (3, 10, 30 mg/kg; p.o.; single daily for 4 weeks) dose-dependently alleviates NASH pathologies in HFMCD-diet-induced mice [1]. Animal Model: Adult male C57BL/6 mice (GAN (Gubra-amylin NASH)-diet induced NASH model) [1]. Dosage: 10 mg/kg Administration: Oral administration; single daily for 12 weeks. Result: Reversed metabolic dysfunction in GAN-induced NASH mice. Reduced GAN-diet-induced hepatic steatosis, injury, inflammation, and fibrosis. Inhibited the hepatic mRNA expression involved in lipid metabolism, inflammatory signaling, and fibrogenesis in GAN-diet-induced mice. Significantly antagonized intestinal FXR signaling and bile acid reabsorption. Animal Model: Adult male C57BL/6 mice (HFMCD-diet induced NASH model) [1]. Dosage: 3, 10, 30 mg/kg Administration: Oral administration; single daily for 4 weeks. Result: Significantly decreased serum ALT and AST levels at 30 mg/kg, and markedly lowered the hepatic TG concentration in both 10 and 30 mg/kg. Lowered hepatic hydroxyproline level.

2295804-68-9

C36H59NO5

585.86

(< 1 mg/ml refers to the product slightly soluble or insoluble )
Powder: -20°C for 3 years
In solvent: -80°C for 2 years