Fezagepras (Setogepram) sodium acts as an orally active agonist for GPR40 and as an antagonist or inverse agonist for GPR84 Fezagepras sodium decreases renal, liver and pancreatic fibrosis Fezagepras sodium exerts anti-fibrotic, anti-inflammatory and anti-proliferative actions . In Vitro Fezagepras sodium (500 μM; 24 hours) inhibits TGF-β (10 ng/mL)-activated human hepatic stellate cells (HSCs) proliferation. ?\nFezagepras sodium (250 or 500 μM; 24 hours) dose-dependently arrests HSCs at the G0/G1 phase without inducing apoptosis. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Cell Proliferation AssayCell Line: HSCs Concentration: 250 or 500 µM Incubation Time: 24 hours Result: Inhibited TGF-β-activated HSC proliferation. TGF-β (10 ng/mL) increased HSC proliferation by 10%. Cell Cycle AnalysisCell Line: HSCs Concentration: 250 µM, 500 µM Incubation Time: 24 hours Result: Inhibited cell cycle progression. In Vivo Fezagepras sodium (100 mg/kg/day; gavage from 8-20 weeks of age) markedly decreases hyperglycemia and markedly improvea glucose tolerance in type 2 diabetes eNOS -/- db/db mice .· MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Type 2 diabetes eNOS -/- db/db mice Dosage: 100 mg/kg/day Administration: Given via daily gavage from 8-20 weeks Result: Compared with vehicle-treated mice, hyperglycemia was markedly decreased, and glucose tolerance was markedly improved. Form:Solid IC50& Target:GPR40, GPR84