KS370G is an orally active hypoglycemic and cardiovascular protective agent. KS370G improves left ventricular hypertrophy and function in pressure-overload mice heart. KS370G reduces renal obstructive nephropathy. In Vivo KS370G (1 mg/kg; oral; once daily for 8 weeks) improves left ventricular function and inhibited cardiac hypertrophy through the decrease of the phosphorylation of ERK, AKT and GSK3β in pressure-overload mice heart . KS370G (10 mg/kg; oral; once daily for 13 days) attenuates unilateral ureteral obstruction-induced renal fibrosis by the reduction of inflammation and oxidative stress in mice. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Pressure-overload ICR mice model Dosage: 1 mg/kg Administration: Oral gavage, once daily for 8 weeks Result: Inhibited cardiac hypertrophy and improved cardiac function induced by pressure overload. Decreased the plasma levels of atrial natriuretic peptide and lactate dehydrogenase. Significantly reduced pressure overload-induced increase of α-SMA and phosphorylation of ERK, AKT and GSK3β. Reduced cardiac collagen accumulation. Animal Model: Male ICR mice, unilateral ureteral obstruction (UUO) modelDosage: 10 mg/kg Administration: Oral, once daily for 13 days Result: Significantly attenuated collagen deposition in the obstructed kidney and inhibited UUO-induced renal fibrosis markers expression, including fibronectin, type I collagen, vimentin, and α-smooth muscle actin (α-SMA). Significantly lowered the expression of renal\ninflammatory chemokines/adhesion molecules and monocyte cells marker (MCP-1, VCAM-1, ICAM-1 and CD11b). Reduced renal malondialdehyde levels and reversed the expression of renal antioxidant enzymes (SOD and catalase) after UUO. Significantly inhibited UUOinduced elevated plasma AngII and TGF-β1 levels, TGF-β1 protein expression and Smad3 phosphorylation. Form:Solid