Pravastatin sodium (CS-514 (sodium)), an HMG-CoA reductase inhibitor, inhibits sterol synthesis with IC50 of 5.6 μM.

HMG-CoA reductase:5.6 μM

Pravastatin (30 mg/kg/day) reduced malnutrition-induced lesions by 34%. In female Wistar rats exposed to radiation, which presented with decreased CCN2 levels, Pravastatin (30 mg/kg/day) could restore muscle structure. A single dose of 40 mg of Pravastatin lowered cholesterol synthesis by 62% in monocytes from healthy individuals and by 47% in patients with hypercholesterolemia. Moreover, treatment with Pravastatin (40 mg/day for 8 weeks) in hypercholesterolemic patients increased LDL degradation by 57% while inhibiting cholesterol synthesis by 55%.

In murine peritoneal macrophages (MPM), the J-774 A.1 macrophage-like cell line, and human monocyte-derived macrophages (HMDM), Pravastatin exhibits a dose-dependent inhibition of cholesterol synthesis. Upon LDL addition, concentrations of Pravastatin below 0.19 μg/mL enhance the esterification of cellular cholesterol, whereas levels below 100 μg/mL suppress esterification. At less than 0.5 mM, Pravastatin attenuates the Rho/ROCK pathway activity in human ileal and colonic transplants, reducing CCN2 mRNA levels. Pravastatin at concentrations less than 1 mM also induces the inhibition of CCN2 in primary human smooth muscle cells. In all cases, Pravastatin at less than 0.5 mM reduces the mRNA levels of type I collagen and fibronectin. Pravastatin facilitates vasodilation in aortic rings, achieving 62.8% endothelium-dependent relaxation at 10 μM after 8 minutes. Pravastatin-Na at 10 μM inhibits sterol synthesis with 50% greater efficacy than in peripheral blood mononuclear cells. In bovine aortic endothelial cells, Pravastatin at less than 10 μM stimulates NOS activity and NO release within 10 minutes, with L-arginine further enhancing NO production in response to Pravastatin.