Rovas Mechanism of Action

Pharmacology: Pharmacodynamics: Mechanism of action: Rosuvastatin is a selective, competitive inhibitor of 3-hydroxymethylglutaryl-CoA (HMG-CoA) reductase, an enzyme that catalyzes the conversion of HMG-CoA to mevalonate (an early and rate-limiting step in cholesterol biosynthesis). Rosuvastatin reduces total and low-density lipoprotein (LDL)-cholesterol, apolipoprotein B (apo B), non-high-density lipoprotein (HDL)-cholesterol, and triglyceride concentrations, and increase HDL cholesterol concentration in patients with primary hyperlipidemia or mixed dyslipidemia.
Pharmacokinetics: Rosuvastatin is incompletely absorbed from the gastrointestinal tract, with an absolute bioavailability of about 20%. Peak plasma concentrations occur 5 hours after an oral dose. It is about 90% bound to plasma proteins. Rosuvastatin is not extensively metabolized; approximately 10% of a radiolabeled dose is recovered as metabolite. The major metabolite is N-desmethyl rovastatin, which is formed principally by cytochrome P-450 (CYP) isoenzyme 2C9. Rosuvastatin and its metabolites are mainly eliminated in feces about 90% following oral administration. The elimination half-life of rosuvastatin is about 19 hours.