Surotin Mechanism of Action

Pharmacology: Pharmacodynamics: Rosuvastatin calcium is synthetic heptenoic acid-derivative antilipemic agent. The drug 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 cholesterol, LDL-cholesterol, apolipoprotein B (apo B), non-HDL-cholesterol and triglyceride concentrations and increases HDL-cholesterol concentrations in patients with primary hyperlipidemia or mixed dyslipidemia. Rosuvastatin also reduces triglyceride concentration in patients with primary hypertriglyceridemia.
Pharmacokinetics: Rosuvastatin is incompletely absorbed from the gastrointestinal tract, with an absolute bioavailability of about 20%. Peak plasma concentrations occur about 5 hours after an oral dose. It is about 90% bound to plasma protein.
Rosuvastatin undergoes limited metabolized; approximately 10% of a radiolabeled dose is recovered as metabolite. The major metabolite is N-desmethyl rosuvastatin, which is formed principally by cytochrome P-450 (CYP) isoenzyme 2C9.
Based on in vitro studies, N-desmethyl rosuvastatin has approximately 17-50% of the HMG-CoA reductase inhibitory activity of the parent drug. The parent drug accounts for greater than 90% of the active plasma HMG-CoA reductase inhibitory activity.
Rosuvastatin and its metabolites are mainly eliminated in feces (90%) following oral administration. The elimination half-life of Rosuvastatin is approximately 19 hours.