Cholestor Mechanism of Action

Pharmacology: Mechanism of Action: Rosuvastatin calcium is a 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 and low density lipoprotein(LDL)-cholesterol, and triglyceride concentrations, and increases HDL-cholesterol concentrations in patients with primary hyperlipidemia or mixed dyslipidemia. Rosuvastatin also reduces triglyceride concentrations in patients with primary hypertriglyceridemia.
Pharmacodynamics: Inhibit HMG-CoA reductase, the rate-limiting enzyme that converts HMG-CoA to mevalonate, a precursor of cholesterol.
Pharmacokinetics: Absorption: The absolute bioavailability of rosuvastatin is approximately 20%. Peak plasma concentrations of rosuvastatin were reached 3 to 5 hours following oral dosing.
Distribution: Mean volume of distribution at steady-state of rosuvastatin is approximately 134 liters. Rosuvastatin is 88% primarily bound to plasma proteins, mostly albumin.
Metabolism: Rosuvastatin is metabolized by cytochrome P450 2C9. Approximately 10 % of radiolabeled dose is recovered as metabolite. The major metabolite is N-desmethyl rosuvastatin, which has approximately one-sixth to one-half the HMG-CoA reductase inhibitory activity of Rosuvastatin.
Excretion: Following oral administration, rosuvastatin and its metabolites are primarily excreted in the feces (90%). The elimination half-life (t1/2) of rosuvastatin is approximately 19 hours.