Starez Mechanism of Action

Pharmacology: Pharmacodynamics: Rosuvastatin is a selective and competitive inhibitor of HMG-CoA reductase, the rate-limiting enzyme that converts 3-hydroxy-3-methylglutaryl coenzyme A to mevalonate, a precursor of cholesterol. In vivo studies in animals, and in vitro studies in cultured animal and human cells have shown rosuvastatin to have a high uptake into, and selectivity for, action in the liver, the target organ for cholesterol lowering. In in vivo and in vitro studies, rosuvastatin produces its lipid-modifying effects in two ways. First, it increases the number of hepatic LDL receptors on the cell-surface to enhance uptake and catabolism of LDL. Second, rosuvastatin inhibits hepatic synthesis of VLDL, which reduces the total number of VLDL and LDL particles.
Pharmacokinetics: Rosuvastatin is incompletely absorbed from the gastro-intestinal tract, with a bioavailability of about 20%. Peak plasma concentrations are achieved about 5 hours after an oral dose. It is taken up extensively by the liver, its primary site of action, and undergoes limited metabolism, mainly by the cytochrom P450 isoenzym CYP2C9. It is about 90% bound to plasma proteins. The plasma elimination half-life of rosuvastatin is about 19 hours. About 90% of an oral dose of rosuvastatin is excreted in the faeces, including absorbed and nonabsorbed drug, and the remainder is excreted in the urine; about 5% of a dose is excreted unchanged in the urine.