RiteMed Rosuvastatin Mechanism of Action

HMG-CoA Reductase Inhibitor.
Pharmacology: Pharmacodynamics: Pharmacodynamics Rosuvastatin 20mg Film-Coated Tablet 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. Studies in animals, and studies in cultured animal and human cells have known Rosuvastatin to have a high uptake into, and selectively for, action in the liver, the target organ for cholesterol lowering. In studies, Rosuvastatin produces its lipid-modifying effects in two ways. First, it increases the number of hepatic LDL (low-density lipoprotein) receptors on the cell-surface to enhance uptake and catabolism of LDL. Second, Rosuvastatin inhibits hepatic synthesis of VLDL (very low-density lipoprotein), which reduces the total number of VLDL and LDL particles.
Pharmacokinetics: Absorption: In clinical pharmacology studies in man, peak plasma concentrations of Rosuvastatin were reached 3 to 5 hours following oral dosing. The absolute bioavailability of Rosuvastatin is approximately 20%.
Distribution: Mean volume of distribution at steady-state of Rosuvastatin is approximately 134 liters.
Metabolism: Rosuvastatin is not extensively metabolized; approximately 10% of a radiolabeled dose is recovered as metabolite. The major metabolite is N-desmethyl rosuvastatin, which is formed principally by cytochrome P450/2C9.
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. After an intravenous dose, approximately 28% of the total body clearance was via the renal route, and 72% by the hepatic route.
20 mg: Distribution: Rosuvastatin is 88% bound to plasma proteins, mostly albumin. This binding is reversible and independent of plasma concentrations.