Rovex 10/Rovex 20 Mechanism of Action

Pharmacological Classification: HMG CoA Reductase Inhibitor. ATC Code: C10AA07.
Pharmacology: Mechanism of action: Rosuvastatin is a selective and competitive inhibitor of HMG-CoA reductase, the rate-limiting enzyme that converts 3-hydroxy-3-methylglutaryl coenzymeA to mevalonate, a precursor for cholesterol. The primary site of action of rosuvastatin is the liver, the target organ for cholesterol lowering.
Rosuvastatin increases the number of hepatic LDL receptors on the cell-surface, enhancing uptake and catabolism of LDL and it inhibits the hepatic synthesis of VLDL, thereby reducing the total number of VLDL and LDL particles.
Pharmacodynamics: Rosuvastatin is a synthetic, enantiomerically pure antilipemic agent. It is used to lower total cholesterol, low density lipoprotein-cholesterol (LDL-C), apolipoprotein B (apoB), non-high density lipoprotein-cholesterol (non-HDL-C), and triglyceride (TG) plasma concentrations while increasing HDL-C concentrations. High LDL-C, low HDL-C and high TG concentrations in the plasma are associated with increased risk of atherosclerosis and cardiovascular disease. The total cholesterol to HDL-C ratio is a strong predictor of coronary artery disease and high ratios are associated with higher risk of disease. Increased levels of HDL-C are associated with lower cardiovascular risk. By decreasing LDL-C and TG and increasing HDL-C, rosuvastatin reduces the risk of cardiovascular morbidity and mortality.
Pharmacokinetics: Absorption: Absolute bioavailability is about 20%. C_max is reached in 3 to 5 h. Administration with food did not affect the AUC.
Distribution: The mean steady-state Vd is about 134 L. Rosuvastatin is 88% protein bound, mainly to albumin.
Metabolism: Rosuvastatin's major metabolite is formed by CYP2C9. Not extensively metabolized; approximately 10% is recovered as metabolite.
Elimination: Primarily excreted in the feces (90%). The elimination half-life is approximately 19 h.