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Pharmacology: Rosuvastatin is a hypolipidaemic agent; it is a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA reductase), the rate-determining enzyme for cholesterol synthesis. HMG-CoA reductase inhibitors (sometimes called "statins") reduce total cholesterol, low-density lipoprotein (LDL)-cholesterol and very-low-density lipoprotein (VLDL)-cholesterol concentrations in plasma. They also tend to reduce triglycerides and to increase high-density lipoprotein (HDL)-cholesterol concentrations. They are considered to exert their hypocholesterolaemic action by stimulating an increase in LDL-receptors on hepatocyte membranes thereby increasing the clearance of LDL from the circulation.
Pharmacokinetics: Rosuvastatin is administered orally in the active form with peak plasma levels occurring 5 hours after dosing. Exposure increases linearly over the dose range. The half life is 19 hours and does not increase with increasing dose. Absolute bioavailability is 20%. There is minimal accumulation on repeated once daily dosing.
Rosuvastatin undergoes first pass extraction in the liver, which is the primary site of cholesterol synthesis and LDL-C clearance. Rosuvastatin is approximately 90% bound to plasma proteins, mostly albumin. The parent compound, accounts for greater than 90% of the circulating active HMG CoA reductase inhibitor activity.
Rosuvastatin undergoes limited metabolism (approximately 10%), mainly to the N-desmethyl form, and 90% is eliminated as unchanged drug in the feces with the remainder being excreted in the urine.
