Pharmacodynamics:

Rosuvastatin is a lipid regulating drug with actions on plasma lipids and competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG CoA reductase), the rate determining enzyme for cholesterol synthesis. Inhibition of HMG CoA Reductase leads to reduced cholesterol synthesis in the liver and lower intracellular cholesterol concentrations. This stimulates in low-density lipoprotein (LDL)-cholesterol receptors on hepatocyte membranes, thereby increasing the clearance of LDL from the circulation. HMG CoA reductase inhibitors (also called statins) reduce total cholesterol, LDL-cholesterol, and very low-density lipoprotein (VLDL)-cholesterol concentrations in the plasma. 

Pharmacokinetics:

Peak plasma concentrations of Rosuvastatin were reached 5 hours following oral dosing. The

absolute bioavailability of Rosuvastatin is approximately 20%. Rosuvastatin is 90% bound to plasma proteins, mostly albumin. This binding is reversible and independent of plasma concentrations. Mean volume of distribution at steady-state of Rosuvastatin is approximately 134 liters. 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. Overall, greater than 90% of active plasma HMG-CoA reductase inhibitory activity is accounted for by Rosuvastatin in the parent compound. Following oral administration, Rosuvastatin and its metabolite are primarily excreted in feces (90%). The elimination half-life of Rosuvastatin is approximately 19  hours.

Indications: 

For the management of hyperlipidaemias, including primary hypercholesterolaemia (type IIa), mixed dyslipidaemia (type IIb), and hypertriglyceridaemia (type IV), it may also be used in patients with homozygous familial hypercholesterolaemia.