The major therapeutic action of statin drugs is reduction in levels of circulating atherogenic lipoproteins as a result of inhibition of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase mainly in the liver. The magnitude of reduction of atherogenic lipoproteins differs among various statins. It is suggested that an ideal statin would maximize the pharmacodynamic activity in the liver and minimize the inhibitory activity outside the liver, particularly in some vulnerable tissues, such as skeletal muscle. An additional advantage would be a low risk of undesirable interactions with other drugs. Compared with other statins, rosuvastatin has been found to be a relatively potent inhibitor of HMG-CoA reductase and to have a high degree of selectivity for effect in liver cells compared with a range of non-hepatic cells, including cultured human skeletal muscle cells. In addition, rosuvastatin undergoes relatively little metabolism by the hepatic CYP system; it has a moderate degree of systemic bioavailability and a relatively long elimination half-life. On the basis of these criteria, rosuvastatin represents a step forward in efforts to optimize the pharmacologic properties of the statin class.