Elevated cholesterol and low-density lipoprotein (LDL) levels are significant risk factors for the development of cardiovascular disease. Rosuvastatin inhibits the enzyme HMG-CoA reductase, which plays a central role in endogenous cholesterol biosynthesis. The drug acts mainly in the liver, where the number of LDL receptors is increased, allowing more LDL to be taken up and broken down, and also inhibits the synthesis of VLDL (very low density lipoprotein). This leads to a decrease in LDL and VLDL in plasma. At the same time, HDL cholesterol (High Density Lipoprotein) is increased and triglycerides are decreased.
Rosuvastatin has an oral bioavailability of 20% and is 50% absorbed. Maximum plasma concentration is reached after approximately 5 hours. The drug binds 88% to plasma proteins and is absorbed primarily in the liver, where only about 10% is metabolized by the cytochrome P450 enzyme family. The half-life is approximately 19 hours but does not increase with increasing dose. Rovastatin is excreted unchanged 90% in the stool, the remainder in the urine.
It takes between two to four weeks for the effects of the statin to occur.
Because rosuvastatin is minimally metabolized via the cytochrome P450 system, fewer interactions occur (in contrast to atorvastatin, lovastatin, and simvastatin) with drugs metabolized by the same enzyme system.