Abstract
Cerivastatin is a synthetic and enantiomerically pure 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor. It has been recognized for its high pharmacologic potency, uncomplicated pharmacokinetic profile, and low drug-interaction potential. The efficacy of cerivastatin has been demonstrated in a number of clinical trials involving patients with primary hypercholesterolemia and mixed dyslipidemia. Cerivastatin was found to have dose-dependent reduction in total cholesterol and low-density lipoprotein (LDL) cholesterol. At the 0.4 mg daily dose, cerivastatin was found to lower LDL cholesterol by approximately 35% (mean reductions of 33-39%). The triglyceride-lowering effect of cerivastatin is also dose dependent; however, there is a much stronger association between baseline triglyceride levels and the triglyceride-lowering effect of cerivastatin. A dosage of 0.4 mg daily has been shown to reduce triglycerides by a mean of 28% in patients with baseline triglyceride levels of > 300 mg/dL. At the time of its initial approval by the US Food and Drug Administration (FDA) in 1997, cerivastatin was available only in 0.2 mg and 0.3 mg strengths. The recent FDA approval of the 0.4-mg strength dose has made cerivastatin a more competitive drug in lipid-lowering efficacy among the HMG-CoA reductase inhibitors.