Statins in multiple sclerosis

Abstract

Statins are orally administered inhibitors of the enzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, which catalyzes the conversion of HMG-CoA to L-mevalonate, a key intermediate for cholesterol biosynthesis1 (Figure 32.1a). Since 1987, when lovastatin was the first statin to be approved in the United States for the treatment of hypercholesterolemia, statins have established themselves as safe and well-tolerated drugs. A number of statins have been approved for the treatment of dyslipidemia: simvastatin (Zocor®, Lipex®), mevastatin (Compactin®), lovastatin (Mevacor®, Altocor®) and pravastatin (Pravachol®) are natural fungal derivatives, whereas fluvastatin (Lescol®), cerivastatin (Baycol®), atorvastatin (Lipitor®) and rosuvastatin (Crestor®) are synthetic statins. All statins resemble HMG-CoA in chemical structure, and thereby competitively bind and inhibit HMGCoA reductase (Figure 32.1b). Although synthetic statins are considered the more potent agents, there is no significant difference in the recommended total daily dose between natural and synthetic statins.