The rate-limiting step in cholesterol biosynthesis is controlled by the enzyme 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. Inhibitors of this enzyme lower serum cholesterol very efficiently by increasing cellular uptake of cholesterol-rich, low-density lipoproteins. Pravastatin, a derivative of mevastatin and in the same class as lovastatin, lowers total cholesterol concentrations by 20–30 percent in patients with hypercholesterolemia. In patients who also have hypertriglyceridemia, serum triglyceride levels are decreased. Detailed pharmacokinetic data and long-term adverse-effect experience with pravastatin are extremely limited. The issue of tissue-selectivity for pravastatin has given rise to the marketing terminology “second-generation” HMG-CoA reductase inhibitor, but any clinical advantage of pravastatin over other HMG-CoA reductase inhibitors remains to be demonstrated.
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