As with other statins,<unk>  is a competitive inhibitor of HMG-CoA reductase. Unlike most others, however, it is a completely synthetic compound. HMG-CoA reductase catalyzes the reduction of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) to mevalonate, which is the rate-limiting step in hepatic cholesterol biosynthesis. Inhibition of the enzyme decreases de novo cholesterol synthesis, increasing expression of low-density lipoprotein receptors (LDL receptors) on hepatocytes. This increases LDL uptake by the hepatocytes, decreasing the amount of LDL-cholesterol in the blood. Like other statins,<unk>  also reduces blood levels of triglycerides and slightly increases levels of HDL-cholesterol. In people with acute coronary syndrome, high-dose<unk>  treatment may play a plaque-stabilizing role. At high doses, statins have anti-inflammatory effects, incite reduction of the necrotic plaque core, and improve endothelial function, leading to plaque stabilization and, sometimes, plaque regression. There is a similar thought process with using high-dose statins to prevent recurrence of thrombotic stroke. Pharmacodynamics The liver is the primary site of action of<unk> , as this is the principal site of both cholesterol synthesis and LDL clearance. It is the dosage of<unk> , rather than systemic medication concentration, which correlates with extent of LDL-C reduction. In a Cochrane systematic review the dose-related magnitude of<unk>  on blood lipids was determined. Over the dose range of 10 to 80 mg/day total cholesterol was reduced by 27.0% to 37.9%, LDL cholesterol by 37.1% to 51.7% and triglycerides by 18.0% to 28.3%.
Atorvastatin
Clofibrate
Simvastatin
Fenofibrate
Lovastatin
Ezetimibe
Fluvastatin
Pravastatin