ATC Group: C10AA HMG CoA reductase inhibitors

Atorvastatin is a selective, competitive inhibitor of HMG-CoA reductase. Atorvastatin lowers plasma cholesterol and lipoprotein serum concentrations by inhibiting HMG-CoA reductase and subsequently cholesterol biosynthesis in the liver and increases the number of hepatic LDL receptors on the cell surface for enhanced uptake and catabolism of LDL.

Fluvastatin, a fully synthetic cholesterol-lowering agent, is a competitive inhibitor of HMG-CoA reductase, which is responsible for the conversion of HMG-CoA to mevalonate, a precursor of sterols, including cholesterol. Fluvastatin reduces total-C, LDL-C, Apo B, and triglycerides, and increases HDL-C in patients with hypercholesterolaemia and mixed dyslipidaemia.

Lovastatin, which is an inactive lactone, is hydrolysed after oral administration to the corresponding β-hydroxyacid. This is the major metabolite and an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, an enzyme that catalyses an early and rate-limiting step in the biosynthesis of cholesterol.

Pitavastatin competitively inhibits HMG-CoA reductase, the rate-limiting enzyme in the biosynthesis of cholesterol, and inhibits cholesterol synthesis in the liver.

Pravastatin is a competitive inhibitor of 3-hydroxy–3-methylglutaryl-coenzyme A (HMG-CoA) reductase, the enzyme catalyzing the early rate limiting step in cholesterol biosynthesis, and produces its lipid lowering effect in two ways.

Rosuvastatin is a selective and competitive inhibitor of HMG-CoA reductase. Rosuvastatin increases the number of hepatic LDL receptors on the cell-surface, enhancing uptake and catabolism of LDL and it inhibits the hepatic synthesis of VLDL, thereby reducing the total number of VLDL and LDL particles.

Simvastatin has a potent activity in inhibiting HMG-CoA reductase (3-hydroxy–3-ethylglutaryl-CoA-reductase). Simvastatin has been shown to reduce both normal and elevated LDL-C concentrations.