Duvaztor-20/Duvaztor-40 Mechanism of Action

Pharmacotherapeutic group: Lipid modifying agents, HMG-CoA-reductase inhibitors.
Pharmacology: Pharmacodynamics: Atorvastatin (Duvaztor) is a selective, competitive inhibitor of HMG-CoA reductase, the rate-limiting enzyme responsible for the conversion of 3-hydroxy-3-methyl-glutaryl-coenzyme A to mevalonate, a precursor of steroids, including cholesterol.
Triglycerides and cholesterol in the liver are incorporated into very low-density lipoproteins (VLDL) and released into the plasma for delivery to peripheral tissues. Low-density lipoprotein (LDL) is formed from VLDL and is catabolized primarily through the high affinity LDL (LDL receptor).
Atorvastatin (Duvaztor) 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.
Atorvastatin (Duvaztor) reduces LDL production and the number of LDL particles. Atorvastatin (Duvaztor) produces a profound and sustained increase in LDL receptor activity coupled with a beneficial change in the quality of circulating LDL particles. Atorvastatin (Duvaztor) is effective in reducing LDL-C in patients with homozygous familial hypercholesterolaemia, a population that has not usually responded to lipid-lowering medicinal products.
Atorvastatin (Duvaztor) has been shown to reduce concentrations of total-C (30%-40%), LDL-C (41%-61%), apolipoprotein B (34%-50%), and triglycerides (14%-33%), while producing variable increases in HDL-C and apolipoprotein A1 in a dose response study. These results are consistent in patients with heterozygous familial hypercholesterolaemia, nonfamilial forms of hypercholesterolaemia, and mixed hyperlipidaemia, including patients with non-insulin-dependent diabetes mellitus.
Reductions in total-C, LDL-C, and apolipoprotein B have been proven to reduce risk for cardiovascular events and cardiovascular mortality.
Pharmacokinetics: Atorvastatin (Duvaztor) is rapidly absorbed after oral administration, maximum plasma levels occur within one to two hours. Although food reduces the rate and extent of absorption, LDL-C reduction is similar whether Atorvastatin (Duvaztor) is given with or without food. Atorvastatin (Duvaztor) is approximately 98% bound to plasma proteins. Atorvastatin is extensively metabolised and eliminated primarily in bile. The mean plasma elimination half-life of Atorvastatin in humans is approximately 14 hours, but the half life of inhibitory activity for HMG-CoA reductase is 20-30 hours.