Vogdia Mechanism of Action

Pharmacology: Pharmacodynamics: Pravastatin sodium is a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, which is the rate-limiting enzyme involved in de novo cholesterol synthesis. This reduction in cholesterol leads to an increased LDL-receptors, improved receptor-mediated catabolism and clearance of circulating LDL. It also blocks the production of LDL by inhibiting the synthesis of its precursor, very low density lipoprotein (VLDL), in the liver. In addition to the ability of HMG-CoA reductase inhibition, Pravastatin sodium also possess pleiotropic properties including improved endothelial function, reduced inflammation at the site of the coronary plaque, inhibition of platelet aggregation, and anticoagulant effects.
Pharmacokinetics: Absorption: Pravastatin sodium is rapidly absorbed. The average absorption is 34% of the administered dose, with bioavailability of 17%. Time to peak concentration is in the range of 1 to 1.5 hours.
Distribution: Protein binding is approximately 50%. The volume of distribution is 0.46 L/kg.
Metabolism: Pravastatin sodium undergoes extensive first-pass metabolism by the liver. The primary metabolite of Pravastatin sodium is the 3-alpha-hydroxy-iso-Pravastatin (2.5% to 10% activity of parent drug).
Excretion: Plasma elimination half-life in adults is 77 hours (including all metabolites), approximately 2 to 3 hours (Pravastatin sodium), approximately 1.5 hours (3-alpha-hydroxy-iso-Pravastatin). About 70% of an oral dose of Pravastatin sodium is excreted in the feces, and about 20% is excreted in the urine.