Pharmacology: Pharmacodynamics: Atorvastatin as well as some of its metabolites, are pharmacologically active in humans. The liver is the primary site of action and the principal site of cholesterol synthesis and LDL clearance. Drug dosage, rather than systemic drug concentration, correlates better with LDL-C reduction individualization of drug dosage should be based on therapeutic response.
Pharmacokinetics: Atorvastatin is rapidly absorbed from the gastrointestinal tract. It has low absolute bioavailability of about 12% due to presystemic clearance in the gastrointestinal mucosa and/or first-pass metabolism in the liver, its primary site of action. Atorvastatin is metabolized by the P45O isoenzyme CYP3A4 to a number of compounds which are also active inhibitors of HMG-CoA reductase. The mean plasma elimination of atorvastatin is about 14 hours, although the half-life of inhibitory activity for HMG-CoA reductase is approximately 20 to 30 hours due to the contribution of the active metabolites. It is 98% to plasma proteins. Atorvastatin is excreted as metabolites primarily in the bile.
                                
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