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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Clinical pharmacokinetics of pravastatin.

The hypolipidaemic agent pravastatin differs from other US Food and Drug Administration (FDA)-approved HMG-CoA reductase inhibitors (e.g. lovastatin and simvastatin) because it has greater hydrophilicity, as a result of the hydroxyl group attached to its decalin ring. The hydrophilic nature of pravastatin accounts for its minimal penetration into the intracellular space of nonhepatic tissues, including an apparent inability to cross the blood-brain barrier. The drug is also well tolerated because it is rapidly absorbed and excreted, and does not accumulate in plasma even with repeated administration. Pravastatin is taken up into the liver by an active transport carrier system, and the hepatic extraction ratio is high (0.66). The drug and its metabolites are cleared through both hepatic and renal routes (53 and 47%, respectively). The dual route of elimination reduces the need for dosage adjustment if the function of either of these organs is impaired. Dosage adjustments are also not required on the basis of age or gender. Furthermore, the drug can be given without regard to food intake, an important consideration for compliance since lipid-lowering therapy is generally required long term. The drug is approximately 50% protein bound, and, therefore, compared with other members of its class the tendency for displacement of highly protein bound drugs such as warfarin is decreased. This minimal potential for drug-drug interactions is important for patients who are taking multiple drugs because of concomitant medical problems. However, as with any HMG-CoA reductase inhibitor, caution should be exercised when pravastatin is given with nicotinic acid (niacin), gemfibrozil or cyclosporin, because of increased risk for myopathy in patients receiving combination therapy.[1]


  1. Clinical pharmacokinetics of pravastatin. Quion, J.A., Jones, P.H. Clinical pharmacokinetics. (1994) [Pubmed]
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