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Active ingredient: Pravastatin - Brands, Medical Use, Clinical Data

Brands, Medical Use, Clinical Data

Drug Category

  • Anticholesteremic Agents
  • HMG-CoA Reductase Inhibitors

Dosage Forms

  • Tablet

Brands / Synonyms

Compactin; Elisor; Lipostat; Lovastatin; Mevalotin; Mevastatin; Mevinolin; Oliprevin; Pravachol; Pravaselect; Pravastatin Sodium; Pravastatina [Spanish]; Pravastatine [French]; Pravastatinum [Latin]; Selectin; Selipran; Vasten


For the treatment of hypercholesterolemia to reduce the risk of myocardial infarction.


Pravastatin, an antilipemic agent, is used to treat primary hypercholesterolemia. Unlike lovastatin and simvastatin, pravastatin is relatively hydrophilic and does not require hydrolysis for activation.

Mechanism of Action

Like lovastatin and simvastatin, pravastatin inhibits hydroxymethylglutaryl-CoA (HMG-CoA) reductase. As HMG-CoA is necessary for the intracellular synthesis of cholesterol, its inhibition results in increased clearance of circulating LDL. Pravastatin also inhibits hepatic synthesis of VLDL, the precursor for LDL, reducing circulating cholesterol and LDL cholesterol.


Average oral absorption of pravastatin is 34% and absolute bioavailability is 17%.


Rhabdomyolysis; LD50=mg/kg (orally in rat)

Biotrnasformation / Drug Metabolism

Hepatic, there is a small amount of metabolism by P450 enzymes, but this effect is so minimal that inhibitory pharmacokinetic drug interactions have no real effect on its overall activity and elimination. An in vitro study which found moderate affinity for P450 2C9 (major), 2D6 and 3A4.


Hypersensitivity to any component of this medication.

Active liver disease or unexplained, persistent elevations of serum transaminases .

Pregnancy and Lactation. Atherosclerosis is a chronic process and discontinuation of lipid-lowering drugs during pregnancy should have little impact on the outcome of long-term therapy of primary hypercholesterolemia. Cholesterol and other products of cholesterol biosynthesis are essential components for fetal development (including synthesis of steroids and cell membranes). Since HMG-CoA reductase inhibitors decrease cholesterol synthesis and possibly the synthesis of other biologically active substances derived from cholesterol, they are contraindicated during pregnancy and in nursing mothers. Pravastatin should be administered to women of childbearing age only when such patients are highly unlikely to conceive and have been informed of the potential hazards. If the patient becomes pregnant while taking this class of drug, therapy should be discontinued immediately and the patient apprised of the potential hazard to the fetus.

Drug Interactions


Immunosuppressive Drugs, Gemfibrozil, Niacin (Nicotinic Acid), Erythromycin
Cytochrome P450 3A4 Inhibitors

In vitro and in vivo data indicate that pravastatin is not metabolized by cytochrome P450 3A4 to a clinically significant extent.
This has been shown in studies with known cytochrome P450 3A4 inhibitors (see diltiazem and itraconazole below). Other examples
of cytochrome P450 3A4 inhibitors include ketoconazole, mibefradil, and erythromycin.


Steady-state levels of diltiazem (a known, weak inhibitor of P450 3A4) had no effect on the pharmacokinetics of pravastatin. In
this study, the AUC and Cmax of another HMG-CoA reductase inhibitor which is known to be metabolized by cytochrome P450 3A4 increased
by factors of 3.6 and 4.3, respectively.


The mean AUC and Cmax for pravastatin were increased by factors of 1.7 and 2.5, respectively, when given with itraconazole (a potent
P450 3A4 inhibitor which also inhibits p-glycoprotein transport) as compared to placebo. The mean tĹ was not affected by itraconazole,
suggesting that the relatively small increases in Cmax and AUC were due solely to increased bioavailability rather than a decrease
in clearance, consistent with inhibition of p-glycoprotein transport by itraconazole. This drug transport system is thought to affect
bioavailability and excretion of HMG-CoA reductase inhibitors, including pravastatin. The AUC and Cmax of another HMG-CoA reductase
inhibitor which is known to be metabolized by cytochrome P450 3A4 increased by factors of 19 and 17, respectively, when given with


Since concomitant administration of pravastatin had no effect on the clearance of antipyrine, interactions with other drugs metabolized
via the same hepatic cytochrome isozymes are not expected.


Concomitant administration resulted in an approximately 40 to 50% decrease in the mean AUC of pravastatin. However, when pravastatin
was administered 1 hour before or 4 hours after cholestyramine or 1 hour before colestipol and a standard meal, there was no clinically
significant decrease in bioavailability or therapeutic effect.


Concomitant administration of 40 mg pravastatin had no clinically significant effect on prothrombin time when administered in a study
to normal elderly subjects who were stabilized on warfarin.


The AUC0-12hr for pravastatin when given with cimetidine was not significantly different from the AUC for pravastatin when given alone.
A significant difference was observed between the AUCís for pravastatin when given with cimetidine compared to when administered with


In a crossover trial involving 18 healthy male subjects given 20 mg pravastatin and 0.2 mg digoxin concurrently for 9 days, the
bioavailability parameters of digoxin were not affected. The AUC of pravastatin tended to increase, but the overall bioavailability
of pravastatin plus its metabolites SQ 31,906 and SQ 31,945 was not altered.


Some investigators have measured cyclosporine levels in patients on pravastatin (up to 20 mg), and to date, these results indicate no
clinically meaningful elevations in cyclosporine levels. In one single-dose study, pravastatin levels were found to be increased in
cardiac transplant patients receiving cyclosporine.


In a crossover study in 20 healthy male volunteers given concomitant single doses of pravastatin and gemfibrozil, there was a
significant decrease in urinary excretion and protein binding of pravastatin. In addition, there was a significant increase in AUC,
Cmax, and Tmax for the pravastatin metabolite SQ 31,906. Combination therapy with pravastatin and gemfibrozil is generally not

In interaction studies with aspirin, antacids (1 hour prior to PRAVACHOL), cimetidine, nicotinic acid, or probucol, no statistically
significant differences in bioavailability were seen when PRAVACHOL (pravastatin sodium) was administered

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