| Indication | Used as an adjunct to diet for the reduction of elevated total and LDL cholesterol levels in patients with primary hypercholesterolemia and mixed dyslipidemia (Fredrickson Types IIa and IIb) when the response to dietary restriction of saturated fat and cholesterol and other non-pharmacological measures alone has been inadequate. |
| Pharmacodynamics | Cerivastatin, a competitive HMG-CoA reductase inhibitor effective in lowering LDL cholesterol and triglycerides, is used to treat primary hypercholesterolemia and mixed dyslipidemia (Fredrickson types IIa and IIb). |
| Mechanism of action | Cerivastatin competitively inhibits hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase, the hepatic enzyme responsible for converting HMG-CoA to mevalonate. As mevalonate is a precursor of sterols such as cholesterol, this results in a decrease in cholesterol in hepatic cells, upregulation of LDL-receptors, and an increase in hepatic uptake of LDL-cholesterol from the circulation. |
| Absorption | The mean absolute oral bioavailability 60% (range 39 - 101%). |
| Volume of distribution | Not Available |
| Protein binding | More than 99% of the circulating drug is bound to plasma proteins (80% to albumin). |
| Metabolism | Hepatic. Biotransformation pathways for cerivastatin in humans include the following: demethylation of the benzylic methyl ether to form Ml and hydroxylation of the methyl group in the 6'-isopropyl moiety to form M23. |
| Route of elimination | Not Available |
| Half life | 2-3 hours |
| Clearance | Not Available |
| Toxicity | Rhabdomyolysis, liver concerns |