Anacetrapib: Difference between revisions
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Revision as of 14:12, 30 November 2010
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Anacetrapib (MK-0859, Merck) is cholesteryl ester transfer protein inhibitor that raises high-density lipoprotein (HDL) cholesterol and reduces low-density lipoprotein (LDL) cholesterol. Cholesteryl ester transfer protein (CETP), also known as plasma lipid transfer protein, is a plasma protein that amasses triglycerides (TG) from VLDL cholesterol or LDL cholesterol and actively exchanges them for cholesteryl esters from HDL cholesterol. CETP inhibition leads to increase in size of HDL cholesterol particle and apolipoprotein A-I concentration, which is a major HDL protein. Development of Torcetrapib, the first CETP inhibitor, was halted during a phase III randomized clinical trial due to a 25% increase in cardiovascular adverse events within the cohort that received the active treatment. The increase in adverse events was thought to be secondary to "off target" toxicity including elevated aldosterone levels and consequent electrolyte abnormalities and elevated blood pressure.
Results of the Phase II DEFINE Study
Download the DEFINE slides here: media:DEFINE.ppt
DEFINEwas a Phase II randomized, double-blind, placebo-controlled trial designed to assess the safety and lipid-lowering efficacy of anacetrapib. Patients in the study had known coronary heart disease or were at an elevated risk for the devlopment of coronary heart disease. Patients (1,623) were randomized to treatment with either 100 mg of anacetrapib or placebo daily for 18 months. The LDL cholesterol was reduced from 81 mg per deciliter (2.1 mmol per liter) to 45 mg per deciliter (1.2 mmol per liter) at 24 weeks in the anacetrapib group versus 82 mg per deciliter (2.1 mmol per liter) to 77 mg per deciliter (2.0 mmol per liter) among placebo treated patients (P<0.001). This represents a 39.8% reduction with anacetrapib realtive to placebo. Anacetrapib increased the HDL cholesterol level from 41 mg per deciliter (1.0 mmol per liter) to 101 mg per deciliter (2.6 mmol per liter) versus placebo which increased HDL from 40 mg per deciliter (1.0 mmol per liter) to 46 mg per deciliter (1.2 mmol per liter) (P<0.001). This represents a 138.1% increase in HDL associated with anacetrapib treatment versus placebo. Throughout the 76 weeks of therapy there were no changes in either systolic or diastolic blood pressure or electrolyte or aldosterone levels with anacetrapib as compared with placebo.