The class
Review makes the case for pharmacological CETP inhibition as a therapeutic strategy pending clinical trial confirmation (Curr Top Med Chem 2005)
Original title: Cholesteryl ester transfer protein: pharmacological inhibition for the modulation of plasma cholesterol levels and promising target for the prevention of atherosclerosis
This review lays out the rationale for CETP inhibition: CETP normally exchanges cholesteryl esters and triglycerides between antiatherogenic HDL and proatherogenic VLDL and LDL particles, and people with genetic CETP deficiency have higher HDL cholesterol, lower LDL cholesterol, and potentially reduced cardiovascular disease risk. Small-molecule CETP inhibitors then in development appeared to reproduce this beneficial lipoprotein shift pharmacologically, but the authors emphasize that randomized clinical trials would ultimately be required to determine whether CETP inhibition actually reduces cardiovascular events, a question the field's genetic observations alone could not answer.
Original abstract
Cholesteryl ester transfer protein (CETP) facilitates the exchange of neutral lipids (such as cholesteryl esters and triglycerides) between anti-atherogenic HDL particles and pro-atherogenic VLDL and LDL particles in human plasma. Individuals possessing a genetic deficiency for CETP have higher HDL cholesterol and lower LDL cholesterol and may have a reduced risk for developing cardiovascular disease. Small molecule inhibitors of CETP are being developed that would appear to provide a beneficial change in lipoprotein profile. However, randomized clinical trials are ultimately required to determine whether CETP inhibition will afford a reduction in cardiovascular events.
Summary written by cetpinhibition.org from the published abstract; figures as published. Page updated 19 August 2026. Methods.