ezetimibe: http://en.wikipedia.org/wiki/Ezetimibe
Ezetimibe localises at the brush border of the small intestine, where it inhibits the absorption of cholesterol from the intestine. Specifically, it appears to bind to the Niemann-Pick C1-Like 1 (NPC1L1) protein on the gastrointestinal tract epithelialcells as well as in hepatocytes. In addition to this direct effect, decreased cholesterol absorption leads to an upregulation of LDL-receptors on the surface of cells and an increased LDL-cholesterol uptake into cells, thus decreasing levels of LDL in the blood plasma which contribute to atherosclerosis and cardiovascular events.
Even though ezetimibe decreases cholesterol levels, the results of two major, high-quality clinical trials (in 2008 and 2009) showed that it did not improve clinically significant outcomes, such as major coronary events, and actually made some outcomes, such as artery wall thickness, worse. Indeed, a panel of experts concluded in 2008 that it should "only be used as a last resort".[1] In one of those studies, a head-to-head trial in 2009, a much less expensive medication (extended-release niacin) was found to be superior. Ezetimibe actually increased the thickness of artery walls (a measurement of atherosclerosis) and caused more major cardiovascular events.[2] However, in combination with simvastatin, a 2010 trial has shown it to be better than atorvastatin and rosuvastatin at lowering lipid levels.[3] A significantly more positive view of the benefits of Ezetimibe is offered by Britain's NICE.[4]
