SR-BI is a member of CD36 superfamily, and is the primary receptor responsible for mediating selective transport of cholesterol between high-density lipoprotein (HDL) and cells. The mechanism of this transport is poorly understood but it is known to be dramatically different from classic endocytic uptake. In addition to cholesterol, SR-BI can also interact and transport a wide variety of other lipids and ligands. Thus, there is a need for molecular tools to probe the biology of SR-BI further.
There are multiple potential therapeutic applications of SR-BI inhibitors. In addition to its significant influence on lipoprotein metabolism, SR-BI has been shown to influence a wide variety of physiologic and pathophysiologic systems, including hypercholesterolemia and coronary artery disease, female infertility, adrenal insufficiency, anemia, thrombocytopenia, endothelial dysfunction, immune/inflammatory defects, susceptibility to deep vein thrombosis and association with some cancers. In addition, SR-BI acts as a co-receptor for cellular entry of HCV and malaria parasites. In some of these cases (e.g., HCV and malarial infection, cancer), targeting SR-BI presents an attractive approach to therapy.