A method of decreasing accumulation of cholesterol in arteries of humans by administering lecithin-cholesterol acyltransferase (LCAT).

Available for licensing and commercial development is a method of decreasing accumulation of cholesterol in arteries of humans by administering lecithin-cholesterol acyltransferase (LCAT). This method is useful for the therapeutic treatment of subjects at risk for developing atherosclerosis. High plasma concentration of HDL cholesterol is associated with reduced risk of cardiovascular diseases (such as ischemic stroke and myocardial infarction). In contrast, low levels of HDL are associated with increased risk of atherosclerotic diseases. The plasma protein enzyme LCAT plays a critical role in the metabolism of HDL and it facilitates the removal of cholesterol from the body. Individuals with a mutation in the LCAT gene have low HDL plasma levels and exhibit an increased risk for atherosclerosis. Therefore, upregulation of LCAT function has been proposed as an HDL-C increasing therapy, and may have atheroprotective effects. This invention provides for several methods of administering LCAT polypeptide to decrease cholesterol accumulation in arteries. Development Status: Animal data available. Relevant Publication: JM Hoeg et al. Overexpression of lecithin:cholesterol acyltransferase in transgenic rabbits prevents diet-induced atherosclerosis. Proc Natl Acad Sci USA. 1996 Oct 15;93 (21):11448-11453.

U.S. Patent No. 6,635,641 issued on 21 Oct 2003 (HHS Reference No. E-007-1996/0-US-03); PCT Application No. PCT/US96/18159 filed 09 Sep 1996, which was published as WO 1997/17434 on 15 May 1997 (HHS Reference No. E-007-1996/0-PCT-02); Australian Patent No. 728257 issued on 19 Apr 2001; and National Stage filings in Canada and Europe Inventors: Silvia Santamarina-Fojo, Jeffrey M. Hoeg, H. Bryan Brewer (NHLBI)

Licensees sought: Available for non-exclusive or exclusive licensing.