Cholesterol and plasma lipid modifying patents

Abstract

Cholesterol lowering by the 3-hydroxy-3-methylglutaryl co-enzyme A (HMG-CoA) reductase inhibitors (statins) has been shown to have significant effects on mortality due to coronary heart disease (CHD) in several trials reported over the last four or so years. However, it has long been recognised that hypercholesterolaemia is not the only dyslipidaemia which can contribute to CHD. This article reviews patenting activity over the past few years directed towards normalisation of the plasma lipid profile by mechanisms which do not involve modulation of cholesterol synthesis. Such mechanisms might include lowering plasma triglyceride or lipoprotein (a) [Lp(a)] or raising plasma high-density lipoprotein (HDL). Many claimed compounds appear to have effects in animal or cell models, but do not have a defined molecular target. Of the molecular targets defined, the peroxisome proliferator-activated receptors (PPARs) have great promise. Gene therapy is well-represented in the patent claims, but many technical hurdles remain to be overcome before such treatments are routine. Strategies affecting cholesterol absorption, cholesteryl ester synthesis and hydrolysis and bile acid metabolism are not covered.

• apolipoprotein B
• dyslipidaemia
• gene therapy
• high-density lipoprotein
• hypercholesterolaemia
• hypertriglyceridaemia
• lipoprotein (a)
• lipoprotein receptor
• peroxisome proliferator-activated receptors
• scavenger receptor
• very low-density lipoprotein