Crosstalk between lipid peroxidation and inflammation is known to be a pathognomonic feature for the development of coronary heart disease(CHD).In this regard ligand activated liver X receptor(LXR)-α has emerged as a key molecular switch by its inherent ability to modulate an array of genes involved in these two fundamental cellular processes.In addition,LXR-α has also been found to play a role in hepatic lipogenesis and innate immunity.Although several lines of evidence in experimental model systems have established the atheroprotective nature of LXR-α,human subjects have been reported to possess a paradoxical situation in which increased blood cellular LXR-α gene expression is always accompanied by increased coronary occlusion.This apparent paradox was resolved recently by the finding that CHD patients possess a deregulated LXR-α transcriptome due to impaired ligand-receptor interaction.This blood cellular mutated LXR-α gene ex- pression correlated specifically with the extent of coro- nary occlusion and hence need is felt to devise new synthetic ligands that could restore the function of this mutated LXR-αprotein in order to modulate genes involved in reverse cholesterol transport and suppression of the inflammatory response leading to the effective treatment of CHD. In this regard ligand activated liver X receptor (LXR) -α has emerged as a key molecular switch by its inherent ability to modulate an array of genes involved in these two fundamental cellular processes. In addition, LXR-alpha has also been found to play a role in hepatic lipogenesis and innate immunity. Several several lines of evidence in experimental model systems have established the atheroprotective nature of LXR- α, human subjects have been reported to possess paradoxical situations in which increased blood cellular LXR-α gene expression is always accompanied by increased coronary occlusion ..This apparent paradox was resolved recently by the finding that CHD patients possess a deregulated LXR-α transcriptome due to impaired ligand-receptor interaction. This blood cellular mutated LXR-α gene ex-pression correlated specifically with the extent of coro- nary occlusion and therefore need is felt to devise new synthetic ligands that could restore the function of this mutated LXR-αprotein in order to modulate genes involved in reverse cholesterol transport and suppression of the inflammatory response leading to the effective treatment of CHD.