Liver X receptors (LXRs) are ligand-activated transcription factors that belong to nuclear receptor superfamily. LXRs function as sterol sensors protecting cells from cholesterol overload by stimulating reverse cholesterol transport and activating its conversion to bile acids in the liver. Since LXRs play important role in lipid and cholesterol metabolism these receptors may be involved in the development of metabolic diseases such as hyperlipidemia and atherosclerosis. LXR agonists were shown to be effective for treatment of murine models of atherosclerosis, diabetes, anti-inflammation, and Alzheimer's disease. Also it was demonstrated that LXR agonists suppress the proliferation of prostate cancer and breast cancer cells. Unfortunately, known ligands possess undesirable side effects inducing lipogenesis and hypertriglyceridemia by transactivating genes involved in fatty acid biosynthesis. Therefore, development of novel LXR agonists is very important in modern drug design. OTAVA Ltd. offers Liver X receptor (LXR) focused library which is targeted towards Liver X receptor β and comprises 553 compounds. This library includes drug-like compounds only. The library was designed by performing molecular docking of OTAVA's collection of drug-like compounds in crystal structure of human LXRβ (PDB ID: 1UPV). The most important polar interaction of a ligand and LXRβ is a hydrogen bond with His435. This bond is observed in many LXR receptor-ligand complexes, including those with steroid compounds. The presence of this hydrogen bond has been used as criteria for filtering docking results in order to identify the most consistent binding modes. The complexes obtained after filtering were taken for visual inspection to exclude ligands displaying inappropriate binding. This library provides an excellent basis for development of novel therapeutics for lipid disorders, atherosclerosis, chronic inflammation, autoimmunity, cancer and neurodegenerative diseases. More information about this library you can find at www.otavachemicals.com.Read less <