As has been discussed above, nicotinic acid has been used routinely in the treatment of dyslipidemia for several decades, despite its shortcomings. With the discovery of a GPCR with which nicotinic acid interacts (GPR109a), a flurry of effort was initiated in the search of more potent and selective agonists of the receptor. A significant amount of progress in the understanding of how to design compounds that avoid some or all of current liabilities associated with nicotinic acid therapies including flushing, fatty acid rebound, and desensitization has been made. Consequently a number of compounds that interact with the receptor but that have somewhat different profiles from nicotinic acid itself have been described. Several companies have now advanced compounds into early clinical development. The data that have been disclosed thus far could have profound implications for further progress in the field.