PGE synthase inhibitors as an alternative to COX-2 inhibitors

NSAIDs and selective COX-2 inhibitors reduce the formation of prostanoids, particularly PGE2, to diminish inflammation. However, these drugs exhibit toxicities, including gastrointestinal bleeding and myocardial infarction. In cells, arachidonic acid is converted to PGE2 by the action of COX enzymes and terminal PGE synthase. This review discusses the problems associated with selective COX-2 inhibitors and describes the microsomal PGE synthase-1 enzyme, its regulation and role in inflammatory diseases, its known inhibitors, and its potential as an alternative target for the development of novel anti-inflammatory agents.