The prostaglandin (PG) EP 4 receptor subtype is expressed by peripheral sensory neurons. Although a potential role of EP 4 receptor in pain has been suggested, a limited number of selective ligands have made it difficult to explore the physiological functions of EP 4 or its potential as a new analgesic target. Here, we describe the in vitro and in vivo pharmacology of a novel EP 4 receptor antagonist, N- [({2-[4-(2-ethyl-4,6-dimethyl-1H-imidazo [4,5-c] Nonsteroidal anti-inflammatory drugs (NSAIDs) and selective cyclooxygenase (COX)-2 inhibitors are mainstays of the pharmacopoeia for the treatment of signs and symptoms of osteoarthritis and inflammatory pain of various etiologies. Their mechanism of action is to decrease prostaglandin (PG) synthesis by inhibiting COX activities. Two isoforms of COX, COX-1 and COX-2, have been identified. COX-1 is constitutively expressed throughout the body, and it is thought to play an essential role in normal gastrointestinal and renal function, whereas COX-2 is induced in the presence of inflammation. NSAIDs inhibit both isoforms and inhibition of COX-1 is thought to cause the adverse gastrointestinal effects such as gastric erosion, ulceration, and hemorrhage, whereas inhibition of COX-2 is associated with the therapeutic effects of NSAIDs. Thus, inhibition of PG synthesis by NSAIDs has demonstrated clear efficacy in the reduction of K.N. and A.M. contributed equally to this work. Article, publication date, and citation information can be found at

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