| [ Summary ] |
Nearly all available NSAIDs inhibit both COX-l and COX 2. Inhibition of the constitutive components of COX-1 is believedto be the primary cause of the many toxic effects associatedwith NSAIDs, especially gastroduodenal mucosal damage. On theother hand, inhibition of inducible COX-2 results in anti-inflammatory effectss without influencing COX-1 and its important homeostatic functions. Recently, new some compounds, which display selective COX-2 inhibition have been developed. The availability of agents in the new therapeutic class of selective COX-2 inhibitors promises to open a new era in the therapy of arthritis by offering potent antiillflammatory andanalgesic effects without potentially serious toxicities, associated with NSAIDs. In this paper, the mechanism and the clinical effects of selective COX-2, inhibition, and the points at issue, for which further studies would be required, were described. |