COX-2 in Inflammation and Resolution
Mol. Interv. 2006 6: 199-207.
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In view of the widespread and effective use of the nonsteroidal anti-inflammatory drugs (NSAIDs), the importance of limiting the side effects of these agents is self-evident. A major goal for both clinicians and drug developers has thus been to improve the specificity with which novel NSAIDs would inhibit their canonical targets, the cyclooxygenase (COX) enzymes. A number of lessons, in a variety of arenas, have been learned in the pursuit of this goal. Some of these lessons have unearthed new challenges in understanding the biology and pharmacology of the COX enzymes. Particularly important is the growing recognition that the inhibition of the COX enzymes, even with the attainment of absolute specificity for one or both of the major COX isoforms, may itself undermine anti-inflammatory therapy or even exacerbate inflammatory disease.