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Recent advances in the mechanisms of regulation of leukotriene and prostaglandin biosynthesis, as well as their mechanisms of action, have generated a renewed interest in this field. One can cite the cloning of enzymes involved in the lipoxygenase (LOX) and cyclo-oxygenase (COX or PGHS) pathways, such as the leukotriene C
4
synthase and the novel inducible COX enzyme named COX-2, and the cloning of receptors to eicosanoids. The discovery of the inducible prostaglandin synthase, COX-2 or PGHS-2, distinct from the constitutive enzyme, renamed COX-1 (
1
–
4
), opened a new area of research toward the development of novel and selective nonsteroidal anti-inflammatory compounds (NSAIDs) for the improved treatment of inflammatory diseases. Indeed, the specific inhibition of the COX-2 isoenzyme is expected to reduce inflammation without the side effects (gastric and renal toxicity) associated to classical nonselective NSAIDs.