查看文章

The identification and characterization of an inducible form of cyclooxygenase (COX-2) in inflammatory cells in the early 1990s were the start of a race to the development of more selective nonsteroidal antiinflammatory drugs (NSAIDs), with reduced side effects (essentially gastro-intestinal toxicity) compared to classical NSAIDs. The development and the use of these specific inhibitors, collectively called coxibs, were immediately considered as a real breakthrough in antiinflammatory therapy. Thus, the development of the “coxibs” was based on the hypothesis that this isoform mediates inflammation in several organs via the biosynthesis of prostaglandins E2 and I2 (or prostacyclin) and that COX-1 was the source of the same prostaglandins in the gastric epithelium, where they would act as cytoprotective mediators (Figure 1.). Celecoxib (Celebrex) and rofecoxib (Vioxx) were the first two coxibs approved by the FDA …