The potential of selective COX-2 inhibitors in inflammatory and other diseases

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It has been known since the 1960s that prostaglandins play a key role in inflammation, fever and pain. In 1971, Sir John Vane discovered that the efficacy of nonsteroidal antiinflammatory drugs (NSAIDs) is derived by inhibiting a key enzyme in prostaglandin biosynthesis (1). This enzyme has subsequently been identified as cyclooxygenase (COX). Presently, there are two known COX isoforms with distinct physiological functions, COX-1 and COX-2. COX-1 is a constitutively expressed protein found in most tissues. In the gastric mucosa, COX-1 is involved in the production of cytoprotective prostacyclin. In platelets, COX-1 is required for the generation of thromboxane A2, which promotes platelet aggregation leading to thrombus formation. In contrast to COX-1, COX-2 is strongly inducible by a variety of mitogens such as cytokines and growth factors, and plays a key role in the production of inflammatory prostaglandins. A William Harvey Research Conference on Defining the role of COX-2 inhibitors in inflammatory and other diseases in Porto, Portugal brought together 15 invited speakers to present their current findings on the clinical significance of COX-2 and strategies for selectively targeting this isoform. Information presented at the conference is summarized below.

Original languageEnglish
Pages (from-to)181-185
Number of pages5
JournalDrugs of Today
Issue number3
StatePublished - 2001


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