Antiprostaglandins are a group of compounds of differing chemical structure but similar pharmacological action. They produce an anti-inflammatory effect by inhibiting the formation of prostaglandins. Often they have been referred to as Non-Steroidal Anti-inflammatory Drugs or NSAIDs. Others have called them prostaglandin synthetase inhibitors or cyclooxygenase (COX) inhibitors. Regardless of the particular name applied, they function by reducing the production of mediators of the inflammatory process. Compounds with this activity are not new, dating back to aspirin, that was patented in 1908. Compounds commonly used in veterinary medicine include aspirin, phenylbutazone, ketoprofen, carprofen, flunixin meglumine, tolfenamic acid and, to a lesser extent, human products such as indomethacin, ibuprofen, and naproxen. It wasn't until 1971 that the action of any of these compounds was demonstrated.

Recently researchers have determined that there are two forms of cyclooxygenase: COX-1 and COX-2. In vitro studies suggest that COX-1 is the form that produces the "good" effects of prostaglandins, such as regulation of gastric acidity and intestinal mucus flow as well as regulation of renal blood. In contrast, COX-2 is responsible for production of prostaglandins of inflammation. Therefore, ideally an NSAID that blocked only the prostaglandins of inflammation may be a safer form of medication. Much of this theory is extrapolation of laboratory data, but it has not been demonstrated in man or animals. Researchers are actively screening for compounds that have more or less COX-2 activity or a high ratio of activity of COX-2 to COX-1. Currently available NSAIDs are inhibitors of both COX-1 and COX-2, although the degree of inhibition of each may be variable. The science in this arena is too new to draw broad conclusions.


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