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Enantiomers of the anti-inflammatory drugs naproxen, ibuprofen, and flurbiprofen inhibit different functions of cyclooxygenase-2 (COX-2), a key enzyme in biological lipid signaling, a study reports (Nat. Chem. Biol., DOI: 10.1038/nchembio.663). COX-2 normally oxygenates arachidonic acid in a pathway that results in pain and inflammation. The enzyme also oxygenates endocannabinoids, turning off their pain-relieving effects. The clinical activity of arylpropionic acid drugs such as naproxen and the profens involves inhibition of COX-2 arachidonic acid oxygenation by the S enantiomers, shutting down that pain and inflammation path. Vanderbilt University’s Lawrence J. Marnett and colleagues have now found that the R enantiomers inhibit endocannabinoid oxygenation, preserving those compounds’ pain-relieving effects. The finding may point to new possibilities for treating pain, Marnett says. For example, unlike other nonsteroidal anti-inflammatory drugs, (R)-flurbiprofen is inefficiently converted to the S enantiomer in vivo and does not show common gastrointestinal side effects.
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