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Effects of oxaprozin and of other 2-arylpropionic acid derivatives on nuclear factor κB(NF-κB) activation

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image of Inflammopharmacology

The translocation to the nucleus and the binding of NF-κB to DNA is thought to play a fundamental role in the activation of immune and inflammatory cells in order to activate the genes that in turn produce cytokines. We evaluated the ability of some 2-arylpropionic acid derivatives (fenoprofen, flurbiprofen, ketoprofen, S- and R-isomers of ibuprofen, ibuprofen, naproxen, and oxaprozin) to affect NF-κB binding to DNA in human peripheral mononuclear cells. We observed NF-κB inhibition by oxaprozin (IC50 = 50 μM), ibuprofen (185 μM) and S-ibuprofen (51 μM). Since oxaprozin reaches higher concentrations in synovial tissues and fluid (4—5 times higher than in plasma, i.e. around 100 μM) its inhibitory activity is clinically relevant. The inhibitory activity observed with all other tested drugs was outside their clinically relevant concentrations. At the concentrations observed to affect the NF-κB binding, oxaprozin and ibuprofen also inhibited the release of TNF-α and interleukin 1β in cells stimulated by Escherichia coli lipolysaccharide. By administering oxaprozin or ibuprofen at high dosage it should be possible to inhibit NF-κB DNA binding in humans in vivo.


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