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Since the discovery of a cytokine-inducible isozyme of cyclooxygenase (COX-2), its pharmacologic inhibition has been the subject of recent investigations. These include tests for the selectivity of known nonsteroidal antiinflammatory drugs (NSAIDs) on the constitutive enzyme of cyclooxygenase (COX-1) compared with the inducible enzyme COX-2. The interesting question arose whether the R(-)- and S(+)-isomers exhibited different inhibitory potencies for ibuprofen. Results with isolated COX-1 and COX-2 isozymes confirmed the known higher efficacy of S(+)- compared with R(-)-ibuprofen. The R(-)-isomer is almost inactive in inhibiting COX-2. In addition, the S(+) form has a several times lower potency with COX-2 than with COX-1. These data were evaluated in platelets containing mainly the constitutive COX-1, with interleukin-1, pretreated, rat mesangial cells which almost exclusively express COX-2.