Equipotent inhibition by R(−)−, S(+)- and racemic ibuprofen of human polymorphonuclear cell function in vitro.
Article first published online: 5 JUL 2012
1993 The British Pharmacological Society
British Journal of Clinical Pharmacology
Volume 35, Issue 3, pages 235–242, March 1993
How to Cite
Villanueva, M., Heckenberger, R., Strobach, H., Palmer, M. and Schror, K. (1993), Equipotent inhibition by R(−)−, S(+)- and racemic ibuprofen of human polymorphonuclear cell function in vitro. British Journal of Clinical Pharmacology, 35: 235–242. doi: 10.1111/j.1365-2125.1993.tb05690.x
- Issue published online: 5 JUL 2012
- Article first published online: 5 JUL 2012
1. The effects of racemic (rac) ibuprofen and its S(+)- and R(−)− enantiomers on functions of human polymorphonuclear cells (PMN) and platelets were studied in vitro. 2. Rac-ibuprofen inhibited PMN functions (O2- generation, beta-glucuronidase release, LTB4 formation). Similar IC50 values (40-100 microM) were obtained for the S(+)- and R(- )-enantiomers. 3. All forms of ibuprofen inhibited cyclooxygenase- related platelet functions (aggregation, thromboxane formation). The S(+)-enantiomer was about twice as active as the racemate while the R(- )-enantiomer was at least 10-fold less active. This demonstrates that the S(+) is the only cyclooxygenase inhibitory component of the racemate. 4. The concentrations of rac-ibuprofen in PMN and platelets were similar to those in the incubation medium and represented equal concentrations of the enantiomers. This indicates that neither interconversion nor tissue accumulation of the compounds occurred. 5. These data indicate that antineutrophil effects of ibuprofen on human PMN are independent of cyclooxygenase inhibition. Therefore, R(−)− ibuprofen may be superior to the S(+)-isomer for the treatment of PMN- dependent inflammatory diseases. However, effective free drug concentrations may not be obtained in vivo.