Ibuprofen is a non-steroidal anti-inflammatory drug with diverse biochemical actions, most notably inhibiting COX-1 and COX-2 (IC
50s = 2.6 and 1.53, μM, respectively).
1 It is commonly synthesized as a racemic mixture of (S)- and (R)-isomers. (S)-Ibuprofen is an enantiomer that more potently inhibits COX activity, thromboxane formation, and platelet aggregation than the (R)-form.
2,3 (S)-Ibuprofen also inhibits activation of NF-κB more effectively than (R)-ibuprofen (IC
50s = 62 and 122 μM, respectively).
4 However, the enantiomers are equipotent in blocking superoxide formation, β-glucuronidase release, and LTB
4 generation by stimulated neutrophils (IC
50 values range from 0.14 to 0.58 μM).
3 A majority of (R)-ibuprofen can be inverted to (S)-ibuprofen in humans after oral administration.
5,6,7