Suprofen (Suprol) is an IBUPROFEN-type anti-inflammatory analgesic and antipyretic. It inhibits prostaglandin synthesis and has been proposed as an anti-arthritic.

Suprofen inactivates the diclofenac-4-hydroxylase activity of baculovirus-expressed P450 2C9 in a time- and concentration-dependent manner, which is consistent with mechanism-based inactivation. [1] Suprofen is a known generator of singlet oxygen whose participation in the reaction is supported by the effects of quenchers and scavengers. Suprofen photosensitizes the production of alkali-labile cleavage sites in DNA much more efficiently than direct strand breaks. [2] Suprofen sensitizes photo-oxidation of cholesterol, producing 7 alpha- and 7 beta-hydroperoxides but not 5 alpha-hydroperoxide of cholesterol. Suprofen-sensitized photo-oxidation of membrane lipids of liposomes increases leakage of trapped glucose, suggesting photosensitized destabilization of the membrane structure. [3] Suprofen incorporation in the phosphatidylcholine (PC) evaporation vesicles (REV) membrane leads to approximately 5% increase in the encapsulation efficiency (34%) in comparison to standard REV (29%). [4]

Suprofen combined with PGF2 alpha blocks induction of uterine contractions, suggesting the possibility that Suprofen also antagonizes PGF2 alpha receptor binding. [5] Suprofen are effective at preventing BAB disruption after paracentesis in dogs, indicating their potential usefulness for treatment of prostaglandin-mediated ocular disease. [6] Suprofen (3.7 mg/kg, i.v.) induces a marked decrease in the firing evoked in arthritic rats by ankle mobilization. [7]