Zaltoprofen (Soleton) is a Cox-1 and Cox-2 inhibitor, which is used for the treatment of arthritis.

Zaltoprofe is a non-steroidal anti-inflammatory drug (NSAID) that effectively inhibits cyclooxygenase-2 with minimal side effects on the gastrointestinal tract. Zaltoprofe binds to a specific site of the bradykinin B2 receptor protein, therefore, the effect of Zaltoprofen on the bradykinin-evoked response of adult DRG neurons can be investigated to investigate possible interaction sites. Zaltoprofen is the most effective inhibitor of bradykinin enhancing capsaicin-induced Ca2+ uptake into DRG neurons. Zaltoprofen also significantly inhibits bradykinin-induced 12-lipoxygenase (12-LOX) activity and slow bradykinin-induced release of the substance P from DRG neurons. Zaltoprofe showed a potent analgesic effect on BK (i.pl.)-induced hyperalgesia at 1 nmol, whereas loxoprofen or its active metabolite loxoprofen-SRS did not. Zaltoprofe also inhibits [Tyr8]-BK-induced nociception in that it is a type B2 receptor specific agonist; but does not affect the nociception induced by [lysine-DES-Arg9]-BK, which is type B1 BK receptor specific agonist. In primary sensory neurons, Zaltoprofe produces an analgesic effect of a bradykinin-induced nociceptive response by blocking the B(2) receptor-mediated pathway. Zaltoprofe completely inhibits Ca2+ increase induced by bradykinin, which is inhibited by the B(2) antagonist D-Arg-[Hyp(3), Thi(5,8), D-Phe(7)]-bradykinin, but not B(1) Antagonist.

After 8 hours of ConA treatment, mice were administrated of Zaltoprofen(10 mg/kg) resulting in inhibition of ConA-induced body weight loss. The combination of 10 mg/kg Zaltoprofen and ConA resulted in a 4-fold increase in food intake in mice compared to ConA only. Therefore, Zaltoprofen increased weight loss in ConA-treated mice.