Molecular Weight(MW): 298.36
Zaltoprofen is an inhibitor of COX-1 and COX-2 for treatment of arthritis.
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Choose Selective COX Inhibitors
|Description||Zaltoprofen is an inhibitor of COX-1 and COX-2 for treatment of arthritis.|
Zaltoprofen binds to specific sites on the protein of the bradykinin B2 receptor, hence we have examined the effect of zaltoprofen on bradykinin-induced responses of adult DRG neurons to investigate possible interaction sites. Zaltoprofen most potently inhibits bradykinin-enhancement of capsaicin-induced Ca2+ uptake into DRG neurons. Zaltoprofen also significantly inhibits bradykinin-induced 12-lipoxygenase (12-LOX) activity and the slow bradykinin-induced onset of substance P release from DRG neurons.  Zaltoprofen produces an analgesic action on bradykinin-induced nociceptive responses by blocking the B(2) receptor-mediated pathway in the primary sensory neurons. Zaltoprofen completely inhibits the bradykinin-induced increase of [Ca(2+)](i), which is inhibited by B(2) antagonist D-Arg-[Hyp(3), Thi(5,8), D-Phe(7)]-bradykinin, but not by B(1) antagonist.  Zaltoprofen at 1nmol shows strong analgesic action on BK (i.pl.)-induced nociceptive flexor responses, whereas loxoprofen or its active metabolite loxoprofen-SRS does not. Zaltoprofen also inhibits the nociception induced by [Tyr8]-BK, a specific agonist of B2-type BK receptor, but does not affect the nociception by [Lys-des-Arg9]-BK, a specific agonist of B1-type BK receptor.  Zaltoprofen is a non-steroidal anti-inflammatory drug (NSAID) causes potent inhibition of cyclooxygenase-2 with fewer side effects on the gastrointestinal tract.
|In vivo||Zaltoprofen improves the loss in body weight in both Con A-treated mice and carbon tetrachloride-treated rats.  Zaltoprofen (10 mg/kg) administrated at 8 h after Con A treatment is found to inhibit the Con A-induced reduction in body weight. Zaltoprofen (10 mg/kg) combined with Con A results in four times greater food intake than that in mice treated with only Con A. |
-  Tang HB, et al. Neuropharmacology, 2005, 48(7), 1035-1042.
-  Hirate K, et al. Neurosci Res, 2006, 54(4), 288-294.
-  Matsumoto M, et al. Neurosci Lett, 2006, 397(3), 249-253.
|In vitro||DMSO||60 mg/mL (201.09 mM)|
|Ethanol||31 mg/mL (103.9 mM)|
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT01369238||Unknown status||Whiplash Injuries||Korean Pharmacoacupuncture Institute||June 2011||Not Applicable|
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