Piroxicam, a structurally novel anti-inflammatory compound. Mode of prostaglandin synthesis inhibition

Protection against Experimental Allergic Encephalomyelitis with Complete Freund’s Adjuvant Is Unaffected by Prostaglandin Synthesis Inhibition

“…As an inhibitor piroxicam was used because of its extended plasma half life [22] and its low toxicity [23]. In cell culture half-maximal inhi bition of PGE2 production occurred in the presence of arachidonic acid at a piroxicam concentration of 0.5 pM [4], Though in our studies serum piroxicam lev els exceeded this value nearly 200-fold, this treatment was ineffective in restoring responsiveness to EAE in ALU-CFA-pretreated animals. Neither severe clinical nor histological signs of EAE could be detected in these animals.…”

Comparative Effects of Piroxicam and Esculetin on Incidence, Proliferation, and Cell Kinetics of Mammary Carcinomas Induced by 7,12-Dimethylbenz[a]anthracene in Rats on High- and Low-Fat Diets

“…Indomethacin is primarily an inhibitor of the cyclooxygenase involved in prostaglandin synthesis, but at higher concentrations it also inhibits phospholipase A2 [47] and 5-lipoxygenase, which are required for leukotriene synthesis [48], There fore, it would be of interest to determine whether specific changes in the overall cascade are directly associated with alterations in mammary carcinogenesis. Although piroxicam inhibits prostaglandin synthesis less effectively than indomethacin, it exerts its effect at the cyclooxygenase step of prostaglandin synthesis [49], not at the 5-lipoxy genase pathway [20,21], Ross et al [50] reported that piroxicam, the doses of 4 mg/kg twice weekly, inhibited the growth of transplanted DMH-F317 tumors in rats, but that higher doses of this agent were less effective in inhib iting tumor growth or causing tumor regression, whereas Reddy et al [51] have reported that increasing levels of piroxicam in the diet inhibited azoxymethane-induced colon carcinogenesis in male F344 rats in a dose-depen dent manner. The lack of correlation may have contrib uted to different model systems.…”

In vivo platelet aggregation in the rat: dependence on extracellular divalent cation and inhibition by nonsteroidal anti‐inflammatory drugs

“…Therefore, some of the inhibitory effect of indomethacin may be due to actions other than cyclo-oxygenase inhibition. Piroxicam is a specific cyclo-oxygenase inhibitor (Carty, Stevens, Lombardino, Parry & Randall, 1980) and was ten times more active than indomethacin. At the maximum tolerated doses piroxicam and indomethacin became less effective.…”