Traxanox was inactive against classic acute and subacute
inflammation models such as
carrageenin paw
edema, UV
erythema, 6-hr
Evans blue-
carrageenin (E-C)
pleurisy and cotton pellet
granuloma formation, and it failed to inhibit the production of
prostaglandin E2 and a
slow reacting substance from rat peritoneal leucocytes which phagocytize killed bacteria in vitro. On the other hand,
traxanox inhibited the
anaphylactoid reaction and decreased the pleural fluid in 24-hr E-C
pleurisy.
Traxanox (100 mg/kg, p.o.) also showed a tendency to suppress
dextran edema and cotton pellet
granuloma formation in
adjuvant arthritis (AA) in rats. In experimental models of delayed type
hypersensitivity (DTH),
traxanox (100 mg/kg, p.o.) inhibited the accumulation of the exudate and the leucocyte migration in B.
pertussis-induced
pleurisy in rats.
Traxanox (50 mg/kg) did not show any effect on AA in Lewis rats when administered orally for 21 days after the adjuvant inoculation, but the combined administration of
traxanox with
hydrocortisone (10 mg/kg, p.o.) or
indomethacin (0.25 mg/kg, p.o.) resulted in a synergistic inhibition of AA. When the administration of
traxanox was started 21 days before the adjuvant inoculation, it inhibited AA in a dose-dependent manner (50-100 mg/kg, p.o.). On the other hand,
traxanox (100 mg/kg, p.o.) enhanced the
concanavalin A-induced DTH-like skin reaction in guinea pigs. These results indicate that the mode of action of
traxanox on inflammatory responses resembles that of
D-penicillamine or
levamisole, so that it may prove to be clinically effective in treating
rheumatoid arthritis.