No abstract

When given orally to animals ibufenac has a range of potencies 2 to 4 times that of aspirin. It also suppresses thurfyl nicotinate erythema in man. Like certain other analgesic-anti-inflammatory-antipyretic drugs, when administered intravenously it suppresses bradykinin-induced bronchoconstriction in the guinea-pig. It has no glucocorticoid activity. Ibufenac, a compound chemically unrelated to existing antirheumatic drugs, can thus be classified as a non-steroidal anti-inflammatory (antirheumatic) agent.BUFENAC (4-isobutylphenylacetic acid) is a non-steroidal anti-inflam-

No abstract

No abstract

The effects of sodium salicylate and of aspirin on the actions of pancreatic, salivary and serum kallikreins have been investigated. Kinin production by the three enzymes was assessed using a guinea-pig isolated ileum preparation. The esterolytic activity of pancreatic and salivary kallikreins was measured by determining acid release from the synthetic substrate toluene-p-sulphonyl-L-arginine methyl ester. Sodium salicylate (up to 20 mM) or aspirin (up to 5 mM) failed to inhibit kinin production by each of the three enzymes. With salivary kallikrein, a concentration of 50 mm of sodium salicylate was required to produce a 50% inhibition of kinin production. No significant inhibition of esterolytic activity was produced by concentrations up to 5 mm of either sodium salicylate or aspirin. Prior incubation of sodium salcylate or aspirin with the enzymes also resulted in no significant effect of either drug on kinin production or esterolytic activity. Prior incubation of pancreatic or salivary kallikrein with the inhibitor from ox parotid gland (Trasylol) reduced both kinin production and esterolytic activity. Toluene-p-sulphonyl-L-arginine methyl ester (0.5 mM) inhibited kinin production by each of the three enzymes. It is concluded that sodium salicylate and aspirin are poor inhibitors of kallikrein activity in vitro.