Abstract
Timegadine (SR 1368, N-cyclohexyl-N"-4-(2-methylguinolyl)-N'-2-thiazolylguanidine) dose-dependently inhibited carrageenan-, nystatin-, and concanavalin A-induced edema. Detailed studies in adjuvant arthritic rats showed: (a) long dosing regimen with timegadine inhibited primary and secondary lesions, leukocytosis and hyperfibrinogemia, (b) timegadine was significantly active in reducing the severity of the already established disease, (c) a short course of dosing with timegadine at the time of adjuvant injection permanently prevented the development of secondary lesions. The tuberculin hypersensitivity reaction was enhanced by timegadine in both adjuvant arthritic and normal rats. Experimental allergic encephalomyelitis in rats and guinea pigs was not affected. It is concluded that timegadine has a profile or activity which differs from that of known anti-inflammatory drugs.
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