Bramm E, Binderup L, Arrigoni-Martelli E
Agents Actions. 1981 Jul;11(4):402-9. doi: 10.1007/BF01982478.
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.
替美加定(SR 1368,N-环己基-N"-4-(2-甲基喹啉基)-N'-2-噻唑基胍)能剂量依赖性地抑制角叉菜胶、制霉菌素和刀豆球蛋白A诱导的水肿。在佐剂性关节炎大鼠中的详细研究表明:(a) 替美加定的长期给药方案可抑制原发性和继发性病变、白细胞增多症和高纤维蛋白原血症,(b) 替美加定在减轻已确诊疾病的严重程度方面具有显著活性,(c) 在注射佐剂时短期给予替美加定可永久性地预防继发性病变的发展。在佐剂性关节炎大鼠和正常大鼠中,替美加定都增强了结核菌素超敏反应。替美加定对大鼠和豚鼠的实验性过敏性脑脊髓炎没有影响。结论是,替美加定具有与已知抗炎药不同的作用特点和活性。