The interaction of tilorone and RMI 9563DA with the complement system.
RMI 9563DA inhibited the classical complement pathway in rat serum in vitro with an 150 of 51 micrograms/ml in diluted serum and 750 micrograms/ml in undiluted serum. Tilorone was much less active than RMI 9563DA in diluted serum and was inactive in undiluted serum. No complement inhibition could be detected in vivo following a near lethal dose of RMI 9563DA (25 mg/kg i.v.). Thus, complement inhibition is not the mechanism by which these compounds exert their anti-inflammatory activity. Both compounds increase serum hemolytic complement activity 24 h after administration to rats. With RMI 9563DA, this effect is entirely due to the local irritancy produced by s.c. administration of the compound. Tilorone, however, has a specific effect on complement synthesis which may be related to its ability to induce interferon.
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002570:Ceruloplasmin / Q000097:blood; D003171:Complement Pathway, Classical / Q000187:drug effects; D003165:Complement System Proteins / Q000096:biosynthesis*; D005449:Fluorenes / Q000494:pharmacology*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D013994:Tilorone / Q000494:pharmacology*
D000893:Anti-Inflammatory Agents; D005449:Fluorenes; C016919:RMI 9563; D003165:Complement System Proteins; D002570:Ceruloplasmin; D013994:Tilorone