The antitumor antibiotic, anthramycin methyl ether (AME), was shown to be active in increasing survival time in mice bearing various experimental leukemias. Like actinomycin D, it was active against P388 but inactive against P388/38280. AME also was active against the plasma cell tumor LCP, while having no activity against the plasma cell tumor YPC-1. AME had an ID50 of 0.02 µg/ml against L1210 cells in tissue culture.

The effects of AME were studied on other pharmacologic parameters. Hexobarbital sleeping times were doubled in mice receiving daily injections of AME for 4 days, while single injections at times varying from 30 minutes to 4 hours prior to hexobarbital had no effect on sleeping time. AME did not affect the blood pressure, respiration, or EKG in anesthetized dogs, nor did it alter the blood pressure responses to various autonomic stimulants.

AME markedly inhibited uptake of tritiated uridine in both L1210 and P388 leukemic cells in vivo. AME also interfered with uptake of tritiated thymidine by L1210 cells. Spectral studies indicated that the ultraviolet absorption maximum of AME was shifted to longer wave lengths following interaction with DNA, but deoxyguanosine had no effect on the absorption maximum of AME. The anthranilic acid moiety did not form complexes with DNA or deoxyguanosine nor did it have cytotoxic effects in tissue culture in doses up to 1000 times that of the ID50 for AME.


A preliminary report of this study was presented at the Federation of American Societies for Experimental Biology, Chicago, Illinois, 1967.

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