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5-Iminodaunorubicin is a quinone-modified anthracycline that retains antitumor activity[1]. 5-Iminodaunorubicin produces protein-concealed DNA strand breaks in cancer cells[2].

In mouse leukemia L1210 cells, 5-Iminodaunorubicin produces protein-concealed DNA strand breaks. Many of the 5-iminodaunorubicin breaks may arise from apposed single-strand breaks (i.e., double-strand breaks)[2].

In rat, 5-Iminodaunorubicin (5-ID; 1-16 mg/kg) treatment produces widening of the QRS complex, increased R- and S-wave voltage, and prolonged the Q alpha T interval. And the quinone redox cycling is suppressed in 5-Iminodaunorubicin. 5-Iminodaunorubicin shows lower cardiotoxic[1].

[1]. R A Jensen, et al. Electrocardiographic and transmembrane potential effects of 5-iminodaunorubicin in the rat. Cancer Res. 1984 Sep;44(9):4030-9.

[2]. L A Zwelling, et al. Cytotoxicity and DNA strand breaks by 5-iminodaunorubicin in mouse leukemia L1210 cells: comparison with adriamycin and 4’-(9-acridinylamino)methanesulfon-m-anisidide. Cancer Res. 1982 Jul;42(7):2687-91..

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