Idarubicin, a potent anthracycline antileukemic agent, is orally active in its application. It functions by inhibiting topoisomerase II, thus interfering with DNA replication and RNA transcription. Furthermore, Idarubicin induces DNA damage, inhibits DNA synthesis, and suppresses c-myc expression. It also demonstrates inhibitory effects on the growth of bacteria and yeasts [1] [2] [3] [4] [5].

The IC 50 of idarubicin is 3.3 ± 0.4 ng/mL on MCF-7 monolayers and 7.9 ± 1.1 ng/mL in multicellular spheroids [1]. Idarubicin exhibits a greater cytotoxicity than daunorubicin or doxorubicin in various in vitro systems. This has been attributed to a better ability of idarubicin to induce the formation of topoisomerase II -mediated DNA breaks [2]. Idarubicin is about 57.5-fold and 25-fold more active than doxorubicin and epirubicin, respectively [3]. Idarubicin produces a concentration-dependent reduction in MCF-7 cell growth, with an IC 50 of approximately 0.01 μM. Idarubicin produces a concentration-dependent inhibition of DNA synthesis and a time- and concentration-dependent suppression of c-myc expression [4].