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].

Idarubicin demonstrates superior cytotoxicity compared to daunorubicin and doxorubicin across various in vitro models, attributed to its enhanced capability to induce topoisomerase II-mediated DNA breaks [2]. Its IC 50 values of 3.3 ± 0.4 ng/mL for MCF-7 monolayers and 7.9 ± 1.1 ng/mL for multicellular spheroids [1] indicate significant effectiveness. Furthermore, idarubicin is approximately 57.5 times and 25 times more active than doxorubicin and epirubicin, respectively [3]. It also shows a concentration-dependent diminution on MCF-7 cell growth, with an observed IC 50 around 0.01 μM, alongside a concentration-dependent inhibition of DNA synthesis and a time- and concentration-dependent dampening of c-myc expression [4].