Daunorubicins/Doxorubicins

Daunorubicin and doxorubicin are anthracycline anticancer drugs that act through DNA intercalation, topoisomerase II inhibition, DNA double-strand breaks, RNA synthesis inhibition, free-radical production, and apoptosis^[1][2]. Mechanistically, anthracyclines also promote histone eviction from open chromatin, attenuate DNA repair through H2AX eviction, deregulate transcription, and affect cancer cells and heart tissue^[3]. In disease and experimental models, these agents remain relevant for solid tumors, blood cancers, acute myeloid leukemia blasts, HL-60 leukemia cells, cardiomyocytes, and anthracycline-induced cardiotoxicity studies^[2][3][4]. Compared with related topoisomerase II isoforms, TOP2α and TOP2β both serve as drug targets, but TOP2β is identified as a plausible cardiomyocyte target and a major intracellular mediator of doxorubicin-induced cardiotoxicity^[5][6]. For experimental applications, liposomal doxorubicin lowers clinical heart failure versus conventional doxorubicin in adult solid tumors, while dexrazoxane and other catalytic TOP2 inhibitors protect cardiomyocytes without compromising anthracycline antiproliferative effects in HL-60 cells^[4][7].