Cardiotoxicity is a growing concern after completion of successful cancer therapies. Research for mechanisms and potential prophylactic options is hampered by the lack of representative 3D multicellular in vitro models. Here, we combined hiPSC-derived cardiac phenotypes (cardiomyocytes and cardiac fibroblasts) embedded in fibrin hydrogels with 3D-PCL scaffolds printed by melt-electrowriting to generate 2 models of anthracycline toxicity: single or repeated exposure to doxorubicin (doxo). To mimic different exposure regimens, minitissues were exposed to 0, 250 or 2500 nM doxo 7 days after generation. In the single exposure group, doxorubicin was added once, whereas in the repeated exposure, it was provided for 7 consecutive days. Functionality (beating rate), structure and gene expression were analysed for up to 1 week. Our results showed that single or repeated exposition to 2500nM doxo abrogated functionality as beating ceased. Similarly, single exposure to 250nM doxo significantly decreased beating rate from day 3, curiously not significant after repeated exposition. The structure of CMs was altered in both models, with most sarcomeres absent or disarranged by doxo treatment, particularly at 2500nM. At gene expression level, repeated addition of both doses of doxo for 7 days caused a marked reduction of all genes screened, likely caused by the large cell death present. Results support that MEW-based human bioengineered myocardium is a promising model for doxo-induced cardiotoxicity and a notable alternative to the use of animals for early screening of cardioprotective drugs.