Tyrosine kinase inhibitors (TKIs) have contributed to the improvement of the survival of patients with chronic myelogenous leukemia (CML). Growing evidence suggest that cancer therapy-related cardiac dysfunction has become important as the most undesirable side effects of chemotherapy. BCR-ABL TKIs, such as nilotinib and imatinib, has been reported to have a risk of QT prolongation associated with Torsades des Pointes and cardiac failure. We have previously reported that nilotinib caused QT prolongation and early afterdepolarization (EAD) using human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs). However, chronic cardiotoxicity of BCR-ABL TKIs has not been fully understood. In this study, we evaluated the chronic toxicity of imatinib and nilotinib using hiPSC-CMs. We used iCell Cardiomyocyte 2.0 (Cellular Dynamics International). To assess whether imatinib and nilotinib induced chronic cardiotoxicity, we investigated the QT interval recorded by multi-electrode array system (MED64, Alpha MED Scientific) and contractility velocity recorded by motion vector analysis (SI8000, Sony). We found that the imatinib decreased contraction velocity for long-term treatment. In addition, long-term treatment with nilotinib caused QT prolongation and decrease in contraction velocity in a concentration-dependent manner. These results suggest that hiPSC-CMs can be the useful tool for chronic cardiotoxicity assessment. We are planning to evaluate other types of BCR-ABL TKIs with hiPSC-CMs.