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Aim: Imatinib mesylate is a tyrosine kinase inhibitor and is approved as a standard first-line therapy of chronic myeloid leukemia. Oxidative stress, as well as intracellular calcium overload and mitochondrial dysfunction, play an important role in chemotherapy-induced cardiotoxicity. The underlying pathophysiological mechanism associated with imatinib-induced cardiotoxicity is not well understood. In the present study, we investigated alterations in calcium influx, oxidative stress and apoptosis through transient receptor potential melastatin 2 (TRPM2) channels. Also, we aimed to investigate if there is a modulator role of astaxanthin in cardiomyocytes during imatinib mesylate-induced cardiotoxicity. Materials and methods: The cells were divided into seven main control groups: imatinib, imatinib+antranilic acid, imatinib+astaxanthin, imatinib+antranilic acid+astaxanthin, astaxanthin and astaxanthin+antranilic acid groups. Cells in the groups were stimulated with cumene hydroperoxide and inhibited with antranilic acid in related experiments for activation and inactivation of TRPM2 channels, respectively. We measured cytosolic calcium, intracellular reactive oxygene, mitochondrial depolarization, caspase 3 and caspase 9 levels.Results: The apoptosis values were significantly lower in the astaxanthin and the imatinib+astaxanthin group than in the imatinib group of cardiomyocytes (p< 0.001). The cell viability values were significantly higher in the imatinib+astaxanthin+antranilic acid (p