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As an undergraduate researcher at the Ohio State College of Pharmacy, I contributed to the Experimental Cancer Pharmacology Lab under Dr. Alex Sparreboom’s leadership. The primary focus of my undergraduate work was the evaluation of strategies to mitigate the cardiotoxic effects of Doxorubicin (DOX), a widely used anthracycline chemotherapy drug. DOX is used to treat various cancers, including soft tissue and bone sarcomas, breast cancer, acute leukemias, and Hodgkin lymphoma. While effective, DOX administration results in severe cardiotoxicity, with risks escalating significantly with cumulative exposure beyond ~450 mg/m² of body surface area. Symptoms range from mild cardiac dysfunction to life-threatening congestive heart failure, which is an enormous problem in clinical practice. Mechanisms of DOX-induced cardiotoxicity include mitochondrial damage, reactive oxygen species (ROS) generation, DNA breaks, and topoisomerase IIβ inhibition—all reliant on intracellular DOX accumulation in cardiomyocytes. Previous research in our lab identified Organic Cation Transporter 3 (OCT3) as a critical mediator of DOX-induced heart injury. The full disruption of OCT3 function in mice led to complete protection from cardiotoxicity. So, this research aimed to develop an OCT3 inhibition strategy to address the debilitating cardiotoxicity associated with DOX. Our goals were to 1) identify OCT3 inhibitors to use with DOX, preventing cardiac accumulation and thus cardiotoxicity, and 2) to investigate the link between unidentified OCT3 substrates and their contribution to cardiotoxicity.