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Abstract VII- Summary & Conclusion Doxorubicin (DOX), is a highly effective chemotherapeutic agent which is used to treat various types of cancer, including hematological malignancies and other sarcomas. Although having a good therapeutic potential, its uses are limited due to cumulative cardiotoxicity. DOX-induced cardiotoxicity is characterized by decreased left ventricular ejection fraction, cardiomyopathy, and heart failure which can develop many years after successful DOX therapy. At present, dexrazoxane is the only FDA-approved drug available to protect against the cardiotoxic side effects of DOX. However, dexrazoxane has several side effects and can reduce the antitumor efficacy of DOX. Thus, there is an urgent need for the development of effective and safe alternative therapies that can be used to prevent DOX-induced cardiotoxicity. The exact molecular mechanism of DOX cardiotoxicity is not yet fully elucidated. However, there are multiple proposed theories to the pathophysiology of DOX-induced cardiotoxicity including oxidative stress, calcium overload, lipid peroxidation, and mitochondrial dysfunction.Topiramate (TPM) is an antiepileptic drug widely used as the firstline treatment for epilepsy. It inhibits voltage-gated calcium and sodium channels, enhances gamma-aminobutyric acid (GABA) and blocks glutamate alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA)/kainate receptors. Several studies indicated that TPM has antioxidant and anti-inflammatory activities, which suggest that TPM is a potential agent for the management of the disease states characterized by |