Doxorubicin is an effective anticancer drug, but its clinical use is limited by cardiotoxicity caused by oxidative stress, mitochondrial dysfunction, and apoptosis in cardiomyocytes. Hydrogen sulfide (H₂S) has been identified as a potential cardioprotective molecule due to its antioxidant and cytoprotective properties. This study investigated the effects of EV-34, a fast-releasing H₂S donor, in a doxorubicin-induced cardiotoxicity model using H9c2 cells. EV-34 increased intracellular H₂S levels, improved cell viability, and reduced mitochondrial oxidative stress in doxorubicin-treated cells. It also enhanced AMPK activation, while its effect on apoptosis-related proteins was not statistically significant. Overall, EV-34 demonstrates potential cardioprotective effects in vitro; however, further in vivo studies are required to confirm its therapeutic relevance.