This study investigates the cytotoxic effects and mechanisms of pitavastatin on triple-negative breast cancer (TNBC) cells. Pitavastatin, a lipophilic statin, was found to significantly reduce the viability of TNBC cell lines, particularly MDA-MB-231. Pitavastatin induced cell cycle arrest, cell death, and oxidative stress in MDA-MB-231 cells, leading to ferroptosis, a form of iron-dependent cell death. The ferroptotic effect was further confirmed by the reversal of these changes using the iron chelator desferrioxamine (DFO). The study also revealed that pitavastatin-induced ferroptosis was autophagy-dependent and mediated through the mevalonate pathway. In vivo experiments in a TNBC xenograft mouse model showed that therapeutic doses of pitavastatin inhibited tumor growth without significant side effects. These findings suggest that pitavastatin could be a potential adjuvant treatment for TNBC patients, highlighting the potential of ferroptosis as a therapeutic target in this context.This study investigates the cytotoxic effects and mechanisms of pitavastatin on triple-negative breast cancer (TNBC) cells. Pitavastatin, a lipophilic statin, was found to significantly reduce the viability of TNBC cell lines, particularly MDA-MB-231. Pitavastatin induced cell cycle arrest, cell death, and oxidative stress in MDA-MB-231 cells, leading to ferroptosis, a form of iron-dependent cell death. The ferroptotic effect was further confirmed by the reversal of these changes using the iron chelator desferrioxamine (DFO). The study also revealed that pitavastatin-induced ferroptosis was autophagy-dependent and mediated through the mevalonate pathway. In vivo experiments in a TNBC xenograft mouse model showed that therapeutic doses of pitavastatin inhibited tumor growth without significant side effects. These findings suggest that pitavastatin could be a potential adjuvant treatment for TNBC patients, highlighting the potential of ferroptosis as a therapeutic target in this context.