Ferroptosis as a Therapeutic Target: Advances in Drug Development for Cancer and Neurodegenerative Diseases

Background: Ferroptosis is an iron-dependent, regulated form of cell death characterized by lipid peroxidation and oxidative stress, distinct from apoptosis and necrosis. It has emerged as a key therapeutic target in cancer and neurodegenerative diseases due to its dual role in promoting or preventing cell death. Ferroptosis inducers can eliminate drug-resistant cancer cells, while inhibitors may protect neurons in conditions like Alzheimer’s and Parkinson’s disease. Understanding its molecular mechanisms and pharmacological modulation offers new therapeutic possibilities. This review focuses on the pharmacological modulation of ferroptosis, its therapeutic potential in cancer and neurodegeneration, and the associated challenges in clinical translation. Materials and Methods: A narrative literature search was conducted in PubMed, Scopus, and Web of Science for articles published between 2015 and 2024 using the keywords ferroptosis, cancer therapy, lipid peroxidation, and neurodegeneration. Relevant preclinical and clinical studies were included. Results: Ferroptosis inducers like Erastin, RSL3, Sorafenib, and FIN56 sensitize cancer cells by inhibiting glutathione metabolism. Inhibitors Ferrostatin-1 and Liproxstatin-1 are neuroprotective. Though specificity, toxicity, and delivery issues persist, clinical trials attest to their promise. Conclusion: Ferroptosis is a novel oncology and neurology drug target. Future trials must address biomarkers, delivery systems, and their interaction with apoptosis and autophagy for the best treatment strategy.