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Drugs that reduce the proliferation of fast-cycling cells might be less effective in migrating cells, which often rely on OXPHOS and hence are not as dependent on de novo synthesis pathways and DNA replication

whether these radical-trapping antioxidant pathways compensate for GPX4 downregulation in affected kidneys or if their dysfunction exacerbates ferroptosis susceptibility remains unknown, limiting multi-targeted therapeutic design

This is its best-validated and most legitimate application, spanning bioprocessing and stem-cell research, and it is the reason the analog was engineered in the first place

Unfortunately, with about 3,100 known causative mutations in over 50 different genes, each gene target would require a unique treatment [4]