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Concurrent synthetic lethality. Schematic depicting the concept of concurrent synthetic lethality. NRF2 target genes are able to bioactivate both mitomycin C, to generate the potent DNA-damaging agent MMC*, and 17-AAG, to generate the proteotoxic stress-inducing HSP90 inhibitor 17-AAGH2. The parallel NRF2-dependent metabolism of prodrugs which target distinct cell death pathways increases the specificity and toxicity toward tumor cells with aberrant KEAP1-NRF2 pathway activation.
