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Depending on cellular state and stress cues, TP53 can promote ferroptosis by repressing SLC7A11 to limit cystine uptake and GSH synthesis, inducing spermidine/spermine N1-acetyltransferase 1 ( SAT1 ) to enhance ROS generation through polyamine catabolism, and upregulating glutaminase 2 ( GLS2 ) to increase -ketoglutarate production and mitochondrial ROS 154-156

Treatment with an MC3R/MC4R antagonist completely abolished PT-141's cytotoxic effects, confirming receptor-specific activity

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