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Redox homeostasis genes modulate response to APR-246 in a p53-dependent and p53-independent manner Previous studies have characterized APR-246 as a modulator of redox homeostasis and inducer of ROS through depletion of key antioxidants, resulting in both p53-dependent and -independent cell death pathways such as ferroptosis [26,27,28,29]

pre-existent induction of CYP2E1) to develop APAP-induced liver injuries

At the end of the trial, it was determined that treatment with exenatide led to a moderate reduction in BMI and improvement in glucose tolerance and cholesterol

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