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Taken together, these findings suggest that APR-246 could induce tumor cell death through both reactivation of mutant p53 and inhibition of cellular thiol-dependent redox system proteins (GPX4, TXNDR1, GRX1), providing novel combinatorial strategies for AML therapy
21 Oral administration may be beneficial for patients with preclinical toxic effects or hepatic injury, although the presence of altered mental status and vomiting may limit its use
NQO1 has been demonstrated to impede the generation of ROS by diminishing quinones (Talebi et al
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