• A GSH-triggered prodrug targeting tumor cell mitochondria via OATP-mediated uptake. • Release of a parent drug through an GSH-triggered S N Ar mechanism. • Translation of a nicotinic acetylcholine receptor to an antitumor drug. • Anabasine in mitochondria and induce a synergistic ferritinophagy and apoptosis.
Zhang et al. (Thu,) studied this question.