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This exchange is crucial for the formation and maintenance of autophagosomes, which are responsible for sequestering and degrading selective cargo during autophagy [134, 135]

or an N-oxide, crystalline form, hydrate, or pharmaceutically acceptable salt thereof, with the proviso that: when R 3 is ethyl, R 1 and R 2 cannot be both H, O, or when R 3 is ethyl and at least one of R 1 or R 2 is H, R 1 or R 2 cannot be In one aspect of this embodiment, the compound has the structure of formula (II): R 3 is independently selected from the group consisting of H, C 1-12 aliphatic, C 1-6 -alkyl-aryl and C 1-6 -alkyl-heteroaryl

USA 116 , 609618 (2019)

1 Introduction Stroke remains the second-leading cause of death and disability worldwide, with ischemic stroke accounting for approximately 80% of cases ( First described in 2012, ferroptosis is characterized by mitochondrial cristae shrinkage, glutathione peroxidase 4 (GPX4) inactivation, and lethal lipid peroxide accumulation through iron-dependent Fenton reactions ( Emerging evidence identifies ferroptosis as a maladaptive response in stroke, with its unchecked activation exacerbating infarct volume expansion and worsening functional outcomes ( 2 Mechanisms of ferroptosis Ferroptosis is a distinct form of regulated cell death characterized by the accumulation of lipid peroxides to lethal levels ( The hallmark of ferroptosis lies in the peroxidation of polyunsaturated fatty acids within cellular membranes, driven by an imbalance between ROS and the cells antioxidant defense systems (Figure 1)