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By using a reducible disulfide linker, we built in a redox-sensitive release mechanism to facilitate intracellular release of the unmodified NMDA receptor antagonist, enabling the combined cellular actions of GLP-1 receptor agonism and NMDA receptor antagonism

These observations are corroborated at the molecular level, with dysregulation in the expression of pro-proliferative proteins (e.g., cyclin D1) and tight junction proteins (e.g., zonula occludens-1, occludin, and claudin 1, 4, and 8) (Peskar et al., 2023)

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