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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

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~0.01-0.7%(CMV-Hb) compared to the expected 0.2-15% (HbA1c)

The study found that this treatment could enhance the immune recognition function of CD8 + T cells and reduce the immune escape of tumor cells [110]