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Accumulated safety data must now support a favorable benefitrisk assessment

Molecular docking models show that disruption of the A6A11 disulfide bond misaligns key receptor-binding residues (ValA3, TyrA19), reducing IR affinity by ~60%, impairing IRS phosphorylation, PI3K-Akt signaling, and GLUT4 translocation, while allowing unchecked hepatic glucose production and driving hyperglycemia (Figure 2) [5355]

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Released DAMPs engage PRRs such as TLRs, NOD-like receptors (NLRs), and the STING (stimulator of interferon genes) pathway in innate immune cells