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The resulting ORL@Cu-MOF simultaneously triggered cuproptosis and blocked lipid reprogramming, which markedly suppressed primary OSCC growth and cervical lymph-node metastasis while remodeling the immune milieu via up-regulation of PD-1

The more relevant research question is whether triple receptor agonism (GIP + GLP-1 + glucagon) combining elements of both approaches could outperform either dual agonist

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