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The inference that a long-acting IGF-1R agonist should promote muscle growth is mechanistically reasonable given the established role of IGF-1R/PI3K/Akt/mTOR signaling in muscle anabolism [12] and the central place of the Akt node in that control [20] but it is largely an extrapolation from IGF-1 biology rather than a direct body of LR3-specific muscle trials

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