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In biological systems, over 95% of circulating native IGF-1 is sequestered in ternary complexes with IGF binding proteins (primarily IGFBP-3) and the acid-labile subunit (ALS), meaning only a small free fraction is available to activate IGF-1R at any given time

By increasing GLP-1 production or stimulating its release, this approach can complement existing therapies, such as GLP-1RAs and DPP-4 inhibitors, offering additional benefits while potentially reducing side effects

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