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In normal physiology, the majority of circulating IGF-1 is bound to IGFBP-3, forming a large ternary complex with the acid-labile subunit that prevents rapid clearance and buffers free IGF-1 within a tightly controlled range

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The four amino-acid substitutions distinguishing the modified parent from native hGHRH(1-29) confer plasma-stability enhancements without compromising receptor agonism

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