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Semaglutide was developed through rational drug design, involving specific modifications to the native human GLP-1 molecule: Amino acid substitution at position 8 (alanine replaced with aminoisobutyric acid) to prevent DPP-4 degradation Attachment of a fatty acid side chain (via a spacer and linker) that allows the molecule to bind to albumin in the bloodstream These modifications extend the half-life to approximately one week , enabling once-weekly dosing Because semaglutide is structurally based on human GLP-1 rather than lizard peptides , there is no connection to Gila monster venom in its design or composition

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Hberle J (2013b) Clinical and biochemical aspects of primary and secondary hyperammonemic disorders