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A 13-residue N-terminal extension and an arginine-for-glutamate substitution at position 3 sharply reduce the peptide's affinity for the insulin-like growth factor binding proteins (IGFBPs), leaving more free peptide available to activate the IGF-1 receptor and giving IGF-1 LR3 a longer functional half-life and greater potency than native IGF-1 in cell-culture systems