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It incorporates key modifications, including 14E/17R mutations to stabilize an -helical segment via a salt bridge, multiple proline substitutions (25P, 28P, 29P) to reduce -sheet formation, and N-terminal C20 fatty diacid lipidation for reversible albumin binding (Kruse et al

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Additionally, GHK's influence on the miR-339-5p/VEGFA axis played a crucial role in preventing neuronal apoptosis following ICH injury

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However, this approach is not routine first-line treatment in UK practice, is considered off-label, and requires good patient adherence and clinical follow-up

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