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The chemistry of N-terminal acetylation and C-terminal amidation is well-established across peptide pharmacology these modifications reliably extend half-life and increase systemic exposure

This review aims to move beyond simple mechanistic descriptions and critically analyze the interaction of the NTFs-mitochondria axis in PD

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In those experiments, pretreatment with the peptide enhanced subsequent responses to growth hormone stimulation, including increased cell viability, elevated proliferating cell nuclear antigen (PCNA) expression, and greater JAK2 phosphorylation activity [5]

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