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This study was designed to systematically evaluate the therapeutic potential of GHK-Cu in a dextran sulfate sodium (DSS)-induced murine model of UC, with particular emphasis on elucidating its regulatory effects on the NAD-dependent deacetylase sirtuin-1 (SIRT1)/signal transducer and activator of transcription 3 (STAT3) signaling pathway

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More importantly, first-pass metabolism in the liver reduces the fraction that reaches systemic circulation

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In the research context, GHK-Cu is a tool for asking questions about copper delivery to specific copper-dependent enzymes (notably lysyl oxidase) and for studying the cellular consequences of GHK-mediated copper supply