GHK is a tripeptide found in human plasma, saliva, and urine that binds copper(II) with high affinity. Structural work shows GHK and human serum albumin form ternary copper complexes at albumin histidine residues, with conditional binding constants of roughly 2900 and 1700 per molar at pH 7.4, consistent with a role in shuttling the exchangeable copper pool (Bossak-Ahmad 2021, PMID: 34730942). In fibroblast culture, GHK-Cu increases matrix metalloproteinase-2 expression along with the tissue inhibitors TIMP-1 and TIMP-2, so it acts on both the building and the remodeling sides of extracellular matrix turnover rather than simply adding collagen (Simeon 2000, PMID: 11045606). In serum-free culture of human dermal fibroblasts from irradiated tissue, GHK-Cu at 1 nanomolar accelerated population doubling and increased basic fibroblast growth factor and VEGF output relative to untreated controls (Pollard 2005, PMID: 15655171). In mice, GHK-Cu reduced reactive oxygen species and TNF-alpha and IL-6 production in an LPS-induced acute lung injury model, apparently through suppression of NF-kappaB p65 and p38 MAPK signaling (Park 2016, PMID: 27517151). A computational screen using regional emphysema severity signatures across 64 lung tissue samples from 8 smokers with COPD flagged GHK as a compound that reversed the destruction-associated gene expression pattern, and GHK restored collagen contraction in COPD-derived fibroblasts (Campbell 2012, PMID: 22937864). All of this is mechanistically coherent. None of it is a human outcome.
The practical gap is delivery. GHK-Cu is small but hydrophilic and does not meaningfully cross intact stratum corneum on its own, which is why the formulation and delivery route matter more than the percentage printed on a jar.
Independently graded against 173,636 indexed supplements with 177 published clinical interactions, sourced from PubMed, FDA CAERS, openFDA, and NIH DSLD | Last updated: March 2026
Not medical advice. Based on published clinical research and systematic reviews.