GHK-Cu (glycyl-L-histidyl-L-lysine : copper(II)) is a naturally occurring tripeptide first isolated from human plasma by Loren Pickart in 1973. Its plasma concentration declines significantly with age — from ~200 ng/mL at age 20 to ~80 ng/mL by age 60 — correlating with reduced regenerative capacity and skin quality in aging tissue.
Collagen and ECM Synthesis
GHK-Cu stimulates production of collagen types I, III, and IV, along with elastin and proteoglycans. It activates TGF-β1 and downstream Smad signaling — the master pathway governing fibroblast activation and extracellular matrix production. It tunes this pathway rather than simply amplifying it, promoting organized collagen deposition without the disordered fibrosis associated with unchecked TGF-β signaling.
Gene Expression Modulation
A 2012 microarray analysis found GHK-Cu modulates over 4,000 human genes, with upregulation of tissue remodeling and anti-inflammatory genes, and downregulation of genes associated with cancer aggression, inflammation, and neurodegeneration.
Anti-Inflammatory Mechanism: NF-κB Suppression
GHK-Cu suppresses the NF-κB pathway, reducing pro-inflammatory cytokines including TNF-α, IL-1β, and IL-6 without immunosuppression — mechanistically distinct from corticosteroids.
Wound Healing Research
GHK-Cu attracts macrophages and mast cells, promotes nerve outgrowth, stimulates angiogenesis, and activates MMPs to debride wound beds while TIMP-2 regulates that activity. This coordinated matrix remodeling — promoting breakdown of damaged tissue while driving new ECM synthesis — is central to its healing profile.
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GHK-Cu — View Product Page →References
- Pickart L, Margolina A. (2018). Regenerative and Protective Actions of the GHK-Cu Peptide. Int J Mol Sci, 19(7), 1987.
- Pickart L. (2008). The human tri-peptide GHK and tissue remodeling. J Biomater Sci Polym Ed, 19(8), 969–988.
- Dou Y, et al. (2021). GHK Peptide Inhibits Bleomycin-Induced Pulmonary Fibrosis. Front Pharmacol, 12, 618633.