GHK-Cu is a naturally occurring copper-binding tripeptide studied for its roles in collagen synthesis, wound healing, and gene expression regulation. A review of published research.
GHK-Cu is the copper(II) complex of the tripeptide glycine-L-histidine-L-lysine (GHK). It was first identified in human plasma albumin by Loren Pickart in 1973 and has since been studied in the context of tissue remodelling, wound healing, and gene expression modulation (Pickart, 2008).
The compound is endogenous: plasma concentrations of GHK in healthy adults are approximately 200 ng/mL in younger individuals, declining with age. This age-related decline has made it a subject of interest in longevity and regenerative research contexts (Pickart and Margolina, 2018).
Molecular Formula: C14H24N6O4
CAS Number: 49557-75-7
Molecular Weight: 340.38 Da (free peptide); 403.91 Da as copper complex
GHK coordinates copper via its histidine residue, forming a stable square-planar complex. Research has shown that this copper delivery function may support superoxide dismutase (SOD) activity and antioxidant defence at the cellular level (Pickart, Vasquez-Soltero, and Margolina, 2015).
One of the most consistently reported findings in GHK-Cu research is stimulation of collagen and glycosaminoglycan synthesis in fibroblast models. Studies using human dermal fibroblasts have documented upregulation of collagen I, collagen III, and fibronectin following GHK-Cu exposure. The compound also appears to inhibit matrix metalloproteinases (MMPs), enzymes responsible for collagen degradation, suggesting a dual role in ECM homeostasis (Pickart, Vasquez-Soltero, and Margolina, 2015).
A bioinformatic analysis of GHK's effects on gene expression (using the Broad Institute Connectivity Map) identified modulation of over 4,000 human genes. Upregulated pathways included those involved in DNA repair, ubiquitin-proteasome degradation, tissue remodelling, and anti-inflammatory signalling. Downregulated genes were associated with inflammation and oncogenic pathways (Pickart and Margolina, 2018).
Multiple preclinical studies have examined GHK-Cu in wound healing models. These investigations report accelerated wound contraction, increased angiogenesis, and improved epithelialisation compared to controls. The proposed mechanisms include stimulation of VEGF expression and upregulation of fibroblast and keratinocyte proliferation (Pickart, 2008).
Preclinical in-vitro research has investigated GHK-Cu in the context of nerve regeneration, specifically its effect on neurite outgrowth and BDNF expression. These findings are preliminary and derived from cell models rather than in-vivo systems.
| Research Area | Model Used | Key Finding |
|---|---|---|
| Collagen synthesis | Human dermal fibroblasts | Increased collagen I and III expression |
| Wound contraction | Rodent models | Accelerated healing rates |
| Antioxidant activity | Cell models | SOD-like activity via copper coordination |
| Gene expression | Bioinformatic analysis | Modulation of 4,000+ human genes |
| Anti-inflammatory | Cell models | Reduced TNF-alpha and IL-6 expression |
1. Pickart L. "The Human Tri-Peptide GHK and Tissue Remodeling." *Journal of Biomaterials Science, Polymer Edition.* 2008;19(8):969-988.
2. Pickart L, Vasquez-Soltero JM, Margolina A. "GHK Peptide as a Natural Modulator of Multiple Cellular Pathways in Skin Regeneration." *BioMed Research International.* 2015;2015:648108.
3. Pickart L, Margolina A. "Regenerative and Protective Actions of the GHK-Cu Peptide in the Light of the New Gene Data." *International Journal of Molecular Sciences.* 2018;19(7):1987.
Our GHK-Cu 100mg is independently verified at 98.8% HPLC purity with full Certificate of Analysis documentation including mass spectrometry identity confirmation and LAL endotoxin assay.
Disclaimer: All information is based on published preclinical research literature and is provided for educational purposes only. GHK-Cu is sold strictly for in-vitro laboratory and research purposes. Not medical advice.
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