GHK-Cu

What is GHK-Cu?

Glycyl-L-Histidyl-L-Lysine bound to copper represents one of nature's elegant metal-mediated signaling systems. First isolated from human plasma in the 1970s by Dr. Loren Pickart, GHK-Cu demonstrates the biological importance of copper-peptide coordination chemistry. The copper ion, precisely positioned by the peptide's histidine and terminal amine, activates the complex's biological functions: stimulating collagen and glycosaminoglycan synthesis, modulating metalloproteinase activity for balanced extracellular matrix remodeling, and providing localized antioxidant effects.

GHK-Cu's plasma concentration declines with age, correlating with diminished tissue repair capacity—a relationship that has driven extensive research into its role in wound healing, dermal remodeling, and tissue regeneration. The peptide's ability to simultaneously promote matrix synthesis and regulate degradation makes it irreplaceable in studies of balanced tissue remodeling.

Mechanism of Action

GHK-Cu functions through multiple interconnected mechanisms centered on the copper ion's catalytic properties. The tripeptide chelates Cu(II) through nitrogen atoms from the glycine amino terminus, histidine imidazole, and lysine side chain, creating a square planar coordination complex. This copper-peptide complex serves as a signaling molecule that modulates gene expression—studies demonstrate GHK-Cu regulates over 4,000 genes, with particular effects on genes encoding extracellular matrix proteins (collagens I, III, IV), matrix remodeling enzymes (MMPs and TIMPs), and antioxidant enzymes.

The peptide stimulates fibroblast proliferation through activation of the ERK1/2 and Akt signaling pathways, while also enhancing TGF-β secretion which drives collagen synthesis. GHK-Cu modulates matrix metalloproteinase-2 (MMP-2) activity—upregulating it during early wound healing to clear damaged matrix, then suppressing excessive MMP activity during remodeling phases. The copper center also provides localized antioxidant effects through catalytic conversion of superoxide radicals. In keratinocytes, GHK-Cu increases production of decorin, a small leucine-rich proteoglycan that regulates collagen fibril assembly and prevents excessive scar formation.

Key Research Findings

• Stimulates collagen I synthesis by 70% and collagen III by 85% in human dermal fibroblasts at 1-10 μM concentrations (Pickart et al., 2012)
• Demonstrates differential MMP regulation: increases MMP-2 by 180% in early wound healing, then reduces by 45% during remodeling phase (Siméon et al., 2000)
• Modulates expression of 4,000+ genes including 47% increase in decorin and 32% increase in anti-inflammatory IL-10 (Campbell et al., 2012)
• Enhances wound contraction rate by 42% and increases tensile strength of healed tissue by 35% in rat wound models (Mulder et al., 2009)
• Shows copper-dependent VEGF upregulation (60% increase) promoting angiogenesis in ischemic tissue models (Pollard et al., 2005)

Research Applications

• Collagen synthesis mechanisms
• Metalloproteinase regulation
• Copper-dependent enzyme research
• Extracellular matrix remodeling
• Wound healing biology
• Antioxidant copper chemistry
• Tissue regeneration models

Reconstitution & Use

Reconstitute with bacteriostatic water for injection. For detailed reconstitution instructions and dosing protocols for your specific research application, see our reconstitution guide.

Storage & Handling

Store lyophilized at -20°C protected from light (copper complexes are photosensitive). Reconstitute with sterile water; the copper complex remains stable at 2-8°C for 30 days. Avoid oxidizing agents.