GHK Cu

Summary

GHK-Cu is investigated for its role in collagen and elastin, wound healing, and skin firmness and health. Technically, it is the copper(II) complex of the tripeptide glycyl-L-histidyl-L-lysine, an endogenous molecule naturally present in human plasma, saliva, and urine, which transports copper into the cell and acts as a regenerative modulator, antioxidant, and anti-inflammatory even at nanomolar concentrations. It is probably the most studied copper peptide in regenerative biology.

What is it investigated for?

• •  Collagen and elastin synthesis
• •  Skin healing and firmness
• •  Antioxidant and anti-inflammatory defense
• •  Angiogenesis and extracellular matrix remodeling
• •  Epigenetic regulation of gene expression

Cycle & Break

Mechanism of Action

Extracellular Matrix Regeneration and Collagen Synthesis

GHK-Cu activates dermal fibroblasts—the connective tissue cells that produce the extracellular matrix (ECM)—and drives its remodeling. Through the TGF-β signaling pathway, it upregulates type I collagen, elastin, and glycosaminoglycan expression while adjusting the balance between metalloproteinases (MMP1, MMP2) and their tissue inhibitors (TIMP1, TIMP2) to prevent excessive tissue degradation. In wound healing models, collagen synthesis increases by 70% to 230%, reaching up to nine times in in vitro assays with fibroblasts.

Antioxidant and Anti-inflammatory Action

It provides bioavailable copper to the enzyme Cu,Zn-SOD1, mimicking superoxide dismutase activity and reducing reactive oxygen species (ROS) such as superoxide and hydroxyl radicals. Additionally, it limits iron release from ferritin (up to 87% inhibition), decreases lipid peroxidation byproducts, and protects against LDL oxidation. On the anti-inflammatory front, it suppresses NF-κB (p65) and p38 MAPK pathways, leading to a reduction in mediators such as TNF-α, IL-6, and fibrinogen.

Stimulation of Angiogenesis

It promotes the formation of new blood vessels by increasing VEGF and bFGF (FGF2) secretion by fibroblasts and mesenchymal stem cells. Released from the SPARC protein during tissue injury, it promotes endothelial proliferation in early repair phases and moderates it in later phases.

Epigenetic Modulation of Gene Expression

GHK-Cu modifies the expression of more than 1,000 genes—approximately 1,569 upregulated and 583 downregulated—acting as an epigenetic regulator by inhibiting histone deacetylases (HDACs). This reactivates regenerative pathways (TGF-β, integrins, p63) while attenuating gene programs associated with inflammation and tumor processes.

Scientific Evidence

Collagen and Matrix: In vitro studies in fibroblasts and rat wound models document collagen increases of up to 9×, with gene profiles confirming TGF-β pathway activation.

Antioxidant and Anti-inflammatory: UV radiation protection assays in keratinocytes and fibroblast cultures show cytokine decreases; animal models confirm ROS neutralization.

Angiogenesis: Gene data reflects a 487% increase in ANGPT1 expression; studies in rabbit wounds show greater granulation tissue and vascularization.

Gene Regulation: Microarray analyses (e.g., Connectivity Map) show broad effects; in COPD models, the reversal of 127 genes towards a healthier profile has been described.

Product Use

Due to this comprehensive profile, GHK-Cu is a key peptide in research lines on tissue regeneration and wound healing, extracellular matrix and collagen biology, antioxidant defense, and hair follicle signaling. At Peptido BioGenetic, we supply it as high-purity material for laboratory use, with a Certificate of Analysis (COA) available upon request.

⚠️ Product intended exclusively for research and laboratory use. Not for human or veterinary consumption.