GHK-Cu (Glycyl-L-Histidyl-L-Lysine) is a naturally occurring copper peptide complex renowned for its regenerative and reparative properties. It plays a pivotal role in wound healing, tissue remodeling, and skin rejuvenation. GHK-Cu has been extensively studied for its ability to stimulate collagen synthesis, enhance skin elasticity, and exhibit potent antioxidant and anti-inflammatory effects.
GHK-Cu is a natural component of human blood and plays a crucial role in skin regeneration pathways. Research in skin cultures has demonstrated that GHK stimulates both the synthesis and breakdown of collagen, glycosaminoglycans, and other extracellular matrix components such as proteoglycans and chondroitin sulfate. This effect is partly mediated by GHK-Cu’s ability to recruit fibroblasts, immune cells, and endothelial cells. The peptide attracts these cells to injury sites and appears to coordinate their activity to repair damage.
GHK-Cu is commonly used in skin-care and cosmetic products because it improves skin elasticity while tightening and firming. It has also been shown to reduce sun damage, diminish hyperpigmentation, and lessen the appearance of fine lines and wrinkles. Its ability to regulate collagen synthesis is important for reducing scar visibility, preventing hypertrophic healing, smoothing rough skin, and repairing aged skin structure. These functions are partly achieved through increased levels of transforming growth factor-beta (TGF-β). It is likely that GHK-Cu operates via multiple biochemical pathways and influences gene transcription.
Mouse studies indicate that GHK-Cu accelerates burn wound healing by up to 33%. Besides recruiting immune cells and fibroblasts to injury sites, GHK-Cu promotes blood vessel growth. Since burned skin often regenerates blood vessels slowly due to cauterization, these findings suggest new approaches to improve wound care and speed healing in burn units.
Tissue invasion by pathogens is a major factor in delayed or failed wound healing. Bacterial and fungal infections are especially problematic in burn patients and individuals with compromised immune systems (e.g., diabetes, HIV). When combined with certain fatty acids, GHK-Cu forms a potent antimicrobial compound active against several bacteria and fungi that complicate wound healing.
Clinical studies in diabetic patients show that GHK-Cu, combined with standard care, increases wound closure by approximately 40% and reduces infection rates by 27% compared to standard care alone. Similar improvements have been observed in patients with ischemic open wounds.
Neuron death caused by degenerative diseases like Alzheimer’s is poorly understood, complicating treatment development. Research suggests GHK-Cu can counter age-related declines in neuron function that contribute to these diseases. It enhances angiogenesis in the nervous system, promotes nerve outgrowth, and reduces central nervous system inflammation. Evidence also indicates GHK-Cu can reset pathological gene expression, restoring health in dysfunctional neural systems.
GHK-Cu is abundant in the brain but declines with age. Some scientists propose that this decline, rather than new disease onset, drives neurodegeneration. Rat studies suggest GHK-Cu protects brain tissue by preventing apoptosis through the miR-339-5p/VEGFA pathway, which is active following brain bleeds and strokes. In these models, GHK-Cu reduces neurological deficits, brain swelling, and neuron death caused by miR-339-5p overexpression.
Mouse studies reveal that GHK-Cu protects lungs from fibrosis caused by the chemotherapy drug bleomycin. This suggests GHK-Cu could serve as a chemotherapy adjuvant, allowing higher doses of life-saving drugs without increased side effects. The mechanism involves regulating inflammatory molecules TNF-alpha and IL-6, which affect lung extracellular matrix and smooth muscle. By reducing inflammation, GHK-Cu prevents fibrotic remodeling and improves collagen deposition.
Similar lung-protective effects have been observed in mouse models of acute respiratory distress syndrome (ARDS), an often fatal inflammatory lung condition linked to injury, infection, and certain drugs including chemotherapy agents. GHK-Cu mediates its benefits through lowered TNF-alpha and IL-6 expression.
In rat models, GHK-Cu administration produces dose-dependent reductions in pain-related behaviors. The peptide’s analgesic effects are associated with increased levels of the natural painkiller L-lysine. Other studies have shown GHK-Cu also raises levels of L-arginine, another analgesic amino acid. These findings suggest new pain management strategies that avoid addictive opioids and NSAIDs, which can harm cardiovascular health.
GHK-Cu exhibits minimal side effects, with low oral but excellent subcutaneous bioavailability in mice. Mouse dosage does not scale directly to humans. GHK-Cu available from Peptide Sciences is intended solely for educational and scientific research and is not for human consumption. Purchases are restricted to licensed researchers.
GHK-Cu is primarily utilized in scientific studies focusing on:
GHK-Cu is intended strictly for laboratory research and is not approved for human consumption. Handle with care, following appropriate safety protocols. Ensure proper storage conditions to maintain the integrity and efficacy of the compound.
Have questions about our peptides or need personalized guidance? Send us a message through the form below, and we’ll respond promptly to help you make informed choices with confidence.