GHK-Cu
GHK-Cu (Glycyl-L-Histidyl-L-Lysine-Copper) is a naturally occurring tripeptide that chelates copper(II), a trace element essential to enzymatic and reparative biochemical systems. Detected in plasma, saliva, and tissue fluid, it has been investigated for its capacity to modulate gene expression, influence extracellular-matrix (ECM) remodeling, and adjust oxidative and inflammatory signaling in preclinical models.
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The information provided is for educational and informational purposes only and should not be interpreted as medical advice. All products described herein are intended strictly for laboratory and research use. They are not approved for human or veterinary administration, and should only be handled by qualified professionals in controlled research environments. Any clinical research must be conducted under the supervision and approval of an Institutional Review Board (IRB), and all preclinical studies must adhere to Institutional Animal Care and Use Committee (IACUC) guidelines in accordance with the Animal Welfare Act (AWA). Users are encouraged to conduct their own due diligence, referencing trusted scientific sources and verifying all information independently before making any purchasing or experimental decisions.
⚠️ Notice: All products are sold for laboratory and research purposes only. They are not intended for diagnostic, therapeutic, or personal use under any circumstances.
GHK-Cu
Overview
GHK-Cu (Glycyl-L-Histidyl-L-Lysine-Copper) is a naturally occurring tripeptide that chelates copper(II), a trace element essential to enzymatic and reparative biochemical systems. Detected in plasma, saliva, and tissue fluid, it has been investigated for its capacity to modulate gene expression, influence extracellular-matrix (ECM) remodeling, and adjust oxidative and inflammatory signaling in preclinical models. Research indicates endogenous GHK-Cu levels decline with age, corresponding with altered collagen expression and inflammatory-gene activation. Microarray studies have reported transcriptional influence across more than 4,000 genes associated with cellular maintenance, antioxidant defense, and matrix regulation.
Key Research Areas
2. Skin and Matrix-Remodeling Research
- In fibroblast and keratinocyte cultures, exposure to GHK-Cu was associated with increased expression of collagen I/III, elastin, and glycosaminoglycans (Maquart 1988).
- Ex vivo human-skin explants demonstrated increased ECM-gene expression and barrier-protein recovery under experimental conditions (Pickart 2018).
- Observed down-regulation of MMP-2/MMP-9 correlated with decreased collagen degradation in photodamage models; up-regulation of integrin and laminin genes was reported to support organized ECM architecture.
- Antioxidant activity has been observed to mitigate UV-induced oxidative stress and transepidermal water loss in tissue assays.
3. Wound-Healing and Tissue-Repair Models
- Experimental data indicate coordinated angiogenic and proliferative signaling following GHK-Cu exposure, with observed increases in fibroblast migration and VEGF/FGF-2 expression corresponding with neovascular formation in rodent wound models.
- Animal studies reported reductions in inflammatory infiltrates and edema during excisional-wound recovery (Arul 2012), with laboratory findings describing maintenance of oxidative balance and barrier integrity in regenerating tissue.
- Observed modulation of repair processes in nerve, tendon, and bone systems has been documented under preclinical conditions (Borkow 2004).
4. Hair-Follicle and Scalp Research
- In preclinical scalp and follicle models, GHK-Cu exposure was associated with increased VEGF expression and capillary formation near follicular bulbs (Yoon 2018).
- Observed activation of follicular stem-cell markers corresponded with entry into the anagen growth phase; down-regulation of perifollicular inflammatory markers and fibrosis was reported under controlled laboratory settings.
- In vitro assays showed increased hair-shaft-keratin expression and follicular-matrix activity; all findings remain non-clinical.
5. Anti-Inflammatory and Antioxidant Research
- GHK-Cu has been observed to suppress NF-κB signaling and lower expression of IL-6 and TNF-α (Pickart 2012), with up-regulation of SOD, catalase, and glutathione-pathway enzymes noted in oxidative-stress assays.
- Experimental studies document mitigation of UV- or xenobiotic-induced oxidative injury in dermal and hepatic tissues, suggesting enhanced redox balance through modulation of detoxification-gene networks.
6. Neurobiological and Cognitive Models
- In neuronal-culture systems, GHK-Cu was observed to support neurite extension and synaptic-marker recovery following oxidative insult; reductions in neuroinflammatory cytokines and lipid peroxidation were reported in cortical cultures (Squitti 2014).
- Preclinical data indicate normalization of copper homeostasis and mitochondrial-enzyme activity, with gene-expression analyses revealing up-regulation of pathways linked to neuronal plasticity and antioxidant defense. All neuroprotective findings remain investigational within non-clinical models.
7. DNA-Repair and Cellular-Protection Studies
- Molecular assays show activation of OGG1 and PARP1 enzymes involved in DNA-damage recognition and repair, with observed down-regulation of senescence-associated transcripts and maintenance of balanced proliferative signaling.
- Enhanced expression of mitochondrial-biogenesis and antioxidant genes in cultured cells (Maquart 2005; Pickart 2015) and protection of cultured cells from radiation- or toxin-induced oxidative damage in vitro.
8. Musculoskeletal and Connective-Tissue Research
- Observed stimulation of collagen cross-linking associated with mechanical strength in tendon and ligament assays; reported increases in angiogenic signaling and oxygen- transport capacity within skeletal-muscle repair models.
- Preclinical studies document limitation of fibrotic deposition and scar formation after mechanical injury; observed support of chondrocyte metabolism and ECM turnover in cartilage cell cultures.
9. Immune and Metabolic Studies
- GHK-Cu has been reported to modulate cytokine profiles and reduce chronic-inflammation markers in preclinical settings; observed association with enhanced oxygen diffusion and angiogenic remodeling in laboratory tissues.
- In-vitro metabolic assays show influence on glucose-uptake and insulin-signaling pathways, with maintenance of copper-dependent enzyme activity supporting energy- metabolism balance in cell studies.
Research References
- Maquart F.X. et al. (1988) — GHK-Cu regulation of dermal ECM components.
- Pickart L. et al. (2012, 2015, 2018) — Antioxidant gene expression and microarray analyses.
- Arul V. et al. (2012) — Wound-healing responses in rodent models.
- Borkow G. et al. (2004) — Copper peptide activity in connective-tissue regeneration.
- Yoon J.I. et al. (2018) — Follicular angiogenesis and VEGF signaling.
- Squitti R. et al. (2014) — Copper balance and neuroprotective effects.
- Maquart F.X. et al. (2005) — DNA-repair modulation and oxidative-stress protection.
Product Specifications
C₁₄H₂₄CuN₆O₄
403.86 g/mol
89030-95-5
Copper Tripeptide-1; Glycyl-L-histidyl-L-lysine copper(II)
Lyophilized powder
Keep refrigerated upon reconstitution
Soluble in sterile water and 0.9% NaCl solution
Research-use only. All information summarizes preclinical and in-vitro studies and is not intended for diagnostic, therapeutic, or personal use.
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