GHK-Cu (Copper Peptide) (Topical)

GHK-Cu is the copper-complexed form of the endogenous tripeptide GHK (glycyl-histidyl-lysine) and is classified as a small regulatory peptide–metal complex studied in molecular biology and tissue-model research. It was originally identified in human plasma and has since been detected in additional biological fluids. Laboratory investigations focus on its interaction with copper-dependent enzymes and its influence on transcriptional pathways associated with extracellular matrix organization and cellular stress responses.

Research interest in GHK-Cu centers on its capacity to bind copper and potentially modulate downstream signaling pathways under defined experimental conditions. Because copper serves as a redox-active cofactor in multiple enzymatic systems, GHK-Cu provides a model for studying controlled copper delivery and its association with gene-regulatory networks. Experimental designs typically compare peptide–copper complexes to peptide-only, copper-only, or untreated controls to isolate metal-dependent biological effects within specific in vitro or animal systems.

Source: PubChem

Copper-coordinated GHK complex
Source: PubMed

Sequence: Gly-His-Lys·Cu
Molecular Formula: C₁₄H₂₃CuN₆O₄
Molecular Weight: 340.384 g/mol
PubChem CID: 73587
CAS Number: 89030-95-5

GHK-Cu is studied in vitro and in animal models to assess measurable molecular and cellular endpoints relative to appropriate control groups. In skin and fibroblast cultures, researchers commonly evaluate collagen-related gene expression, decorin-associated markers, glycosaminoglycan synthesis indicators, and extracellular matrix remodeling proteins. Additional endpoints may include fibroblast proliferation indices, endothelial-cell migration markers, and histological assessments in preclinical tissue models.

Inflammation-related research examines changes in cytokine expression such as TNF-α and IL-6, as well as modulation of NF-κB–associated signaling pathways under controlled laboratory conditions. Oxidative-stress investigations measure reactive oxygen species markers, antioxidant-response gene expression, and redox-regulatory enzyme activity compared to baseline controls.

Transcriptomic studies have reported broad gene-expression changes in defined systems, including pathways associated with DNA-repair markers, proteasome-related components, and apoptosis-related signaling. All findings are interpreted within the constraints of the specific experimental model, concentration range, exposure duration, and assay methodology. Observations are limited to laboratory and preclinical research contexts and do not imply clinical application or therapeutic use.

Mechanistic studies indicate that GHK-Cu interacts with multiple intracellular and extracellular signaling pathways associated with gene transcription regulation, growth factor signaling, and redox homeostasis. In vitro investigations have shown that the peptide complex can influence expression profiles of genes involved in extracellular matrix organization, metalloproteinase regulation, cytokine signaling, and cellular differentiation states. Copper coordination is considered a critical determinant of peptide conformation and bioactivity, enabling redox-sensitive interactions and modulation of copper-dependent enzymes.

In animal model systems, GHK-Cu has been utilized to examine angiogenesis-associated signaling, fibroblast recruitment, immune-cell chemotaxis, and apoptotic pathway regulation. Additional experimental work has explored peptide-mediated effects on microRNA-associated signaling cascades and vascular growth factor regulation, supporting its use as a tool for dissecting complex, multi-node signaling networks.

Relative GHK-Cu distribution across tissues (experimental data)
Source: PubMed

The referenced literature comprises exclusively preclinical investigations conducted in cell-based systems and animal models. These studies examine GHK-Cu–associated modulation of extracellular matrix synthesis, antimicrobial activity in vitro, neurovascular signaling pathways, inflammatory mediator regulation, and apoptosis-related molecular mechanisms. Observations reported in the cited publications are limited to defined experimental contexts and do not extend beyond laboratory research models.

This product is supplied as a lyophilized peptide–copper complex intended for laboratory research use. Analytical characterization commonly includes high-performance liquid chromatography (HPLC) and mass spectrometry to confirm identity, molecular integrity, and purity. Handling and storage should follow established laboratory protocols appropriate for peptide stability and traceability.

The above literature was researched, edited and organized by Dr. Logan, M.D. Dr. Logan holds a doctorate degree from Case Western Reserve University School of Medicine and a B.S. in molecular biology.

Loren Pickart, Ph.D. has released 109 publications and is developing patents and analyzing GHK’s effects on human gene expression of 4,192 genes. In addition to GHK’s published potential uses on skin inflammation, metastatic cancer and COPD, it appears to have beneficial effects on other tissue systems such as the nervous system, gastrointestinal system, and mitochondrial system. His brief but detailed autobiography dives into the motivations and background behind his dedicating to skin, anti-aging, and life-long training.

Loren Pickart, Ph.D is being referenced as one of the leading scientists involved in the research and development of GHK-Cu. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Peptide Sciences and this doctor. The purpose of citing the doctor is to acknowledge, recognize, and credit the exhaustive research and development efforts conducted by the scientists studying this peptide. Loren Pickart, Ph.D is listed in [1] [3] and [8] under the referenced citations.

1. L. Pickart, J. M. Vasquez-Soltero, and A. Margolina, “GHK Peptide as a Natural Modulator of Multiple Cellular Pathways in Skin Regeneration,” BioMed Res. Int., vol. 2015, p. 648108, 2015. [BioMed Research International]
2. A. Gruchlik, E. Chodurek, and Z. Dzierzewicz, “Effect of GLY-HIS-LYS and its copper complex on TGF-β secretion in normal human dermal fibroblasts,” Acta Pol. Pharm., vol. 71, no. 6, pp. 954–958, Dec. 2014. [PubMed]
3. L. Pickart and A. Margolina, “Regenerative and Protective Actions of the GHK-Cu Peptide in the Light of the New Gene Data,” Int. J. Mol. Sci., vol. 19, no. 7, Jul. 2018. [PubMed]
4. X. Wang et al., “GHK-Cu-liposomes accelerate scald wound healing in mice by promoting cell proliferation and angiogenesis,” Wound Repair Regen. Off. Publ. Wound Heal. Soc. Eur. Tissue Repair Soc., vol. 25, no. 2, pp. 270–278, 2017. [PubMed]
5. M. Kukowska, M. Kukowska-Kaszuba, and K. Dzierzbicka, “In vitro studies of antimicrobial activity of Gly-His-Lys conjugates as potential and promising candidates for therapeutics in skin and tissue infections,” Bioorg. Med. Chem. Lett., vol. 25, no. 3, pp. 542–546, Feb. 2015. [Science Direct]
6. G. D. Mulder et al., “Enhanced healing of ulcers in patients with diabetes by topical treatment with glycyl-l-histidyl-l-lysine copper,” Wound Repair Regen. Off. Publ. Wound Heal. Soc. Eur. Tissue Repair Soc., vol. 2, no. 4, pp. 259–269, Oct. 1994. [PubMed]
7. S. O. Canapp et al., “The effect of topical tripeptide-copper complex on healing of ischemic open wounds,” Vet. Surg. VS, vol. 32, no. 6, pp. 515–523, Dec. 2003. [PubMed]
8. L. Pickart, J. M. Vasquez-Soltero, and A. Margolina, “The Effect of the Human Peptide GHK on Gene Expression Relevant to Nervous System Function and Cognitive Decline,” Brain Sci., vol. 7, no. 2, Feb. 2017. [PubMed]
9. H. Zhang, Y. Wang, and Z. He, “Glycine-Histidine-Lysine (GHK) Alleviates Neuronal Apoptosis Due to Intracerebral Hemorrhage via the miR-339-5p/VEGFA Pathway,” Front. Neurosci., vol. 12, p. 644, 2018. [PubMed]
10. X.-M. Zhou et al., “GHK Peptide Inhibits Bleomycin-Induced Pulmonary Fibrosis in Mice by Suppressing TGFβ1/Smad-Mediated Epithelial-to-Mesenchymal Transition,” Front. Pharmacol., vol. 8, p. 904, 2017. [PubMed]
11. J.-R. Park, H. Lee, S.-I. Kim, and S.-R. Yang, “The tri-peptide GHK-Cu complex ameliorates lipopolysaccharide-induced acute lung injury in mice,” Oncotarget, vol. 7, no. 36, pp. 58405–58417, Sep. 2016. [PubMed]
12. L. А. Sever’yanova and M. E. Dolgintsev, “Effects of Tripeptide Gly-His-Lys in Pain-Induced Aggressive-Defensive Behavior in Rats,” Bull. Exp. Biol. Med., vol. 164, no. 2, pp. 140–143, Dec. 2017. [Springer]
13. L. А. Sever’yanova and D. V. Plotnikov, “Binding of Glyprolines to L-Arginine Inverts Its Analgesic and Antiagressogenic Effects,” Bull. Exp. Biol. Med., vol. 165, no. 5, pp. 621–624, Sep. 2018. [PubMed]

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The products offered on this website are furnished for in-vitro studies only. In-vitro studies (Latin: in glass) are performed outside of the body.  These products are not medicines or drugs and have not been approved by the FDA to prevent, treat or cure any medical condition, ailment or disease.  Bodily introduction of any kind into humans or animals is strictly forbidden by law.

For Laboratory Research Only. Not for human use, medical use, diagnostic use, or veterinary use.