GHK-Cu for Research in Canada

GHK-Cu is the copper(II) complex of glycyl-L-histidyl-L-lysine (GHK), a three-amino-acid peptide that occurs naturally in human plasma. Loren Pickart first reported the tripeptide in 1973 as a serum factor that prolonged the survival of normal liver cells in culture^[1], identified its sequence as Gly-His-Lys in 1977^[2], and by 1980 had shown that it binds copper(II) and carries the metal into cultured cells^[3]. Since then the complex has been studied mainly in fibroblast cultures and rodent wound models for its effects on collagen, glycosaminoglycans and matrix-remodelling enzymes^{[5, 6, 7]}, and more recently in mouse models of lung injury, fibrosis and colitis^{[14, 15, 16]}. It has no approved drug form. The vials on this page are lyophilized research-grade material for in-vitro and preclinical laboratory work only.

Key facts

• Peptide: Gly-His-Lys (GHK), a tripeptide; the complex carries one Cu(II) ion per peptide at neutral pH^[4]
• Formula and weight (complex): C₁₄H₂₃CuN₆O₄⁺, 402.92 g/mol — PubChem CID 71587328 (“prezatide copper”); PubChem also lists the doubly deprotonated form as C₁₄H₂₁CuN₆O₄⁻, 400.90 (CID 139035031). The weight depends on which protonation state is counted, so both are shown.
• Formula and weight (free GHK): C₁₄H₂₄N₆O₄, 340.38 g/mol — PubChem CID 73587; ChEMBL CHEMBL1814493 (340.38); the two databases agree
• CAS numbers: 89030-95-5 (GHK-Cu); 49557-75-7 (GHK)
• Other names: copper tripeptide-1, prezatide copper, Cu-GHK, “liver cell growth factor” (PubChem synonyms)
• Origin: human plasma; the same Gly-His-Lys triplet occurs in the α2 chain of type I collagen, which led Maquart and colleagues to propose that it is released by proteases at wound sites^[5]
• Research status: preclinical. Two 2026 systematic reviews describe a large, consistent body of cell and animal data and a thin, fragmented human literature with no adequately powered randomised trial^{[19, 20]}
• Formats on this site: 50mg and 100mg vials and a pen — lyophilized powder, laboratory research only

Where does GHK-Cu come from?

The tripeptide was found before its copper partner was understood. In the 1973 paper, a fraction of human serum prolonged the survival of normal hepatocytes and stimulated growth of hepatoma cells in culture^[1]; four years later the active substance was shown to be glycyl-histidyl-lysine^[2]. During purification the peptide co-isolated with roughly equimolar copper and about one-fifth as much iron, and several tripeptides sharing the histidyl-lysyl linkage were nearly as active — which, together with the resemblance between GHK and the copper-binding sites of albumin and α-fetoprotein, led Pickart’s group to propose that GHK acts as a copper-transport factor^[3]. Spectroscopic work in 1982 established that at neutral pH GHK forms a mononuclear 1:1 complex with Cu(II), coordinated through two or three nitrogen atoms including the histidine imidazole, and that the oxygen-bridged copper pairs seen in the crystal do not persist in solution^[4].

In 1988 Maquart and co-workers reported that GHK-Cu stimulated collagen synthesis in fibroblast cultures from about 10⁻¹² M, peaking at 10⁻⁹ M, without changing cell number, and noted the GHK triplet inside type I collagen^[5]. That observation reframed the peptide as a possible fragment of the extracellular matrix — a “matrikine” — released during tissue breakdown, a view the 2026 reviews still adopt^[19].

Chemical identity

PubChem and ChEMBL agree on the free peptide (340.38). For the complex, the databases list charged species rather than a neutral salt, so the weight of a given lot also depends on its counter-ion and water content — a point the 2026 Pharmaceutics review makes at length when it argues that “GHK-Cu” is often sold and studied without its coordination state being defined^[20].

What has been studied in the laboratory?

Fibroblasts and connective-tissue synthesis (cell culture)

The best-replicated finding is a stimulation of extracellular-matrix synthesis by cultured fibroblasts at nanomolar concentrations: collagen in the 1988 FEBS Letters study^[5], and, in a 2005 serum-free model using human dermal fibroblasts taken from irradiated head-and-neck surgery patients, faster population doubling plus more basic fibroblast growth factor and VEGF production early after exposure to 1 nM GHK-Cu^[11]. Those are dish measurements, not tissue outcomes.

Wound-chamber model (rat)

Maquart’s group implanted stainless-steel mesh cylinders under the skin of rats and injected GHK-Cu or saline into them. Treated chambers showed concentration-dependent increases in dry weight, DNA, total protein, collagen and glycosaminoglycans; collagen synthesis rose about twice as much as non-collagen protein, type I and III collagen mRNAs increased while TGF-β mRNA did not, and a control tripeptide had no effect^[6]. Follow-up work in the same model found that GHK-Cu did not change interstitial collagenase activity but prolonged MMP-9 expression in wound tissue and altered the balance of gelatinases^[7], and that it increased chondroitin- and dermatan-sulfate accumulation and decorin mRNA while lowering biglycan mRNA^[8].

Skin, hair and radiation-injured tissue (mouse, rat, rabbit)

A 1991 report in C3H mice described hair-follicle stimulation by peptide-copper complexes^[9]; no abstract is indexed and the paper is cited here for the model only. In contrast, a 2013 study of irradiated dorsal skin flaps in Sprague-Dawley rats found that ten days of topical GHK-Cu gel produced no difference in flap ischaemia, vessel number or area, or VEGF expression compared with control ointment^[12].

Ligament graft (rat)

In 72 rats undergoing ACL reconstruction, weekly intra-articular GHK-Cu for four weeks reduced side-to-side knee laxity and increased graft stiffness at six weeks, but the differences were gone at twelve weeks and there was no difference in ultimate load, gait or histology — the authors describe the benefit as transient once treatment stopped^[13].

Inflammation models (mouse and cells)

In LPS-stimulated RAW 264.7 macrophages and in LPS-induced acute lung injury in mice, GHK-Cu lowered reactive oxygen species, raised superoxide dismutase activity, and reduced TNF-α and IL-6 through suppression of NF-κB p65 and p38 MAPK signalling^[14]. In bleomycin-induced pulmonary fibrosis in C57BL/6 mice, intraperitoneal GHK-Cu reduced inflammatory cytokines, collagen deposition and MMP-9/TIMP-1 imbalance and partly prevented epithelial–mesenchymal transition via Nrf2, NF-κB and TGF-β1/Smad pathways^[15]. A 2025 study in DSS-induced colitis in BALB/c mice reported reduced disease activity, restored tight-junction proteins and lower cytokines, with SIRT1/STAT3 signalling proposed as the mechanism^[16].

Gene-expression analyses

Pickart and Margolina’s 2018 review collects connectivity-map data suggesting that GHK modulates a large number of human genes and uses that to explain the breadth of reported actions^[17]. Those are computational associations from cultured-cell expression profiles, written by the compound’s discoverer, and the 2026 systematic reviews treat them as hypothesis-generating rather than confirmatory^[20].

Human studies

Human data are sparse. An 86-patient randomised, evaluator-blinded trial in venous stasis ulcers (1992) found that a 0.4% tripeptide-copper cream was no better than placebo, while silver sulfadiazine reduced ulcer size^[10]. The 2026 Pharmaceutics review, covering the literature to August 2026, characterises the cosmetic reports as small or incompletely described, notes a negative 13-participant post-laser study and a positive 18-participant split-face eyebrow study that did not define what species of GHK-Cu was applied, and records a Phase 2 acute-wound trial (NCT07437586) still recruiting with no results^[20]. A separate 2026 systematic review of 64 records reached the same conclusion: no adequately powered human randomised controlled trial exists^[19]. A 2025 review of topical GHK as a cosmetic ingredient adds that skin-permeation data for GHK-Cu are insufficient^[18].

Study summary

What the evidence does not show

• No human efficacy. The one sizeable randomised trial, in venous ulcers, was negative^[10]; the 2026 reviews find no adequately powered RCT and call GHK-Cu “promising but unproven”^{[19, 20]}. Nothing on this page supports any effect on human skin, hair, wounds, ageing or inflammation.
• Not all animal results are positive. Topical GHK-Cu did nothing measurable in irradiated rat flaps^[12], and the ACL-graft benefit in rats disappeared once injections stopped^[13].
• Cell-culture concentrations are not doses. Fibroblast effects were seen at 10⁻¹² to 10⁻⁹ M in a dish^{[5, 11]}; the rat chamber studies injected 2 mg directly into an implanted wound space^{[7, 8]}. Neither translates to any route or amount in a whole organism.
• The material itself is under-defined in much of the literature. Speciation, copper occupancy and stability are rarely reported, and results obtained with one preparation cannot be assumed for another^[20].
• Broad gene-expression claims are computational. The lists of genes “reset” by GHK come from connectivity-map analyses of cultured cells, published by the compound’s discoverer^[17], and have not been validated as outcomes in any organism.
• No regulatory approval anywhere. GHK-Cu is a cosmetic ingredient and a research reagent; it is not a drug in Canada, the US or the EU.

Batch documentation

An independent Janoshik report is posted for the 100mg vial: report #218248, sample received 17 August 2026, analysed 19 August 2026, purity 99.661%, measured GHK-Cu 76.04 mg GHK-Cu (63.73 mg GHK peptide + 12.31 mg copper). The laboratory reported the peptide and the copper separately; their molar amounts (63.73 mg ÷ 340.38 ≈ 0.187 mmol of GHK and 12.31 mg ÷ 63.55 ≈ 0.194 mmol of copper) are close to the 1:1 ratio described for the complex^[4]. The library card lists “N2JKLM26983T” as a batch number; on the report itself that string is the Janoshik verification key, and the batch field reads “unknown”. No report is posted for the 50mg vial at the time of this review. The product page embeds the document.

GHK-Cu is one of the compounds on the page where you can buy peptides online in Canada; every listing there carries the same research-use-only terms and links to its own report where one exists.

Handling and storage in the laboratory

• Form: lyophilized powder in a sealed vial.
• Storage: the site’s guidance is −20 °C for long-term storage of the sealed vial (stated stability up to 24 months) and cool, dry, dark conditions for short periods; avoid repeated freeze–thaw.
• Solution chemistry: copper coordination changes with pH — the 1982 study recorded three optical transitions with apparent pK values of 3.6, 9.2 and 11.4^[4] — so buffer choice and pH affect which species is present. GHK is highly water-soluble and described as unstable in formulation^[18]; prepare only what an experiment needs.
• Protocols: the researcher’s responsibility. Shop Peptides Online publishes no dosing, reconstitution or administration guidance.

References

All references were retrieved from PubMed (NCBI) on 30 September 2026 and cross-checked against Europe PMC; identity data from PubChem and ChEMBL (EMBL-EBI) on the same date. Where a database lists more than one form of the compound, each is shown with its own identifier.

1. Pickart L, Thaler MM (1973). Tripeptide in human serum which prolongs survival of normal liver cells and stimulates growth in neoplastic liver. Nature: New biology 243(124):85-7. PMID 4349963
2. Schlesinger DH, Pickart L, Thaler MM (1977). Growth-modulating serum tripeptide is glycyl-histidyl-lysine. Experientia 33(3):324-5. doi:10.1007/BF02002806. PMID 858356
3. Pickart L, Freedman JH, Loker WJ et al. (1980). Growth-modulating plasma tripeptide may function by facilitating copper uptake into cells. Nature 288(5792):715-7. doi:10.1038/288715a0. PMID 7453802
4. Freedman JH, Pickart L, Weinstein B et al. (1982). Structure of the Glycyl-L-histidyl-L-lysine–copper(II) complex in solution. Biochemistry 21(19):4540-4. doi:10.1021/bi00262a004. PMID 6291585
5. Maquart FX, Pickart L, Laurent M et al. (1988). Stimulation of collagen synthesis in fibroblast cultures by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+. FEBS letters 238(2):343-6. doi:10.1016/0014-5793(88)80509-x. PMID 3169264
6. Maquart FX, Bellon G, Chaqour B et al. (1993). In vivo stimulation of connective tissue accumulation by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+ in rat experimental wounds. The Journal of clinical investigation 92(5):2368-76. doi:10.1172/JCI116842. PMID 8227353
7. Siméon A, Monier F, Emonard H et al. (1999). Expression and activation of matrix metalloproteinases in wounds: modulation by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+. The Journal of investigative dermatology 112(6):957-64. doi:10.1046/j.1523-1747.1999.00606.x. PMID 10383745
8. Siméon A, Wegrowski Y, Bontemps Y et al. (2000). Expression of glycosaminoglycans and small proteoglycans in wounds: modulation by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu(2+). The Journal of investigative dermatology 115(6):962-8. doi:10.1046/j.1523-1747.2000.00166.x. PMID 11121126
9. Trachy RE, Fors TD, Pickart L et al. (1991). The hair follicle-stimulating properties of peptide copper complexes. Results in C3H mice. Annals of the New York Academy of Sciences 642:468-9. doi:10.1111/j.1749-6632.1991.tb24420.x. PMID 1809108
10. Bishop JB, Phillips LG, Mustoe TA et al. (1992). A prospective randomized evaluator-blinded trial of two potential wound healing agents for the treatment of venous stasis ulcers. Journal of vascular surgery 16(2):251-7. doi:10.1067/mva.1992.37086. PMID 1495150
11. Pollard JD, Quan S, Kang T et al. (2005). Effects of copper tripeptide on the growth and expression of growth factors by normal and irradiated fibroblasts. Archives of facial plastic surgery 7(1):27-31. doi:10.1001/archfaci.7.1.27. PMID 15655171
12. Parker NP, Ardeshirpour F, Schmechel SC et al. (2013). Effects of topical copper tripeptide complex on wound healing in an irradiated rat model. Otolaryngology–head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery 149(3):384-9. doi:10.1177/0194599813492644. PMID 23744835
13. Fu SC, Cheuk YC, Chiu WY et al. (2015). Tripeptide-copper complex GHK-Cu (II) transiently improved healing outcome in a rat model of ACL reconstruction. Journal of orthopaedic research : official publication of the Orthopaedic Research Society 33(7):1024-33. doi:10.1002/jor.22831. PMID 25731775
14. Park JR, Lee H, Kim SI et al. (2016). The tri-peptide GHK-Cu complex ameliorates lipopolysaccharide-induced acute lung injury in mice. Oncotarget 7(36):58405-58417. doi:10.18632/oncotarget.11168. PMID 27517151
15. Ma WH, Li M, Ma HF et al. (2020). Protective effects of GHK-Cu in bleomycin-induced pulmonary fibrosis via anti-oxidative stress and anti-inflammation pathways. Life sciences 241:117139. doi:10.1016/j.lfs.2019.117139. PMID 31809714
16. Mao S, Huang J, Li J et al. (2025). Exploring the beneficial effects of GHK-Cu on an experimental model of colitis and the underlying mechanisms. Frontiers in pharmacology 16:1551843. doi:10.3389/fphar.2025.1551843. PMID 40672369
17. Pickart L, Margolina A (2018). Regenerative and Protective Actions of the GHK-Cu Peptide in the Light of the New Gene Data. International journal of molecular sciences 19(7). doi:10.3390/ijms19071987. PMID 29986520
18. Mortazavi SM, Mohammadi Vadoud SA, Moghimi HR (2025). Topically applied GHK as an anti-wrinkle peptide: Advantages, problems and prospective. BioImpacts : BI 15:30071. doi:10.34172/bi.30071. PMID 39963574
19. Najafi N, Maatouk H, Vardanyan KG et al. (2026). A Systematic Review of the Mechanisms and Therapeutic Applications of GHK-Cu (Glycyl-L-Histidyl-L-Lysine-Copper Complex) in Topical Microneedle Delivery: A Case for Expanded Clinical Trials. Archives of internal medicine research 9(3):269-293. doi:10.26502/aimr.0255. PMID 42787770
20. Mateescu DM, Gavrilescu DM, Mincioaga RI et al. (2026). GHK-Cu as a Bioactive Metallopeptide and Drug-Delivery Cargo: Coordination Chemistry, Formulation Science, Therapeutic Evidence, and a Translational Roadmap. Pharmaceutics 18(9). doi:10.3390/pharmaceutics18091077. PMID 42797253