What is GHK-Cu?

GHK-Cu is the tripeptide glycyl-L-histidyl-L-lysine bound to one copper(II) ion. The peptide occurs naturally: Loren Pickart and Marvin Thaler reported a tripeptide in human serum in 1973, and a 1977 paper identified it as glycyl-histidyl-lysine. ^[1][13] A later review describes GHK in human plasma, saliva and urine, at levels that decline with age. ^[14]

The copper came into the story in 1980. While isolating the peptide from plasma, Pickart's group found it co-purified with roughly equimolar copper, and they reported that it forms complexes with copper(II) and increased copper uptake into cultured hepatoma cells. ^[15]

That history explains the names you will see. Chemists write Cu(II)-GHK or GHK-Cu. PubChem lists "prezatide copper" and the cosmetic ingredient name "copper tripeptide-1" as synonyms for the same 1:1 complex. ^[2] GHK-Cu in 50mg vials is in stock with a batch certificate.

GHK-Cu is three amino acids (glycine, histidine, lysine) with a copper(II) ion held by the first two residues. PubChem's record for the 1:1 complex gives the formula C14H23CuN6O4+ and a molecular weight of 402.92 g/mol. ^[2] We checked each value below against PubChem on 29 September 2026.

The identifiers come from PubChem. ^{[2][6][7][16]}

The table carries four masses for one common name. Suppliers, papers and cosmetic labels all say "GHK-Cu", yet the free peptide, the 1:1 complex and the two 2:1 records differ by more than 400 g/mol. A 2026 review of GHK-Cu formulation work makes the same point from the research side: studies often report total peptide and copper content without resolving how much copper is bound, or whether intact GHK-Cu or free GHK and copper were released. ^[3] When you read a certificate, find the mass it quotes and match it to a row above.

GHK binds copper(II) through three nitrogen atoms: the glycine amino group, the deprotonated amide nitrogen between glycine and histidine, and a nitrogen in the histidine imidazole ring. A 2011 X-ray and spectroscopy study confirmed this arrangement for the complex in solution, and reported that the solid form is a dimer in which a carboxylate oxygen fills the fourth position. ^[17]

Earlier work reached the same picture from different directions. A 1982 spectroscopy study found that at neutral pH GHK forms a mononuclear 1:1 copper compound, with one coordinating nitrogen in the histidyl imidazole ring. ^[18]

The binding is strong. Three measurements put numbers on it:

• Affinity. Isothermal calorimetry (ITC) gave a conditional dissociation constant of 7.0 × 10^-14 M for Cu(II)-GHK at pH 7.4, close to the 2.6 × 10^-14 M measured for the albumin-type DAHK motif in the same study. ^[4]
• Competition with albumin. In equilibrium dialysis at pH 7.5, equal concentrations of albumin and GHK left about 42% of the copper on the peptide. ^[5]
• Ternary complexes. A 2021 study with a University of Melbourne co-author found that Cu(GHK) also attaches to histidine side chains of human serum albumin, including His3, with a conditional binding constant of 2900 M-1. ^[19]

Redox behaviour matters in a lab. The 2011 study reported that Cu(II)-GHK is inert under moderate redox potentials, and that it can be reduced to Cu(I) at about -0.62 V (against Ag/AgCl), which releases the copper. ^[17] A strong reducing environment can therefore strip the metal from the peptide.

GHK-Cu's proposed mechanism is copper transport: the peptide carries copper(II) and hands it to cells. Pickart's 1980 Nature paper built this case from two observations. GHK has a copper site resembling the transport sites on albumin, and adding it to hepatoma cells increased their copper uptake. ^[15] The 1981 albumin competition data led its authors to discuss GHK complexes as carriers of copper from blood to tissues. ^[5]

Two later lines of work added detail.

The first concerns where GHK comes from in tissue. A 1988 fibroblast study noted that the GHK triplet occurs in the alpha 2(I) chain of type I collagen, and proposed that proteases could release it at a site of tissue injury. ^[20]

The second is gene expression. In 2012, a Boston University and University of British Columbia group profiled lung tissue from smokers with COPD and used the Connectivity Map database to search for compounds that reverse the emphysema-linked gene signature. GHK came up. In cultured human fibroblasts, GHK reproduced TGF-beta-type gene expression patterns and restored collagen I contraction by fibroblasts from COPD lungs. ^[21] Pickart's own reviews extend this to claims of broad gene regulation across thousands of genes. ^[14]

None of the abstracts we reviewed names a specific cell-surface receptor for GHK-Cu. The mechanism in the literature rests on copper chemistry, the collagen-fragment origin and gene-expression data, most of it from cell culture.

Research on GHK-Cu has examined copper chemistry, cultured cells, rodent wound and injury models, human skin in diffusion cells, and a handful of small human trials. The table lists the studies we checked, by model, with what each abstract reported.

Two entries need a caution. The 1992 trial abstract describes "a biologically active tripeptide copper complex" and does not name GHK, so we list it as probable, unconfirmed. ^[9] The 2006 trial used skin care products containing GHK-Cu alongside other ingredients; its patient questionnaire differed between groups (P = .04) while the computer and blinded-evaluator measures did not. ^[8]

Every finding above describes one model under one set of conditions, reported by the study's own authors.

The GHK-Cu evidence base is long and narrow. A 2026 systematic review screened 1,247 records and retained 64, and concluded that the human literature "remains thin and fragmented", with most randomised trials small and run on facial creams. ^[10] A second 2026 review reached a harder verdict: GHK-Cu "should be regarded as a promising but unproven therapeutic cargo". ^[3]

Four limits stand out.

1. One group wrote much of it. The 2026 systematic review estimates that about 35% of the primary literature in its window includes Loren Pickart or Anna Margolina of Skin Biology as an author, and notes that Pickart held commercial interests in the field for decades. ^[10] The broadest claims, such as regulation of thousands of genes, come from that group's reviews. ^[14][27]
2. The controlled human results are mostly null. The 13-patient laser trial found no objective difference, and the 86-patient ulcer trial found the copper complex cream no different from placebo. ^[8][9] A registered phase 2 study (NCT07437586) was still recruiting at the review's August 2026 search, with no results. ^[3]
3. Animal results are mixed. Rat wound chambers showed more collagen, while irradiated rat flaps showed no difference and the ACL effect faded by 12 weeks. ^[22][24][25]
4. Nobody has measured it in people after systemic exposure. We found no published human pharmacokinetic study. A 1993 paper built an analogue with about ten-fold greater stability in human plasma in vitro, which implies the parent peptide breaks down in plasma. ^[28]

Purity, identity and copper content of a research vial are separate questions, and a batch certificate answers them.

We found no study abstract that reports adverse events for GHK-Cu. The human studies located are small topical studies whose abstracts give no adverse-event data, and we found no human study of any route other than the skin.

Two sources speak to the question from other directions:

• Cell data. In a human keratinocyte model built to test skin irritation, GHK-Cu "was not cytotoxic and did not induce any significant change" in irritation biomarkers. Copper chloride and copper acetate raised IL-1 alpha, IL-8, HSPA1A and FOSL1 in the same study. ^[11]
• A 2026 sports-medicine review covering GHK-Cu among other unapproved peptides states that "rigorous human safety data are scarce, and there is potential for serious harm to patients". ^[29]

The TGA names GHK-Cu among its examples of unapproved peptide products, and lists unknown manufacturing, sterility and contents among the risks of such products. ^[30] An absence of reported events in small topical studies is a gap in the record.

GHK-Cu is not named in the Poisons Standard. The June 2026 instrument (F2026L00633) does list "COPPER COMPOUNDS for human use" in Schedule 4 (prescription only), with exceptions for substances separately specified, for low-copper preparations for internal use, and for other preparations containing 5% or less of copper compounds. ^[31] Schedule 6 carries a separate copper compounds entry with its own exceptions. ^[31] We have not resolved which entry, if any, applies to GHK-Cu, so regard its status as unconfirmed and check with the TGA.

The TGA's safety alert on unapproved peptide products names GHK-Cu among its examples, meaning goods not included in the Australian Register of Therapeutic Goods. ^[30] Sport Integrity Australia lists GHK-Cu among unapproved peptide products being promoted. ^[32]

For sport, GHK-Cu is not named on the WADA 2026 Prohibited List, effective 1 January 2026. Class S0 prohibits at all times any pharmacological substance not addressed elsewhere on the List and with no current governmental approval for human therapeutic use. ^[12] Whether S0 applies depends on approval status, which we did not verify. Our guide to Australian peptide law and the Poisons Standard explains the schedules and group entries.

GHK-Cu has no published storage study for research-grade lyophilised powder. The closest primary data is a 2016 preformulation study from the University of Auckland, which reported that GHK-Cu: ^[33]

• broke down by hydrolytic cleavage under basic and oxidative stress, and to a lesser extent under acidic stress;
• stayed stable in water and in pH 4.5 to 7.4 buffers for at least two weeks at 60 °C;
• is highly hydrophilic, with log D values between -2.38 and -2.49;
• produced three main degradation products, one of them free histidine.

In practice, keep sealed vials cold, dry and dark, and keep solutions near neutral pH and away from oxidising agents. The 2011 redox study adds one more rule: strong reducing agents can release the copper from the peptide. ^[17]

GHK-Cu's water solubility makes aqueous solvents the natural choice. We stock BAC Water (sterile water with 0.9% benzyl alcohol) in 3ml vials. Our guide on reconstituting peptides for laboratory work covers concentration arithmetic, and the peptide storage guide covers temperature, light and freeze-thaw.

Peptides Collective sells GHK-Cu for laboratory research use only, in 50mg vials at A$58. Stock ships from Western Australia with tracking. It sits in our skin research peptides range.

Every batch is tested by an independent lab before sale. The certificate reports purity by HPLC and identity by mass spectrometry, and it is published under the batch number printed on the vial. Search the certificate of analysis library by that number and match the report to the vial in your hand. The testing page sets out what each test covers.

Read the identity result against the structure table. The certificate should state which mass it confirms: 402.92 g/mol for the 1:1 complex, 340.38 g/mol for free GHK, or a 2:1 form near 743 g/mol. ^[2][6] Our guide on how to read a peptide certificate of analysis explains HPLC traces and mass spectra. The GHK-Cu product page links the certificate for the current batch.

GHK-Cu is a naturally occurring tripeptide bound tightly to copper(II), with well-characterised chemistry and five decades of cell and animal research. The controlled human evidence is small, mostly null and concentrated in one research group. In Australia it is not named in the Poisons Standard, its copper compounds status is unresolved, and WADA's 2026 List does not name it. For a research vial, the batch certificate, read against the right molecular mass, settles what is in the vial.