Peptide / SubQ, Topical / 1-2mg daily
GHK-Cu*
GHK was found in 1973 during a search for whatever in young human plasma kept old liver tissue alive, and turned out to be a copper carrier rather than a growth factor in the ordinary sense. Randomized human testing opened with a negative venous ulcer trial in 1992, produced one positive diabetic ulcer trial in 1994, and then settled into cosmetics; the injected form people buy today never traveled that path at all.
In plain words
GHK-Cu is a very short lab-made peptide, just three amino acids, joined to a copper atom. The same peptide occurs naturally in human blood, where it carries copper, and people buy it hoping it will help skin and wound healing. The human evidence is limited, mixed, and entirely about putting it on the skin: a 1992 randomized trial in leg ulcers found the cream no better than an inert placebo, a 1994 randomized trial in diabetic foot ulcers found faster closure and fewer infections, and a 2006 randomized trial on skin recovering from laser treatment found no objective benefit at 12 weeks. Everything else is cell and animal work. No GHK-Cu drug has ever been approved; it settled into cosmetics instead, and the injected form sold in research-chemical vials today has no published human trial behind it at all, so the dose, the schedule and the expectation of a whole-body effect all come from user reports. One more catch is that a badly proportioned batch leaves copper that is not bound to the peptide, which oxidizes tissue rather than being carried into it, and correctly and incorrectly proportioned material are the same shade of blue.
At a glance
| Half-life | 0.063 days |
|---|---|
| Tmax | 0.02 days |
| Route(s) | SubQ, Topical |
| Published dosing range | 1-2mg daily |
| Vial strengths | 50, 100 mg |
Reference data from the DosePlot canon -- not a protocol recommendation.
Serum curve
Single 1.5 mg dose by SubQ, rendered from the same engine that powers the interactive chart. Relative levels, not lab values.
What does the evidence show?
Two things are labeled separately here because they answer different questions. The tier is how a study was built. The distance chips are whether that study touched this molecule, by this route, in a population resembling the reader. A randomized trial of a different molecule keeps its tier and still says nothing about this compound.
| Finding | Tier | Distance from use | Study |
|---|---|---|---|
| In a randomized, evaluator-blinded, vehicle-controlled multicenter trial, a topical GHK-Cu gel applied daily to freshly debrided diabetic foot ulcers reached 98.5 percent median area closure against 60.8 percent for the vehicle, and infection appeared in 7 percent of treated plantar ulcers against 34 percent of vehicle-treated ones. The benefit required application immediately after the first debridement. | rct | not recorded | Mulder GD et al. Enhanced healing of ulcers in patients with diabetes by topical treatment with glycyl-l-histidyl-l-lysine copper.Wound Repair and Regeneration 2(4):259-269, 1994 |
| In 1992, two years before the diabetic foot ulcer trial, randomized human testing of topical GHK-Cu began with a failure. In a prospective randomized evaluator-blinded trial in venous stasis ulcers, 86 evaluable patients completed treatment with a 0.4 percent tripeptide-copper cream, an inert vehicle placebo, or 1 percent silver sulfadiazine cream. Only the silver sulfadiazine arm reduced ulcer size significantly; the copper-peptide cream and the placebo did not differ from each other. | rct | not recorded | Bishop JB, Phillips LG, Mustoe TA, VanderZee AJ, Wiersema L, Roach DE, Heggers JP, Hill DP Jr, Taylor EL, Robson MC. 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):251-257, 1992 |
| A randomized trial in 13 patients applying topical GHK-Cu after carbon dioxide laser resurfacing found no measurable advantage. Blinded evaluators and computer image analysis showed no difference in how quickly redness resolved, and no difference in wrinkles or overall skin quality at 12 weeks. Only self-reported satisfaction favored the peptide. | rct | not recorded | Miller TR, Wagner JD, Baack BR, Eisbach KJ. Effects of topical copper tripeptide complex on CO2 laser-resurfaced skin.Archives of Facial Plastic Surgery 8(4):252-259, 2006 |
| GHK-Cu raised collagen synthesis in fibroblast cultures across picomolar to nanomolar concentrations, peaking near one nanomolar, with no change in cell number. The effect is on how much each cell makes, not on how many cells there are. | preclinical | not recorded | Maquart FX, Pickart L, Laurent M, Gillery P, Monboisse JC, Borel JP. Stimulation of collagen synthesis in fibroblast cultures by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+.FEBS Letters 238(2):343-346, 1988 |
| Injected into wound chambers implanted in rats, GHK-Cu produced a concentration-dependent rise in dry weight, DNA, total protein, collagen, and glycosaminoglycan content, with collagen synthesis stimulated roughly twice as much as non-collagen protein synthesis. | preclinical | not recorded | Maquart FX et al. In vivo stimulation of connective tissue accumulation by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+ in rat experimental wounds.Journal of Clinical Investigation 92(5):2368-2376, 1993 |
| GHK was singled out by software rather than by a chemist. A Connectivity Map search for compounds predicted to reverse a 127-gene signature of emphysematous lung destruction returned GHK, and treating fibroblasts taken from COPD lungs with it restored their ability to contract and remodel collagen. | preclinical | not recorded | Campbell JD et al. A gene expression signature of emphysema-related lung destruction and its reversal by the tripeptide GHK.Genome Medicine 4(8):67, 2012 |
| Copper-free GHK given by intraperitoneal injection reduced bleomycin-induced lung fibrosis in mice at all three doses tested, lowering inflammatory cell infiltration and interstitial thickening by suppressing TGF-beta1/Smad signaling. The same peptide that raises collagen output in skin fibroblasts reduced fibrotic collagen in lung. | preclinical | not recorded | Zhou XM et al. GHK Peptide Inhibits Bleomycin-Induced Pulmonary Fibrosis in Mice by Suppressing TGFbeta1/Smad-Mediated Epithelial-to-Mesenchymal Transition.Frontiers in Pharmacology 8:904, 2017 |
| Subcutaneous injection at roughly 1 to 2 mg daily is a community practice with no published human trial behind it. Every controlled human study of GHK-Cu applied it to skin. The dose, the schedule, and the expectation of a systemic effect all come from user reports, and users commonly describe transient blue-tinted swelling or stinging at the injection site. | anecdotal | not recorded | community reports aggregated from reddit, MESO-Rx, and similar forumsno study |
How did it get here?
- preclinical1973
- Pickart and Thaler, chasing a factor in human plasma that made old human liver tissue behave like younger tissue, narrow it to three amino acids: glycine, histidine, lysine. Activity at nanogram concentrations is unusual for a molecule that small, and it is unclear at this point why it works.
- preclinical1980
- The peptide keeps arriving with copper and iron attached through every purification step, roughly equimolar copper and about one-fifth molar iron. Work in Nature shows it readily forms complexes with copper(II) and increases uptake of the metal into cultured hepatoma cells, and notes that its copper site resembles the transport sites at the N-terminus of albumin and alpha-fetoprotein. GHK is reclassified as a copper transport peptide. The stoichiometry of the complex in solution is not settled here; that comes in 1982.
- preclinical1988-1993
- A group in Reims shows GHK-Cu drives collagen synthesis in fibroblast culture at picomolar concentrations, and then raises collagen and glycosaminoglycan content inside wound chambers implanted in rats. The compound becomes a serious wound-healing candidate rather than a laboratory curiosity.
- first-human1992-1994
- Randomized human testing happens twice in this window, two years apart, with opposite results. In 1992 a prospective randomized evaluator-blinded trial in venous stasis ulcers finds a 0.4 percent tripeptide-copper cream no better than an inert vehicle placebo across 86 evaluable patients, and behind the 1 percent silver sulfadiazine comparator. In 1994 a randomized, vehicle-controlled multicenter trial of a topical GHK-Cu gel in diabetic foot ulcers reports faster closure and fewer infections. The 1994 result is the high-water mark of the drug program, and nothing better ever follows it.
- clinical-adoption1995-2012
- No approved GHK-Cu drug arrives. The 1994 trial had tested a named commercial wound-care gel, so the drug route was real; it simply stops here. Wider adoption happens through cosmetics instead, where copper peptide becomes a standard over-the-counter cream ingredient sold on the strength of the wound-healing literature. The one later randomized test in people, on skin recovering from laser resurfacing, finds no objective benefit at 12 weeks.
- grey-market2010s-2026
- GHK-Cu reappears as a lyophilized blue powder in research-chemical vials, reconstituted at home and injected under the skin at 1 to 2 mg daily. No published source dates the start of that vial trade, so the decade is the tightest honest boundary. The published human record covers none of it. The topical trials are what gets cited for it, and they tested a different route, a different dose, and a different tissue.
How is it made?
Production happens in three stages.
1. Building the tripeptide. GHK is three amino acids long - glycine, histidine, lysine - which makes it one of the simplest peptides in commercial use. It is assembled by solid-phase synthesis: the lysine is anchored to a resin bead, then histidine and glycine are coupled on in turn. That is two coupling reactions, where a thirty-residue peptide needs twenty-nine, so the crude material is correspondingly cleaner. Histidine and lysine both carry reactive side chains, which are capped with protecting groups during assembly and stripped off with acid at the end.
2. Adding the copper. This is not a synthesis step. The purified peptide is dissolved and mixed with a soluble copper(II) salt at controlled pH, and the metal binds on its own, displacing two protons and turning the solution deep blue. The ratio is the whole job. One copper per peptide is the intended product; anything past that stays behind as free copper, which oxidizes tissue rather than being carried into it.
3. Drying and filling. The solution is sterile-filtered, dispensed into vials, and freeze-dried to a blue cake. Regulated manufacture tests identity, potency, sterility, endotoxins, and free metal content on every batch. Sterile fill and batch testing are what vary outside that setting, and here they carry an extra problem: correctly proportioned material and copper-heavy material are the same shade of blue, so the attribute that matters most is the one nobody can check by eye.
Worth knowing
The molecule in the vial and the molecule in the body are not the same shape. X-ray work on crystalline copper-GHK found a polymer of oxygen-bridged copper pairs. Spectroscopy in solution found something else: a single copper on a single peptide, with one of its nitrogen ligands placed inside the histidine imidazole ring by electron spin-echo measurement. The crystal structure, the authors concluded, does not exist in solution.
Freedman JH, Pickart L, Weinstein B, Mims WB, Peisach J. Structure of the glycyl-L-histidyl-L-lysine-copper(II) complex in solution.Biochemistry 21(19):4540-4544, 1982
Copper is about 16 percent of the complex by mass, 63.5 daltons of metal on a 402-dalton molecule, so a 2 mg dose delivers roughly 0.3 mg of elemental copper. For scale, the adult recommended intake is 0.9 mg per day and the tolerable upper intake level is 10 mg per day. Those are dietary reference values, set for copper that is swallowed and taken up through the gut, so they size the injected load as a mass comparison only and do not define a safe injected amount. The sharper question is unbound copper left over from a badly proportioned batch, because free copper(II) catalyzes oxidation instead of being carried.
Institute of Medicine (US) Panel on Micronutrients. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc.National Academies Press, NCBI Bookshelf NBK222310, 2001
GHK has no gene of its own. The sequence sits inside larger proteins and is thought to be released by proteases when tissue is damaged. One documented source is SPARC, a matrix protein that endothelial cells put out at injury sites: peptides from its cationic region, carrying the sequence KGHK, stimulated new vessel formation in culture and in animals. The same study found copper binding was not required for that particular effect, which is a useful correction to the assumption that the metal is always the active half.
Lane TF, Iruela-Arispe ML, Johnson RS, Sage EH. SPARC is a source of copper-binding peptides that stimulate angiogenesis.Journal of Cell Biology 125(4):929-943, 1994
Reconstitution
GHK-Cu* ships lyophilized and is mixed before use; the published vial strengths are 50, 100 mg. The water volume you add sets the concentration, not the dose -- the calculator turns a vial size and a water volume into mg/mL, draw volume, and units on an insulin syringe.
Open in the reconstitution calculatorWritten and reviewed by Evan Marlow, developer of DosePlot · Updated 2026-08-27
Not medical advice. DosePlot is an informational tool, not a healthcare provider, and using it creates no provider-patient relationship. Do not start, stop, or change any protocol without the approval of a licensed healthcare professional.
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