compound
GHK-Cu
A copper-binding tripeptide that occurs in human plasma, covered claim by claim: what the two randomized human trials found, what the cell and rodent work measured, and where the FDA compounding record now stands.
GHK-Cu is a peptide three amino acids long, glycine then histidine then lysine, holding a single copper(II) ion. The peptide part occurs in human plasma, and it entered the literature in 1973 in a paper reporting that a tripeptide isolated from human serum prolonged the survival of normal liver cells in culture. It has been sold since under two very different labels: as a cosmetic ingredient applied to skin, where its INCI name is copper tripeptide-1, and as a lyophilised powder in a vial intended for injection.
Those two products are the same molecule and two entirely separate evidence questions, which is why this site already carries a page setting the topical and injected routes apart. The literature is lopsided between them. Almost everything published is topical or in a dish. Injection into a body has been done in rodents, five studies of it, and never in a person for any purpose.
This page grades each claim area separately, names the model system on every result, and reports what the two randomized human trials measured and what they found. The reference list runs to 29 numbered sources: 22 primary research papers and reviews with every identifier checked against PubMed, three registry records read in full through the ClinicalTrials.gov API, and four FDA documents fetched from the agency. The regulatory section is current to 8 August 2026 and it has moved twice this year, which most writing about this compound has not caught up with.
| Property | Value | Source |
|---|---|---|
| Category | Copper-binding tripeptide, sold as a topical cosmetic ingredient and as an injectable | PMID 18644225 |
| Also known as | Copper tripeptide-1, glycyl-L-histidyl-L-lysine copper, GHK-Cu(II), copper peptide, tripeptide copper complex | PMID 26236730 |
| Sequence | Gly-His-Lys, bound to a copper(II) ion | PMID 22666519 |
| Molecular formula of the free peptide | C14H24N6O4, giving 340.4 g/mol | PubChem CID 73587 |
| Molecular formula of the complex | Not a single answer. PubChem carries several separate records for the copper complex at different charges and stoichiometries, so a formula quoted for GHK-Cu depends on which record it came from | PubChem CID 139035031 |
| Present in the body | Yes. Plasma GHK was measured at 133.0 plus or minus 54.54 nanograms per millilitre in eleven age-paired healthy adults in a 2023 study, and lower in the nine patients with chronic obstructive pulmonary disease it compared them against | PMID 36905132 |
| Molecular target | Not settled. The most specific published proposal is peroxiredoxin 6, identified as a binding target in a 2024 silicosis study; the mechanism section covers the second candidate and the group both came from | PMID 38879894 |
| Half-life in people | Never measured. No pharmacokinetic study of administered GHK-Cu in a person has been published, on any route | PMID 39795193 |
| Largest completed human trial | The 1992 venous stasis ulcer trial, 86 evaluable patients, in which a tripeptide copper complex cream did not differ from an inert vehicle. The human-record section carries it and the 2006 trial in full | PMID 1495150 |
| Registered trials whose intervention is GHK-Cu itself | 1. A phase 2 split-wound study of a topical gel, recruiting since 2 February 2026, primary completion estimated 14 February 2027. A search returns two further records that are not trials of the compound, and the human-record section reads all three | NCT07437586 |
| FDA 503A, non-injectable routes | In category 1, bulk drug substances under evaluation. Removed on 22 April 2026 when the nominations were withdrawn, then restored after a nominator clarified on 5 May 2026 that it meant to withdraw only the injectable route | FDA 503A list, May 2026 |
| FDA 503A, injectable routes | Previously in category 2, bulk drug substances that raise significant safety risks. The nomination was withdrawn and it now sits in FDA's withdrawn table, with the agency's safety rationale still published beside it | FDA category 2 record |
| Cosmetic status | Sold topically under the INCI name copper tripeptide-1. FDA does not evaluate cosmetic ingredients before they go on sale, and what a seller says a product is for can move it out of that category altogether. The regulatory section sets out both halves | FDA authority over cosmetics |
| Approved drug anywhere | No approved product. A search of FDA's Drugs@FDA dataset for copper tripeptide returned no record on 8 August 2026 | Drugs@FDA |
Not medical advice
This page reports what has been documented about a compound. It is not medical advice, not a diagnosis, not a dosing protocol, and not a recommendation to obtain or use anything described here. Talk to a licensed clinician about anything concerning your health. Read the full disclaimer.
Reviewed against editorial standards Updated
Key takeaways
- GHK-Cu has been through two randomized human trials, in 1992 and 2006, and in neither of them did the copper peptide arm separate from its control on an objective measure. That is unusual in this category: most compounds sold alongside it have never been tested in a person at all. [Human RCT] [1] [2]
- One measure did separate in the 2006 trial, and it was the patients' own questionnaire on overall skin quality, at P equal to .04, in a study whose blinded and computer-assisted assessments found no difference. [Human RCT] [2]
- Neither trial is open access. Everything this page reports from them comes from the published abstract and the indexed record, and the human-record section says so in its own row.
- FDA's compounding position moved twice in 2026 and splits by route: the non-injectable form sits in 503A category 1 under evaluation, while the injectable form was in category 2 for significant safety risks before its nomination was withdrawn.
- FDA states it intends to consult the Pharmacy Compounding Advisory Committee about GHK-Cu before the end of February 2027. The committee's meeting of 23 and 24 July 2026 did not cover it: the seven substances voted on across those two days were BPC-157, KPV, TB-500, MOTS-c, emideltide, epitalon and semax.
- Two ex vivo studies of human skin disagree about whether topical GHK-Cu gets through it. A 2010 diffusion-cell study measured copper crossing dermatomed skin and forming a depot in it; a 2015 microneedle study reports that almost no peptide or copper crossed intact skin without pretreatment. [In-vitro] [3] [5]
- Whether the copper is the active half is not established. Copper-free GHK produced similar effects to the copper complex on keratinocyte stemness, and in two fibroblast studies copper chloride on its own moved the same markers in the same direction as the complex did. [In-vitro] [8] [9] [10]
- The only published animal work using the injected route is a rat knee study, and its difference against saline was gone by twelve weeks once the injections stopped. [Animal] [11]
- The figures repeated most often for this compound, on gene expression and on collagen, come from review articles rather than from trials, and those reviews share a first author who is also the person who described the tripeptide.
- The hair-growth study cited for GHK-Cu does not test it. It tests a two-component complex of 5-aminolevulinic acid and copper-free GHK, with no arm isolating the peptide, and it found no difference in hair length or thickness at six months. [Anecdote] [21]
- SEQUENCE
- Gly-His-Lys
- RANDOMIZED HUMAN TRIALS
- 2
- NUMBERED SOURCES
- 29
- EVIDENCE GRADE
- B
Who researches GHK-Cu?
Readers arrive at this compound from three directions, and the published work speaks to them very unevenly.
The largest group is reading about skin: fine lines, firmness, texture, or recovery after a laser or needling procedure. That is where the human evidence sits, which makes this one of the few compounds in the catalogue where the question a reader arrives with has actually been asked.
The second group is reading about the injected form, usually framed as systemic repair or as an anti-ageing protocol. Nothing in the published record addresses that. There is one rat study using injections into a joint, a set of rodent studies giving the compound into the abdominal cavity for lung and muscle endpoints nobody markets it for, and no human study of any design on any injected route.
The third group arrives from the regulatory question, usually after seeing GHK-Cu described as FDA-cleared or as banned. Neither is right, and the actual record is more interesting than either: it splits by route, it changed twice in 2026, and there is a committee consultation on the calendar.
What is GHK-Cu?
Plain-English version: a chain of three amino acids, glycine then histidine then lysine, wrapped around a single copper ion.
The peptide on its own is glycyl-L-histidyl-L-lysine, written GHK: fourteen carbons, formula C14H24N6O4, 340.4 grams per mole. The histidine in the middle is what makes it interesting chemically, because that side chain binds copper(II) tightly, and the tripeptide plus the ion is what the market calls GHK-Cu or copper tripeptide-1 [20].
It arrived in the literature by accident rather than by design. A 1973 paper in Nature New Biology reported that a tripeptide isolated from human serum prolonged the survival of normal liver cells in culture and stimulated growth in neoplastic liver [28]. Everything sold under this name descends from that observation, which was about liver tissue in a dish and not about skin.
GHK is present in people. A 2023 respiratory study measured it in plasma by reversed-phase high-performance liquid chromatography and reported 133.0 plus or minus 54.54 nanograms per millilitre across eleven age-paired healthy adults, against 70.27 plus or minus 38.87 in the nine patients with chronic obstructive pulmonary disease it compared them with [14]. That endogenous presence is the observation almost all of the marketing rests on, usually in the form of a claim that the level falls with age.
One thing worth knowing before reading any figure attached to this compound: the complex does not have one settled molecular description. PubChem carries several separate records for GHK with copper at different charges and stoichiometries, from a singly charged anion at 400.9 grams per mole to a two-peptide species above 742. A molecular weight quoted for GHK-Cu therefore depends on which record it was taken from, and vendor documents rarely say. It is the same class of identity question FDA raised about the injectable form, and it is answered on a certificate of analysis or not at all.
Gly-His-Lys · C14H24N6O4, 340.4 g/mol for the free peptide
How strong is the evidence, claim by claim?
Every claim area this compound is discussed for gets a row, including the ones with the weakest support. The tier records what the row rests on, and the last column states what that work can and cannot show. Each tier links to its definition on the methodology page.
| Evidence Area | What Has Been Studied | Evidence Level | What It Can and Cannot Show |
|---|---|---|---|
| Wrinkles, firmness and overall skin appearance | One randomized trial in people, published in 2006. Thirteen patients completed. After circumoral carbon dioxide laser resurfacing, patients were randomized to a skin care regimen with or without GHK-Cu, with erythema assessed by computer software and by blinded evaluators, wrinkles and overall skin appearance assessed at twelve weeks, and a validated patient questionnaire completed before treatment and twelve weeks after it [2] | [Human RCT] | Supports the finding that adding GHK-Cu to a post-laser skin regimen produced no measurable difference in erythema, wrinkles or overall skin quality at thirteen patients. The one measure that separated was the patients' own questionnaire on overall skin quality, at P equal to .04, and a patient questionnaire in a study of this size cannot distinguish a difference in the skin from a difference in expectation. Does not settle the question either way at that number of patients. |
| Wound healing and skin repair | One randomized trial in people, published in 1992 and still the largest human study of this compound. Eighty-six evaluable patients with venous stasis ulcers, evaluator-blinded, three arms: silver sulfadiazine 1 percent cream, a tripeptide copper complex 0.4 percent cream, and an inert vehicle placebo. The outcome reported is reduction in ulcer size [1] | [Human RCT] | Supports the finding that a copper tripeptide cream did not differ from an inert vehicle on ulcer size in the largest randomized test this compound has had, while a third arm in the same trial did beat both. Does not establish that the compound is inert: it is one concentration, one formulation and one wound type, thirty-four years ago. The published abstract reports no per-arm numbers and no p-values, and the full text could not be obtained. |
| Joint, ligament and connective tissue repair from the injected form | One rat study, and the only published work delivering GHK-Cu into a joint, which is the closest published route to how the injectable is sold. The four rodent studies further down this table used the abdominal cavity instead. Seventy-two rats had an anterior cruciate ligament reconstructed and were randomized to saline or to one of two GHK-Cu concentrations, with injections into the joint beginning two weeks after surgery and continuing for four weeks. Knee laxity, graft pull-out and histology were measured at six weeks and again at twelve [11] | [Animal] | Supports a smaller side-to-side difference in knee laxity at six weeks in a rat, while treatment was still running, and higher graft stiffness in the lower-concentration group at the same point. Does not show anything in a person, and the authors report that the difference had gone by twelve weeks once injections stopped, with no difference in ultimate load, gait or histology at any point. |
| Lung, airway and muscle work using systemic administration | Four rodent studies from one research group, all giving GHK-Cu into the abdominal cavity. Bleomycin-induced pulmonary fibrosis in mice, measuring collagen deposition and inflammatory markers; crystalline silica-induced silicosis in mice, with peroxiredoxin 6 identified as a binding target; ovalbumin-induced airway remodelling in mice, through sirtuin 1 in airway epithelial cells; and cigarette-smoke-induced skeletal muscle loss in mice, also through sirtuin 1, measuring muscle mass, cross-sectional area and grip strength [12] [13] [14] [15] | [Animal] | Supports a consistent set of anti-inflammatory and anti-fibrotic readouts across four rodent disease models, which is more internal replication than most claims in this category have. Does not show anything in a person, and does not speak to what the compound is sold for: nobody markets GHK-Cu for silicosis, asthma or chronic obstructive pulmonary disease. All four come from one group, so the replication is within a laboratory rather than across laboratories. |
| Longevity and ageing | One study in the nematode Caenorhabditis elegans, published in 2026. GHK-Cu extended lifespan and changed a set of ageing-related measures including resistance to oxidative and thermal stress, movement, pharyngeal pumping and lipofuscin accumulation, with mitochondrial membrane potential and the DAF-16 and SKN-1 pathways proposed as the mechanism [16] | [Animal] | Supports a lifespan extension in a millimetre-long worm with about a thousand cells and a three-week life. Does not show anything about ageing in a mammal, let alone a person. Lifespan extension in this organism has been reported for a very long list of compounds and it is a screening result rather than a finding about people. |
| Collagen and connective tissue building | Cell culture in normal human fibroblasts. The most specific measurement is a 1992 study of glycosaminoglycan synthesis: GHK-Cu produced a dose-dependent increase that peaked between one nanomolar and ten nanomolar and fell back towards control at higher concentrations, preferentially raising extracellular dermatan sulfate and cell-layer heparan sulfate, with no influence on hyaluronic acid observed. The collagen figures that circulate are summarised in review articles rather than measured in them [7] [18] [20] | [In-vitro] | Supports a concentration-dependent change in what cultured human fibroblasts secrete, with a peak at a concentration the experimenters chose and a fall-off above it. Does not show a change in collagen in living skin, and no human study has measured one. The response is biphasic, which means more is not more, and no published work establishes what concentration living dermis reaches. |
| Whether topical GHK-Cu reaches living skin | Four laboratory studies, none of them in a living person. Two used real human skin removed from a body and reached opposite conclusions: a 2010 flow-through diffusion-cell study across isolated stratum corneum, heat-separated epidermis and dermatomed skin, measuring copper by mass spectrometry over 48 hours, and a 2015 study whose untreated-skin condition was the control arm of a microneedle experiment run over nine hours. A 2008 study used a liposome membrane standing in for the horny layer rather than skin at all, and a 2025 review examined whether the measurement methods themselves are ready. The figures each one reports are in the benefits section [3] [4] [5] [6] | [In-vitro] | Supports the conclusion that this is an open question rather than a settled one, and that a technique which breaches the barrier changes the answer. Does not show what happens in living skin with a circulation underneath it: every one of these is ex vivo human tissue or a synthetic membrane, and a reader taking either number as an in-vivo result has been misled. Both cannot be right about intact skin, and no published work reconciles them. |
| Gene expression, ageing and the percentage figures | Review articles. The claim that GHK influences a large share of human genes traces to a 2014 review titled GHK and DNA: resetting the human genome to health, and the collagen and skin-regeneration figures to a 2015 review from the same authors, with a 2012 review covering oxidative stress and conditions of ageing. The underlying measurements those reviews summarise are gene-expression and cell-culture work, not clinical endpoints [17] [18] [19] | [In-vitro] | Supports the statement that these figures exist and where they come from. Does not show an effect in a person, because a review is a summary of other work rather than a new measurement, and gene-expression modelling in cells is several steps from an outcome anyone can see. Read the percentage as a property of a dataset, not as a property of skin. |
| Skin inflammation and redness | Two studies in normal human dermal fibroblasts from the same laboratory. The first measured interleukin-6 secretion driven by tumour necrosis factor alpha and reported that GHK, GHK-Cu, copper chloride and a copper ferment preparation all lowered it. The second, at one nanomolar, measured transforming growth factor beta-1 secretion driven by insulin-like growth factor 2, and reported that GHK, its copper complex and free copper ions all lowered that too [8] [9] | [In-vitro] | Supports a change in two inflammatory signals released by cultured human skin cells. Does not show anything about redness on a person, and the 2006 trial is the only work that measured that and found no difference. Neither study isolates the peptide, because copper chloride alone moved the same markers in the same direction in both. |
| Hair growth and hair loss | Vendor product pages and community writing, where the claim is that GHK-Cu matches or approaches an approved hair-loss drug. No published study tests GHK-Cu for hair growth. The paper cited for it is a 2016 randomized trial in 45 men, and its intervention is a two-component complex of 5-aminolevulinic acid and copper-free GHK at two concentrations against placebo [21] | [Anecdote] | Records what is being claimed and names the nearest published study. Shows nothing about GHK-Cu, because that trial has no arm isolating the peptide, no copper in the peptide it used, no significant difference in hair length or thickness among the three groups at six months, and a dose response that runs backwards, since the lower concentration produced the larger hair-count increase. |
Rolled up, that puts GHK-Cu at evidence grade B Human data, endpoint missed . Human evidence for the marketed use has read out, and it did not separate from control: all 2 randomized trials that tested it missed the primary endpoint. The grade describes how much and how good the research is, not which way it came out, so a compound that has been tested and beaten grades above one nobody has tested at all. A grade describes the quality of the research, not whether something works and not whether anyone should use it. The derivation is published.
How GHK-Cu is thought to work
Mechanism work on GHK-Cu falls into two questions that get answered as though they were one. What the molecule does to cells has a long literature going back to the 1970s. What it binds to in order to do it has two candidate answers, both recent, both from the same research group, and neither confirmed elsewhere. A third question sits under both of them and is rarely asked out loud: whether the copper is the part doing the work.
1. Changing what dermal fibroblasts secrete, altering the mix of building material the cells in skin release (the oldest and best-replicated readout)
Fibroblasts are the cells in the dermis that manufacture the scaffolding skin is built from: collagen, and a family of sugars called glycosaminoglycans that hold water in the tissue. The clearest single measurement of what GHK-Cu does to them is from 1992. Normal human fibroblasts were incubated with radiolabelled glucosamine and sulfate, and GHK-Cu produced a dose-dependent rise in the glycosaminoglycans they secreted [7].
The shape of that response matters more than the fact of it. Stimulation peaked between one and ten nanomolar and then fell back towards control as the concentration rose, so the curve is biphasic rather than a ladder. The rise was also selective: extracellular dermatan sulfate and cell-layer heparan sulfate went up, and the authors report that no influence on hyaluronic acid was observed [7].
Two later studies measured signalling rather than structure, in the same cell type. Interleukin-6 released in response to tumour necrosis factor alpha fell under GHK, under GHK-Cu and under copper chloride [8]. Transforming growth factor beta-1 released in response to insulin-like growth factor 2 fell under the same three [9]. [In-vitro] [7] [8] [9]
Our takeThree decades apart, in the same cell type, pointing the same way. The biphasic curve is the part that should travel further than it does, because it means a higher concentration is not a stronger version of the same result.
2. Whether the copper is the active half, the question the name of the compound assumes has been answered (unresolved, and the evidence cuts against the assumption)
The product is sold as a copper peptide, and the implication is that the pairing is what produces the activity. Three published results make that harder to hold.
A 2012 study set copper-free GHK against the copper complex in cultured human keratinocytes and in skin-equivalent models. Copper-free GHK raised keratinocyte proliferation, made basal cells more cuboidal, produced linear and intense integrin staining along the basement membrane, and raised the count of p63-positive and proliferating-cell-nuclear-antigen-positive cells. The authors' own conclusion is that copper-free GHK showed similar effects to copper-GHK [10].
In both fibroblast studies above, copper chloride on its own moved the same markers in the same direction as the complex did [8] [9]. And the 2016 hair trial, which is the study most often cited for GHK-Cu, names its peptide as glycyl-histidyl-lysine and mentions copper nowhere [21]. [In-vitro] [8] [9] [10]
Our takeThree results, three systems, one direction: the peptide without copper and the copper without the peptide each reproduce part of what the complex does. Nothing published settles which half is carrying the result, and the name of the product asserts an answer the literature has not given.
3. Binding to sirtuin 1, a protein cells use to switch other proteins on and off (two studies, one research group)
Sirtuin 1 removes acetyl groups from other proteins, which changes what those proteins do. Two 2023 papers put GHK-Cu on it directly.
In cigarette-smoke-exposed mice, GHK-Cu bound and activated sirtuin 1 with a computed binding energy of minus 6.1 kilocalories per mole, and the muscle effects were reported as sirtuin-1-dependent. Downstream, the authors describe inhibition of FoxO3a transcriptional activity, deacetylation of Nrf2, and raised PGC-1 alpha expression [14].
In ovalbumin-challenged mice, the same target was proposed in airway epithelial cells, with the reduction in transforming growth factor beta-1 attributed to sirtuin 1 activation [15]. [Animal] [14] [15]
Our takeA specific, testable target with two papers behind it, both from the same group and both in mice. It is the strongest mechanistic proposal this compound has, and it has never been checked by anyone else.
4. Binding to peroxiredoxin 6, an enzyme cells use to mop up oxidative damage (one study)
A 2024 silicosis paper from the same group identified peroxiredoxin 6 as a molecular target, reported that GHK-Cu binds it, and attributed the reduction in lung inflammation and fibrosis partly to suppression of silica-induced oxidative stress in alveolar macrophages [12].
Two proposed targets from one laboratory, in two different tissues, are not necessarily in conflict: a small molecule can bind more than one protein. What they do not yet amount to is a settled answer, and no independent group has tested either. [Animal] [12]
Our takeWorth watching rather than repeating. A target identified in the same laboratory that reports the effect is the beginning of a mechanism story, not the end of one.
What we do not know
The two ex vivo permeation results on human skin disagree with each other and nobody has reconciled them [3] [5]. That is the single most consequential gap on this page, because almost every product built on this molecule is applied to intact skin.
No pharmacokinetic measurement of administered GHK-Cu exists in a person on any route: no half-life, no clearance, no bioavailability figure. A 2025 review states plainly that the methods for measuring skin transport of liposome-encapsulated GHK-Cu are still being developed [6], and the injected route has no measurement of any kind.
The copper question above is open in both directions. Nothing published establishes that the complex outperforms the free peptide, and nothing establishes that it does not.
The two proposed molecular targets come from one research group, and the four rodent disease studies behind them come from that same group [12] [13] [14] [15]. Concentration of authorship is a quality signal this site reports on every compound, and it is not an accusation: a group that builds an assay keeps using it, and small fields are small.
Whether the endogenous plasma level has anything to do with what a product does is unmeasured. Two of those studies report lower plasma GHK in patients with a lung condition [14] [15]. An association between a measured level and a disease is not evidence that adding more of it changes the disease, and no trial has tested that step.
What this evidence can and cannot show
These results come from mice, rats and nematodes in reconstructed knee ligaments, chemically induced lung fibrosis and airway remodelling, smoke-induced muscle loss, and cultured human skin cells, not from people. An animal model is a deliberate simplification: the injury is created on purpose, the animal is young and healthy, the dose is scaled to body weight in a way that does not translate directly, and the outcome is measured at a fixed point rather than lived with. Cell and tissue work is a further step removed, because the concentrations that produce an effect in a dish are often far above anything a body reaches. Mechanism is a reason to run a trial. It is not a substitute for one, and compounds that looked mechanistically convincing have failed in people many times.
Has GHK-Cu been tested in humans?
Two randomized controlled trials of GHK-Cu in people have been published, thirty-four and twenty years ago. Both are topical. Both are in the table below with what they measured and what they found.
The table also carries the three registry records that a search for this compound returns, because only one of them is a trial of the compound itself, and the last row records a limit on this page's own sourcing that a reader is entitled to know about.
| Study | People | What was done | Result | Evidence level |
|---|---|---|---|---|
| Bishop 1992, venous stasis ulcers [1] | 86 evaluable | Prospective, randomized, evaluator-blinded, three arms: silver sulfadiazine 1 percent cream, a tripeptide copper complex 0.4 percent cream, and an inert vehicle placebo. Ulcer size was the reported outcome | Silver sulfadiazine reduced ulcer size against both other arms. In the authors' words, there was no difference between the latter two treatments, meaning the copper tripeptide cream and the inert vehicle. The report predates the convention of naming one endpoint the primary, so ulcer size is simply the outcome it reports, and the abstract gives no per-arm numbers and no p-values | [Human RCT] |
| Miller 2006, after CO2 laser resurfacing [2] | 13 completed | Randomized to a post-treatment skin care regimen with or without GHK-Cu after circumoral carbon dioxide laser resurfacing. Erythema assessed by computer software and by blinded evaluators through the post-treatment period; wrinkles and overall skin appearance assessed at twelve weeks; a validated questionnaire completed by patients before treatment and twelve weeks after | No statistically significant difference between groups in resolution of erythema, on either the computer analysis or the blinded evaluators. All patients improved in wrinkles and skin quality, with no difference between groups. The patient questionnaire showed a significant difference in improvement of overall skin quality for the GHK-Cu group, at P equal to .04 | [Human RCT] |
| Lee 2016, hair growth. NOT a study of GHK-Cu [21] | 45 randomized | Three arms over six months in male pattern hair loss, testing a two-component complex of 5-aminolevulinic acid and glycyl-histidyl-lysine at two concentrations against placebo. The abstract names that peptide as glycyl-histidyl-lysine and mentions copper in neither direction, so on the published record it is the free peptide rather than the copper complex. No arm isolates it from the 5-aminolevulinic acid | Hair count rose in both active arms and the lower-concentration arm was the one that separated from placebo, which is a dose response running backwards. No significant difference in hair length or hair thickness among the three groups at six months. This row is in the table because the study is cited for GHK-Cu constantly. The tier beside it records what that trial was, which is a randomized trial of something else: a different molecule inside a two-component product. Nothing in it reaches this compound's claim set or its grade | [Human RCT] |
| NCT07437586, registered phase 2 [22] | 60 estimated | Randomized, double-blind, vehicle-controlled, quadruple-masked split-wound study of a topical GHK-Cu gel on standardized acute wounds in healthy adults. Each participant receives two wounds, one randomized to the gel and one to vehicle. Sponsor Hudson Biotech | Recruiting. Actual start 2 February 2026, primary completion estimated 14 February 2027, study completion estimated 17 March 2028. The primary outcome is time to complete re-epithelialization of each wound. No results posted. This is the only registered study whose intervention is GHK-Cu itself, against a vehicle that differs from it in nothing else. Read the registration itself before weighing it: the record was first submitted 22 February 2026 and first posted on the 27th, which is after the start date it reports, and it has not been updated since. Its single site is Peking University Shenzhen Hospital; both listed contacts use an email domain that does not match the sponsor name; the oversight block records the study as not FDA-regulated; and two of its intervention and arm strings are truncated mid-word | not a claim about effect |
| NCT05932732, the trial usually miscounted [23] | 27 | Phase 4, open-label, single-group study of three facial device treatments 28 days apart, in adults of Fitzpatrick skin types I to VI. Three registered interventions: two device systems, and a booster serum applied through the device handpiece during every treatment, to every participant. That serum is a drug intervention and its registered description does name the compound, in a list of ingredients that also includes a heptapeptide | Completed 9 October 2024, no results posted. This record is why a free-text search returns a phase 4 trial for GHK-Cu, and it is worth being precise about rather than dismissing. It did put the compound on 27 people. What it cannot do is say anything about the compound, because it is open-label, has no control arm, gave the serum to everyone, and delivered it alongside two devices and at least one other active ingredient. Nothing in it separates GHK-Cu from any of that | not a claim about effect |
| NCT07706361, measurement rather than intervention [29] | 100 estimated | Two-part study of a wearable patch, part one single-arm and open-label, part two randomized and placebo-controlled. The interventions are the patch and a placebo patch | Not yet recruiting, estimated start January 2027. Its four primary outcomes are changes in circulating GHK and GHK-Cu levels from baseline to day 8. GHK-Cu is what is being measured here, not what is being given | not a claim about effect |
| Full-text access for the two trials, checked 8 August 2026 | Not applicable | PubMed Central, Europe PMC, OpenAlex, Semantic Scholar, and the publishers' own sites at the registered DOI for both papers | Neither trial is open access anywhere, and both publishers refused an unauthenticated request. Everything this page reports from 1992 and 2006 therefore comes from the published abstract and the indexed record. Where an abstract does not give a number, this page does not give one either, which is why no per-arm figures appear for the 1992 trial | not a claim about effect |
Why we are not calling this proof
Two randomized trials against a control is more human testing than most compounds in this catalog have ever had, and it is worth being exact about what that buys and what it does not.
It buys a real answer to a narrow question, twice. A copper tripeptide cream at one concentration did not shrink venous stasis ulcers faster than an inert vehicle, in a trial where a third arm did. A GHK-Cu skin regimen did not clear post-laser redness faster than the same regimen without it, and did not change wrinkles or skin quality on any assessment an evaluator made. Neither of those is a verdict on the molecule. They are results for one formulation, one concentration and one clinical situation each.
It does not buy an answer about anything else this compound is sold for. Nothing in the human record touches the injected route, the anti-ageing framing, hair, or systemic repair. The 2006 trial ran to thirteen patients, which is small enough that it could miss a real difference as easily as it could report a false one.
One word in the grade explanation above needs its own line, because the two trials do not use the term the same way. The 2006 report names its objective outcomes and its questionnaire separately, so calling the objective ones its primary endpoints is fair. The 1992 report predates that convention and simply reports ulcer size. The grade explanation says both trials missed their primary endpoint, and what that means precisely, for both of them, is that the arm receiving the copper peptide did not differ from its control on the outcome the trial reported.
The FTC sets the substantiation bar for a health claim at randomized controlled human trials and says animal work, laboratory work and observational data are generally not enough on their own. GHK-Cu has two of the first, and both came back the same way on their objective measures. That is the whole human picture, and the recruiting phase 2 is the first registered study capable of changing it.
That trial deserves the same reading this page gives the older literature, because a registration is a document like any other and this one has features worth knowing. It is sponsored by Hudson Biotech, runs at a single site, Peking University Shenzhen Hospital, and lists both of its contacts at an email domain that does not match the sponsor's name. Its oversight block records it as not FDA-regulated. It was first submitted on 22 February 2026 and first posted five days later, which is after the start date it reports, and nothing in the record has been updated since. Two of its intervention and arm strings are cut off mid-word. None of that says the trial is not running or that its result will not count. It does say that the strongest thing on this page's horizon rests on one unamended registration at one site, and a reader weighing it is entitled to that before February 2027 rather than after.
Benefits: what the research shows
Each heading below is a claim people make about GHK-Cu, not a finding. Under each one is what was measured, in what, and by whom.
Four review articles cover most of this ground and are worth naming, because they are frequently cited as though they contained data of their own [17] [18] [19] [20]. They summarise cell and animal work. None of them adds a human result.
Wrinkles, firmness and overall skin appearance
This is the claim the market is built on, and it is one of the very few in this category with a randomized human trial behind it. The trial is in the matrix above. What the matrix cannot hold is the shape of the disagreement inside it, and that shape is the interesting part.
Three assessment routes were used. Computer software measured erythema. Blinded evaluators assessed erythema, wrinkles and overall skin appearance. Patients filled in a validated questionnaire before treatment and twelve weeks after. The first two found nothing. The third found a significant difference in improvement of overall skin quality for the patients using GHK-Cu, at P equal to .04 [2].
The authors' own conclusion states both halves: objective evaluation found no significant improvement in wrinkles or overall skin quality, and patient satisfaction was significantly higher. Reporting only one of those halves misrepresents the paper, and both directions of that error are common in writing about this compound. [Human RCT] [2]
Our takeA patient-reported difference with no assessor-measured difference behind it, at thirteen patients. It is a real result and it is the weakest kind of real result, because a questionnaire cannot separate a change in skin from a change in expectation.
Wound healing and skin repair
The 1992 trial is the largest human test this compound has ever had and it is almost never cited on the pages that rank for it. Its design is in the matrix above. What the matrix cannot hold is the reason the result is harder to set aside than a bare null would be, and that reason is the third arm.
Silver sulfadiazine, in the same trial, in the same patients, on the same measure, did reduce ulcer size against both the copper tripeptide arm and the placebo [1]. So this was not a trial too blunt to detect anything. It detected a difference, and the difference was somewhere else. The wounds themselves are also worth a line: venous stasis ulcers are chronic, they arise from a circulation problem in the leg, and the authors record a recurrence rate approaching seventy percent even after successful treatment.
What it does not establish is that GHK-Cu does nothing for a wound. It tested one concentration of one formulation in one wound type, in 1992, and venous stasis ulcers are a hard problem with a vascular cause that a topical peptide would have to work around rather than through. The recruiting phase 2 is testing a different question entirely: standardized acute punch-biopsy wounds in healthy adults, with each participant acting as their own control [22]. [Human RCT] [1]
Our takeA negative result with a positive control inside the same trial is worth more than most positive results in this category. It is also thirty-four years old and narrow, and treating it as a verdict on the molecule would be the same error in the other direction.
Collagen and connective tissue
The percentage figures attached to this claim come from reviews. The measurement underneath them is cell culture, and the clearest one is the 1992 glycosaminoglycan study in the matrix above [7].
Two features of that study deserve to travel with the claim and rarely do. The response peaked between one and ten nanomolar and fell back towards control above it, so the relationship between concentration and effect is an arch, not a ramp. And the rise was selective rather than general: dermatan sulfate and heparan sulfate rose, and no influence on hyaluronic acid was observed [7].
No human study has measured collagen or glycosaminoglycan content in skin after GHK-Cu. The 2006 trial measured what a person and an evaluator could see, which is the closer question for a cosmetic claim, and found no assessor-measured difference [2]. [In-vitro] [7] [18] [20]
Our takeReal laboratory work with a specific shape that gets flattened into a percentage on the way to a product page. The biphasic curve is the detail worth keeping.
Whether topical GHK-Cu gets anywhere
Two studies used real human skin and they do not agree. Both are ex vivo, meaning skin removed from a body and mounted in an apparatus, with no circulation underneath it.
The 2010 study mounted isolated stratum corneum, heat-separated epidermis and dermatomed skin in flow-through diffusion cells under infinite dose conditions and measured copper by inductively coupled plasma mass spectrometry. Copper applied as the tripeptide permeated dermatomed skin at 2.43 plus or minus 0.51 times ten to the minus four centimetres per hour, with 136.2 plus or minus 17.5 micrograms per square centimetre crossing over 48 hours and 82 plus or minus 8.1 retained in the tissue as a depot. The authors concluded that the amounts were potentially relevant to treating inflammatory disease [3].
The 2015 study reports the opposite for intact skin. Its purpose was to test whether a polymeric microneedle array improves delivery, and its baseline finding is that almost no peptide and almost no copper crossed untreated human skin, against 134 plus or minus 12 nanomoles of peptide and 705 plus or minus 84 nanomoles of copper across microneedle-treated skin in nine hours [5].
The differences between the two are the obvious place to look: one measured copper by mass spectrometry under infinite dose over 48 hours, the other measured peptide and copper over nine hours as the control condition in a device study. Neither paper addresses the other, and a 2025 review of this exact measurement problem concludes that the methods for assessing GHK-Cu transport through skin are still being worked out and that liposome-encapsulated GHK-Cu has received little attention [6]. A 2008 study often cited alongside these used a liposome membrane standing in for the horny layer rather than skin at all [4]. [In-vitro] [3] [4] [5] [6]
Our takeThe most important unresolved question about this compound, and one that a reader is entitled to have flagged rather than tidied away. Anyone quoting either number as proof that copper peptides do or do not cross skin is quoting one ex vivo result and ignoring the other.
Skin inflammation and redness
Two fibroblast studies from one laboratory measured inflammatory signalling, and both reported that GHK-Cu lowered it [8] [9]. What both also report, and what the claim never carries, is that free copper chloride lowered the same signals in the same experiments.
The 2006 trial is the only work that measured redness on a person, in the situation where redness is most reliably present, which is skin immediately after laser resurfacing. Neither the computer analysis nor the blinded evaluators found a difference [2]. [In-vitro] [8] [9]
Our takeA cell result and a human result pointing in different directions on the same claim area, with the human one carrying more weight and getting cited less.
Gene expression, and where the percentages come from
Every page ranking for this compound carries a version of the same figure: that GHK influences some large percentage of human genes, or resets gene expression. It traces to a 2014 review whose title is GHK and DNA: resetting the human genome to health [17], and to a 2015 review from the same authors [18].
Two facts about those sources belong beside the figure. They are review articles, so the number summarises other people's measurements rather than reporting a new one, and the measurements summarised are gene-expression work in cells rather than clinical endpoints. And the reviews share a first author, who is the same person named first on the 1973 paper that introduced this tripeptide [28], writing from a company research and development department. That is a statement about a paper's authorship, and it is checkable on the papers themselves.
None of that makes the underlying work wrong. It does mean the figure most repeated about this compound has never been measured in a person, and that the sources it comes from are a summary written by the people closest to the subject. [In-vitro] [17] [18] [19]
Our takeA number describing a dataset, quoted as if it described skin. Trace any percentage in this category back to what was measured and in what, and most of them shorten dramatically.
Joint and ligament repair, and the injected form
The injected form is sold for connective tissue and joint recovery, and there is exactly one published study using that route in any species. Seventy-two rats, anterior cruciate ligament reconstruction, randomized to saline or one of two GHK-Cu concentrations, with injections into the joint starting two weeks after surgery and running for four weeks [11].
The result is genuinely mixed and the timing is the whole story. At six weeks, while treatment was still running, the treated groups had a smaller side-to-side difference in knee laxity than saline, and the lower-concentration group had higher graft stiffness. At twelve weeks, after treatment had stopped, no difference remained. Across both time points there was no significant difference in ultimate load, in gait parameters or in histological scores, and every graft failed mid-substance in the pull-out test [11].
The authors' own summary is that the beneficial effects could not last as treatment discontinued. No study has given GHK-Cu by injection to a person for any purpose. [Animal] [11]
Our takeOne rat study, cited for the first half of its result. The second half, that the difference disappeared once injections stopped, is in the same abstract and it is the more useful half.
The lung, airway and muscle studies, and why they are not the marketed claim
The largest recent body of work on this compound has nothing to do with skin. Four rodent studies gave GHK-Cu into the abdominal cavity and measured lung and muscle endpoints: bleomycin-induced pulmonary fibrosis [13], crystalline silica-induced silicosis [12], ovalbumin-induced airway remodelling [15], and cigarette-smoke-induced skeletal muscle loss [14].
Read as a set they are the most internally consistent thing in the file: anti-inflammatory and anti-fibrotic readouts across four different injuries, with two proposed molecular targets and mechanism work behind each. Read as evidence for what the compound is sold for they are close to irrelevant, because nobody markets GHK-Cu for silicosis, asthma or chronic obstructive pulmonary disease.
Two of the four also carry human measurements, and they are worth stating precisely because they are easy to over-read. Both report lower plasma GHK in patients with a lung condition than in healthy controls, at nine and eleven patients in the muscle study [14] [15]. Those are observations of the level people already have. Neither gave anything to a person. [Animal] [12] [13] [14] [15]
Our takeThe strongest preclinical work on this compound is in tissues and diseases nobody sells it for, and it comes from a single research group. Both halves of that sentence matter.
Longevity
A 2026 study reported that GHK-Cu extended lifespan in the nematode Caenorhabditis elegans and improved a set of ageing-related measures, with mitochondrial function and the DAF-16 and SKN-1 pathways proposed as the route [16].
C. elegans is the standard first screen in ageing research: it is transparent, it has about a thousand cells, and it lives around three weeks, which makes a lifespan experiment cheap. A very long list of compounds extends its lifespan and almost none of them has gone on to show anything in a mammal. [Animal] [16]
Our takeA screening result reported as a screening result by its authors, and repeated elsewhere as an anti-ageing finding. The distance between those two readings is the whole of the claim.
Hair growth
The hair claim is the clearest case in this file of a study being counted for a compound it does not test. The 2016 trial randomized 45 men with pattern hair loss across three arms for six months, and its intervention is a complex of 5-aminolevulinic acid and glycyl-histidyl-lysine [21].
Two things disqualify it as evidence about GHK-Cu, and either would be enough on its own. The abstract names the peptide as glycyl-histidyl-lysine and never mentions copper in any direction, so on the published record it is the free peptide rather than the copper complex, and that is an inference from what the paper says rather than a statement the paper makes. And the product has two components with no arm isolating either, so nothing in the trial separates the peptide's contribution from the 5-aminolevulinic acid's.
The result inside it is also less supportive than the citation implies. Hair count rose in both active arms, but hair length and hair thickness showed no significant difference among the three groups at six months, and the between-group significance against placebo belonged to the lower of the two concentrations rather than the higher [21].
No published study tests GHK-Cu for hair growth in a person. The comparison to an approved hair-loss drug that circulates for this compound has no source behind it that this site could find. [Anecdote] [21]
Our takeA different molecule, inside a two-component product, with a dose response running backwards, cited as though it settled the question. It is the single most misused reference in this compound's literature.
The honest bottom line on benefits
What the two trials leave is a narrow answer rather than a verdict, and the narrowness runs both ways. Most writing about this compound avoids the result entirely; a smaller amount treats it as proof the molecule is inert. Neither reading survives contact with what was actually tested, which was one cream in one chronic wound and one regimen after one procedure.
There is a second thing to say, and it cuts the other way from how counts usually get used. The preclinical file is not as independent as its length suggests. Four of the rodent studies and both proposed molecular targets come from one research group [12] [13] [14] [15]. Two of the three fibroblast studies come from a second [8] [9]. The four reviews that carry the most-repeated figures share a first author [17] [18] [19] [20]. A reader weighing a long reference list should know that it represents fewer independent lines of work than the number of entries implies.
Set against that, the thing this compound has that its shelf-mates do not is a live, registered, vehicle-controlled trial of the topical form with a real primary outcome and a date on it [22]. Between February 2027 and whatever FDA does after its advisory committee consultation, the record on this page is likely to look different within about eighteen months.
What anyone does with that is a judgement rather than a fact, and it belongs to the reader. This site reports what has been documented. It does not prescribe what should be done.
How long GHK-Cu stays in the body
Two different quantities get discussed under this heading and only one of them has ever been measured. The first is the level a person already carries, which is the plasma figure in the opening section [14]. It is a baseline, and it says nothing about what a product delivers.
The second is what an administered amount does once it is in, and that has no published measurement in any species: no half-life, no clearance figure, no bioavailability figure. Any such number in circulation therefore came from somewhere other than a measurement of this compound, and the most likely source is arithmetic on the first quantity.
For the topical route, the closest thing to a measurement is the pair of contradictory ex vivo permeation studies above [3] [5], and a 2025 review whose conclusion is that the analytical methods for answering this question are still being developed [6]. For the injected route there is nothing at all: the one animal study using injections into a joint measured outcomes rather than exposure [11].
No half-life, clearance or bioavailability figure has been reported for administered GHK-Cu in any species. What exists instead is a measurement of the level people already carry in plasma, and two ex vivo skin-permeation results that disagree with each other. [In-vitro] [3] [5] [6] [14]
What is documented about dosing
No study has established an amount of GHK-Cu for a person, so there is no dosing section on this site in the sense other properties use the phrase. What can be reported is what published studies used, in the model they used, and what kind of figures circulate elsewhere.
Commonly cited protocols (extrapolated, not validated)
Nothing here is a dosing recommendation. Statements about dosing reflect community and research reports only.
| Study | What was given | Frequency | Duration | Notes |
|---|---|---|---|---|
| Human venous stasis ulcers, topical. Bishop 1992 [1] | A tripeptide copper complex cream at 0.4 percent, against silver sulfadiazine 1 percent cream and an inert vehicle placebo | Not stated in the abstract | Not stated in the abstract | The largest human study of this compound. The paper is not open access, so nothing beyond the concentrations is available to report |
| Human skin after CO2 laser resurfacing, topical. Miller 2006 [2] | A commercial skin care regimen containing GHK-Cu, against the same regimen without it. No concentration is given in the abstract | Not stated in the abstract | Assessments ran to twelve weeks | Thirteen patients completed. A regimen is a product rather than a substance, so even a stated concentration would not have been a figure for the peptide alone |
| Rat knee, injection into the joint. Fu 2015 [11] | 0.3 or 3 mg per millilitre GHK-Cu in solution, against saline | Once a week, beginning two weeks after surgery | Four weeks of treatment, with harvest at six and at twelve weeks | Seventy-two rats, and the only published work on this compound using an injected route in any species |
| Mouse lung fibrosis, into the abdominal cavity. Ma 2020 [13] | 0.2, 2 and 20 micrograms per gram of body weight in phosphate-buffered saline | On alternate days | Through the bleomycin fibrosis model | A body-weight-scaled amount in a mouse. Scaling between species is unreliable even for two mammals on the same route, and this route is not one anyone markets |
| Mouse skeletal muscle, into the abdominal cavity. Deng 2023 [14] | 0.2 and 2 mg per kilogram of body weight | Per the study protocol | Through the cigarette-smoke exposure period | The companion muscle study to the lung work, from the same group and on the same route |
| Human fibroblasts and keratinocytes, in culture. Wegrowski 1992, Gruchlik 2012 and 2014, Choi 2012 [7] [8] [9] [10] | Culture concentrations chosen by the experimenter, from one nanomolar upwards | Single treatment per assay | Per the assay | Cells in a dish. A culture concentration is not an amount for a body and does not convert into one, and the 1992 response was biphasic, peaking between one and ten nanomolar and falling back above it |
| Registered phase 2, topical gel. NCT07437586 [22] | The registered protocol states a concentration and an amount. This page does not reproduce them | The registered protocol states a schedule. This page does not reproduce it | Primary completion estimated 14 February 2027 | A trial protocol is a set of instructions for investigators. Reprinting one here would supply an instruction to a reader, which is the thing this site exists not to do |
| Community write-ups and vendor pages | Figures circulate. This site does not republish them | Figures circulate | Figures circulate | No trial established an amount for a person, so any figure in circulation is an extrapolation from an animal study, a copy of a product label, or has no origin at all |
Two things in that table are worth pulling out. The first is that the human trials tested products rather than substances: a cream and a skin care regimen, each with a formulation that shapes what reaches skin as much as the peptide concentration does.
The second is that the culture work has a shape that a single number destroys. The 1992 glycosaminoglycan response peaked between one and ten nanomolar and returned towards control above it [7], so a higher concentration is not a stronger version of the same result, and no published work establishes what concentration living skin reaches under any product.
Main routes people compare, and what each source class actually reported, are set out on the documented protocols page.
Reported effects and what has been measured
What the two human trials report
Both randomized trials were conducted in patients and both completed, at 86 evaluable and 13 completed respectively [1] [2]. Neither abstract reports a safety or tolerability endpoint, and neither paper is open access, so this page cannot say what either study recorded on that question.
That is a gap in what can be read rather than a finding in either direction. An abstract omitting safety is not a study reporting none, and this site does not convert one into the other. [Human RCT] [1] [2]
What FDA has said about the injected form
The one agency statement that addresses harm rather than paperwork is FDA's rationale for putting the injectable form in category 2. In the agency's own words: compounded injectable drugs containing GHK-Cu may pose risk for immunogenicity due to the potential for aggregation and peptide-related impurities, and there are limited data in humans to inform safety-related considerations. The regulatory table below carries the same finding with its document and date.
Two precisions matter and both are routinely lost. That statement is about injectable routes and nothing else, so it says nothing about a cream. And a risk the agency calls potential is one it has not ruled out, not a harm it has documented. Those are the two opposite ways this sentence gets misread.
Aggregation is worth a plain-language line, because it is the mechanism behind the concern. Peptide molecules can clump together into larger particles, and an immune system is more likely to react to a clump than to a single small molecule. FDA raises it here as an unassessed possibility rather than as something measured in this compound.
What the toxicology record contains
What the record holds on toxicology is a pair of remarks made inside efficacy studies. The 2024 silicosis paper states that GHK-Cu attenuated lung inflammation and fibrosis in mice without significant systemic toxicity [12]. The rat knee study's abstract does not mention adverse findings either way, in an experiment designed to measure ligament healing rather than harm [11].
An observation made in passing in a study built to measure something else is not a toxicology result. A compound with a clean fourteen-day rodent toxicology study has a measurement behind it. This one has remarks.
The formal package that would carry those measurements was not located for this page under this compound's name: no acute study, no repeat-dose study, no genotoxicity study, no reproductive study and no carcinogenicity study appears in the published literature. [Animal] [11] [12]
The copper question, which is specific to this molecule
This compound carries a metal, which makes exposure a different question from the one that applies to a plain peptide. Copper is an essential trace element at low intake and toxic at high intake, and the amount a body handles depends on how much arrives and how often.
Nobody has measured that for this compound in a person on any route. The two ex vivo permeation studies measured copper crossing removed human skin and disagreed with each other by a wide margin [3] [5], which means the input side of the question is unsettled before the exposure side can be asked. No published study has measured serum or tissue copper in a person using a topical or injected GHK-Cu product.
This is not a statement that harm has been observed. It is a statement that the measurement that would answer the question has not been made. [In-vitro] [3] [5]
What has not been characterised
The identity question raised in the opening section belongs here too. The complex has no single settled molecular description in the public chemistry databases, which carry several records at different charges and stoichiometries. A substance whose composition is described more than one way cannot have its impurity profile described precisely either, and FDA named aggregation and peptide-related impurities as its concern for the injected form.
No published stability or shelf-life study of GHK-Cu was located, in any presentation. No degradation product has been characterised. And no published work describes what happens to the compound in a product over time or under handling, which is a question every certificate of analysis is silent about.
Long-term exposure has been characterised in no species. The published studies ran days to weeks, and the longest human assessment on record is twelve weeks.
Talk to a licensed clinician about anything concerning your health.
Sourcing and quality
What a credible product should show
A certificate of analysis is the document that matters, and for this compound it has to answer one question that does not arise for a plain peptide: which copper species is in the vial or the jar, and in what ratio to the peptide. The public chemistry records carry several forms at different charges and stoichiometries, so a certificate naming only GHK-Cu has not identified the material.
Three things make any certificate checkable: a lot number that matches the container in front of you, a test date, and the name of the laboratory that ran the test rather than the name of the company selling the material.
What the common tests establish is narrower than it looks. High performance liquid chromatography separates what is in a sample and reports relative peak area, which is a statement about chromatographic purity rather than about identity. Mass spectrometry addresses identity by measuring molecular weight, and for the free peptide that should land at 340.4. Neither test says how much is in the container: that is net peptide content, reported separately if at all. And neither says how much copper is present, which for this compound requires its own elemental measurement.
Red flags
A certificate with no lot number cannot be tied to the container in your hand, whatever else it says. A certificate reproduced from a supplier without an independent test is a supplier's claim rather than a verification. A certificate dated well before the material was made covers a different batch.
A purity figure with no method named is not a purity figure. Ninety-nine percent by which measurement, against which reference standard, with how much material in the container, and with how much copper are five separate questions, and one percentage answers none of them.
A molecular weight quoted for the complex without saying which species it refers to is a specific problem here rather than a general one, because there is more than one right answer and the databases carry several.
Widely circulated statistics about what fraction of products in this market are underdosed, or what fraction of certificates are fabricated, trace back to affiliate content sites rather than to a published testing program. This site does not publish them, because nobody has traced them to primary data.
This site names no company adversely and names none favourably either. There is no best-vendor list here, no rating and no top pick, and there will not be one.
Will it show on a drug test?
The question people ask is whether a copper peptide product could produce a positive test, and the honest answer starts with a fact that makes the question harder than it looks: GHK is already in everyone's blood. A 2023 study measured it in plasma at 133.0 plus or minus 54.54 nanograms per millilitre across eleven healthy adults [14].
So a test looking for the peptide itself would have to distinguish an administered amount from the amount a person already carries, and no published work establishes what a topical or injected product adds to that baseline. No pharmacokinetic study of administered GHK-Cu in a person exists on any route, which means nothing published supports or refutes a detection claim in either direction.
Anti-doping status is decided by an athlete's own anti-doping organization against the current Prohibited List, and this site publishes no reading of that list for this compound because it has not verified one against the primary document. The KPV review sets out how the S0 Non-Approved Substances category reaches a compound that is not named on the list, which is the mechanism most likely to be relevant here, and an athlete's own organization is the only body whose answer counts.
Workplace testing and anti-doping testing are different systems with different panels, and neither publishes a position on this compound.
Storage
Storage is a two-part question for this compound and only for compounds like it, because the molecule is a peptide holding a metal ion by a coordination bond rather than a covalent one. The peptide can degrade and the complex can come apart, and a measurement of one is not a measurement of the other.
Published work addresses neither for a marketed product. No stability study of GHK-Cu was located in any presentation, and no shelf life has been published for it. That is the whole of the record on this question.
This site publishes no handling or preparation procedure. That is a standing rule and the reasoning is on the editorial policy page.
Regulatory status, as of 8 August 2026
| Body | Position | Date | Document |
|---|---|---|---|
| FDA, 503A interim policy, non-injectable routes | GHK-Cu (except for injectable routes of administration) is in category 1, bulk drug substances under evaluation. FDA records that it was removed from category 1 on 22 April 2026 because the nominations were withdrawn by the nominators, that on 5 May 2026 one nominator clarified it intended to withdraw only the injectable route and would like to retain its nomination for non-injectable routes, and that the substance will be added back to category 1 | Document updated 2026-05-14 | FDA, Bulk Drug Substances Nominated for Use in Compounding Under Section 503A, fda.gov/media/94155/download |
| FDA, 503A interim policy, injectable routes | GHK-Cu (for injectable routes of administration) appears in FDA's table of bulk drug substances previously in category 2 whose nominations were withdrawn by the nominators. Category 2 is the category for substances that raise significant safety risks, and FDA's published rationale is that compounded injectable drugs containing GHK-Cu may pose risk for immunogenicity due to the potential for aggregation and peptide-related impurities, with limited data in humans to inform safety-related considerations | Page content current 2026-04-22 | FDA, Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks |
| FDA, advisory committee consultation | FDA has announced it intends to consult the Pharmacy Compounding Advisory Committee before the end of February 2027 regarding the potential inclusion of GHK-Cu on the 503A Bulks List. No meeting date has been published | Stated in the document updated 2026-05-14 | FDA, Bulk Drug Substances Nominated for Use in Compounding Under Section 503A |
| Pharmacy Compounding Advisory Committee, July 2026 | GHK-Cu was not on the agenda and was not voted on. Seven substances were put to the committee across the four sessions, each on two questions covering a free base and an acetate salt: BPC-157 and KPV on the morning of 23 July, TB-500 and MOTS-c that afternoon, emideltide and epitalon on the morning of 24 July, and semax that afternoon | 2026-07-23 and 2026-07-24 | FDA, Questions for PCAC regarding whether FDA should include certain bulk drug substances on the 503A Bulks List, fda.gov/media/193711/download |
| FDA, cosmetics | Cosmetic products and ingredients do not need FDA premarket approval, with the exception of color additives. A product intended for a therapeutic use, or to affect the structure or function of the body, is a drug under section 201(g) of the FD&C Act even where it also affects appearance | Page content current 2025-11-18 | FDA, FDA Authority Over Cosmetics |
| Approval status | No approved drug product containing this compound. A search of FDA's Drugs@FDA dataset for copper tripeptide returned no record | Checked 2026-08-08 | Drugs@FDA, accessdata.fda.gov |
The regulatory position on GHK-Cu is the part of its file that changed most recently, and it splits by route in a way almost nothing written about this compound reflects.
Start with what category 1 means, because it is the single most misreadable fact here. Under FDA's interim policy on compounding with bulk drug substances, category 1 covers substances that were nominated for the 503A Bulks List with enough supporting information for the agency to evaluate them, that do not appear on any other list, and that the agency is still evaluating. FDA states that it does not intend to take action against a compounder using a category 1 substance provided the conditions in the guidance are met. That is a stated enforcement posture during an evaluation. It is not approval, it is not endorsement, and it is not a finding that anything has been established about the substance [24].
The 2026 sequence is worth stating in order, because a single sentence about it will be wrong. GHK-Cu for routes other than injection was in category 1. On 22 April 2026 it came off, because the nominations for GHK-Cu were withdrawn by the nominators. On 5 May 2026 one of those nominators clarified that it had meant to withdraw only its nomination of the injectable route and wished to keep its nomination for non-injectable routes, and FDA records that the substance will be added back to category 1 [24].
The injectable side went the other way and is a separate record. That route had been placed in category 2, which FDA uses for nominated substances where it has identified significant safety risks pending further evaluation, and its nomination was withdrawn as well. The agency's stated rationale is quoted in the second row of the table above and is discussed in the safety section [25]. What matters structurally is that the two routes now sit in different places in the same policy, so a sentence about GHK-Cu and FDA is wrong unless it says which route it means.
The next event is already on the record. FDA states it intends to consult the Pharmacy Compounding Advisory Committee about the potential inclusion of GHK-Cu on the 503A Bulks List before the end of February 2027 [24]. This page publishes no prediction about what the agency will decide, and no meeting date has been posted. What can be said is that the committee's meeting of 23 and 24 July 2026, which several write-ups have attached to this compound, did not cover it: the questions document for that meeting runs to seven substances across four sessions and GHK-Cu is not one of them. A case-insensitive search of the document for the letters GHK returns nothing [26].
The cosmetic side is a different statute and gets confused with all of the above. A topical product carrying copper tripeptide-1 is lawfully sold without any agency having evaluated it, because FDA does not run a premarket approval step for cosmetic ingredients [27]. That absence is not evidence about the ingredient in either direction, and reading it as clearance is the mirror of reading category 1 that way.
The line between the two statutes is drawn by intended use rather than by contents, and that is the part with practical consequences. Under section 201(g) a product intended for a therapeutic use, or to affect the structure or function of the body, is a drug even where it also affects appearance [27]. So a jar of cream can move across that line on the strength of what its seller writes about it, with nothing inside the jar changing. It is the same reasoning FDA applied to research-use-only labelling, and it is why the editorial standard this site publishes under is stricter than an independent publisher's.
GHK-Cu compared with other peptides sold for repair and skin
| Compound | Evidence grade | What the human record covers | Read more |
|---|---|---|---|
| KPV | D | No human study of any design, on any route, confirmed four separate ways including by FDA's own literature search | Its full evidence review, 32 numbered sources |
| BPC-157 | Not graded here yet | Two registrations, neither reported: a phase 1 first posted December 2015 with status unknown, and a randomized phase 2 in acute hamstring strain recruiting since February 2026. One published retrospective report of injection into the knee | Covered on the healing and recovery page |
| TB-500 | Not graded here yet | One registration naming TB-500 itself, not reported. The eighteen usually counted for it tested thymosin beta-4, a different and much larger molecule, in the eye and in skin | Covered on the healing and recovery page |
| GHK-Cu, topical against injected | One grade covers both | Both randomized trials tested topical products. The injected route has one rat study and no human study of any design, and FDA treats the two routes separately in its compounding record | The topical and injected routes have a page of their own |
Two of these four compounds carry a grade and two do not, and that is deliberate: a grade on this site is derived from tiered claim rows, and the source review behind those rows has not been run on BPC-157 or TB-500.
The comparison worth understanding is the one between GHK-Cu and KPV, because it shows what the grade scale does and does not measure. KPV sits at D because nobody has ever tested it in a person. GHK-Cu sits at B because it has been tested twice, and neither test separated it from its control. The letter records how much research exists and how good it is, not which way the research came out, which is why the sentence beside the badge on this page carries the direction in words.
The route split within this compound is a bigger practical difference than any of the comparisons above, and it has its own page.
What GHK-Cu typically costs
GHK-Cu is sold in two completely different formats: as an ingredient inside finished topical products, where the peptide is a fraction of what is being bought, and as a lyophilised powder in vials. What any of it costs is not published here, and the price comparison page sets out why, along with the four things that actually move a listing.
The one thing worth carrying away is that nothing in a price says anything about identity, content or testing, and for this compound that includes which copper species is present. Those are certificate questions, and they are covered in the sourcing section above.
Frequently asked questions
The studies say GHK in some places and GHK-Cu in others. Which did each one test?
It varies, it is rarely flagged, and it changes what a study can be cited for. The copper complex was tested in the 1992 and 2006 human trials, the rat knee study, all four rodent lung and muscle studies, the 1992 fibroblast work and the worm study. Copper-free GHK was what the 2012 keratinocyte stemness study used [10] and what sits inside the 2016 hair product [21], and both fibroblast papers ran the free peptide, the complex and plain copper chloride side by side [8] [9]. A citation that says GHK where the product says GHK-Cu is not automatically wrong, but it is a different substance and worth checking before the result is carried across.
What would change what this page says?
Not the letter, and that is worth understanding. Grade B already covers a compound whose randomized evidence has read out without settling the question, and grade A needs two trials at phase 3 scale agreeing across separate programs, which is a long way from here. What the recruiting phase 2 can change is the direction the sentence beside the badge reports. Its design answers the objection to both published trials: each participant gets two standardized wounds, one randomized to the gel and one to a vehicle identical in everything else, with blinded assessors reading photographs [22]. That removes the differences between people a 13-patient parallel trial cannot, and it tests the peptide rather than a finished product. Primary completion is estimated for 14 February 2027.
Why is the grade B if both trials came back that way?
Because the grade measures how much research exists and how good it is, not which way it came out. Two randomized controlled trials of the marketed use have read out, which is what grade B describes, and a compound nobody has ever tested sits lower. That is exactly why the explanation beside the badge on this page says in words that the evidence did not separate from control: a letter alone cannot carry a direction, so the direction travels with the sentence.
Does GHK-Cu increase collagen?
No human study has measured collagen in skin after GHK-Cu. What exists is cell culture: in normal human fibroblasts, GHK-Cu produced a dose-dependent rise in glycosaminoglycan synthesis that peaked between one and ten nanomolar and fell back towards control above that, selectively raising dermatan sulfate and heparan sulfate [7]. The percentage figures that circulate come from review articles summarising work of that kind [18] [20].
Does topical GHK-Cu get through skin?
The two studies that tested it on real human skin disagree, and both are ex vivo. A 2010 diffusion-cell study measured copper crossing dermatomed skin and forming a depot in it [3]. A 2015 study reports that almost no peptide and almost no copper crossed intact skin without microneedle pretreatment [5]. Neither addresses the other, and a 2025 review concludes the measurement methods are still being developed [6]. Anyone quoting one of those results as settled is quoting half the record.
Is the copper the part that does the work?
That has not been established, and three published results cut against the assumption. Copper-free GHK produced similar effects to the copper complex on keratinocyte stemness, with the authors concluding as much [10]. In two fibroblast studies, copper chloride on its own moved the same markers in the same direction as the complex [8] [9]. And the hair trial usually cited for GHK-Cu names its peptide as glycyl-histidyl-lysine, with no mention of copper anywhere in its abstract [21].
Does GHK-Cu regrow hair?
No published study has tested it for hair growth. The trial cited for it tests a two-component complex of 5-aminolevulinic acid and copper-free GHK, with no arm isolating either component, and it found no significant difference in hair length or thickness among its three groups at six months [21]. The comparison to an approved hair-loss drug that circulates for this compound has no source this site could find.
Has anyone injected GHK-Cu in a study?
In animals, yes, and the route matters. One study used a joint as the site: seventy-two rats received weekly injections into a reconstructed knee for four weeks; the treated groups had less knee laxity at six weeks and no difference at twelve, after treatment stopped [11]. Four more used the abdominal cavity for lung and muscle endpoints [12] [13] [14] [15]. No published study has given GHK-Cu by injection to a person, for any purpose.
Is GHK-Cu approved by the FDA?
No. There is no approved drug product containing it, and a search of Drugs@FDA for copper tripeptide returned no record on 8 August 2026. Topically it is sold as a cosmetic ingredient, and FDA states that cosmetic products and ingredients need no premarket approval other than color additives [27], so nothing has been evaluated on that side either.
What does it mean that GHK-Cu is in FDA category 1?
It means the non-injectable form was nominated for the 503A Bulks List with enough supporting information for FDA to evaluate it, and that the agency is still evaluating it. FDA states it does not intend to act against a compounder using a category 1 substance while the conditions in its guidance are met. That is an enforcement posture during a review [24]. It is not an approval, not an endorsement, and not a finding about the substance.
Why does FDA treat the injectable form differently?
Because it placed that form in category 2, the category for nominated substances where the agency has identified significant safety risks pending further evaluation. Its published rationale is that compounded injectable drugs containing GHK-Cu may pose risk for immunogenicity due to the potential for aggregation and peptide-related impurities, with limited data in humans to inform safety-related considerations [25]. That statement is about injection and it does not extend to a topical product.
Was GHK-Cu part of the July 2026 advisory committee meeting?
No. The questions document FDA published for 23 and 24 July 2026 covers seven substances, each on two voting questions: BPC-157 and KPV on the morning of 23 July, TB-500 and MOTS-c that afternoon, emideltide and epitalon on the morning of 24 July, and semax that afternoon [26]. GHK-Cu appears nowhere in it, and a case-insensitive search of the document for the letters GHK returns nothing. FDA has separately stated it intends to consult the same committee about GHK-Cu before the end of February 2027, and no date for that has been published [24].
How many registered trials of GHK-Cu are there?
Three records come back, and only one of them can answer anything about the compound: a phase 2, randomized, double-blind, vehicle-controlled split-wound study of a topical gel, recruiting since 2 February 2026 with primary completion estimated for 14 February 2027 [22]. Of the other two, one is a completed open-label facial device study in 27 people that applied a multi-ingredient booster serum containing the compound to everyone, with no control arm and no way to separate it from the devices or the other ingredients [23]; the other has not started and measures circulating GHK and GHK-Cu levels rather than giving anything [29]. Counting all three as trials of GHK-Cu is the commonest error made about this compound.
How does GHK-Cu compare with KPV?
KPV sits at grade D because no human study of it exists on any route. GHK-Cu sits at B because two randomized trials have read out. The comparison is worth understanding precisely: B is the higher letter and it belongs to the compound that was tested and did not separate from its control, which is what the grade scale can and cannot say in a single character.
References
- 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. J Vasc Surg. 1992. PMID 1495150 DOI 10.1067/mva.1992.37086
- Miller TR, Wagner JD, Baack BR, Eisbach KJ. Effects of topical copper tripeptide complex on CO2 laser-resurfaced skin. Arch Facial Plast Surg. 2006. PMID 16847171 DOI 10.1001/archfaci.8.4.252
- Hostynek JJ, Dreher F, Maibach HI. Human skin retention and penetration of a copper tripeptide in vitro as function of skin layer towards anti-inflammatory therapy. Inflamm Res. 2010. PMID 20703511 DOI 10.1007/s00011-010-0214-4
- Mazurowska L, Mojski M. Biological activities of selected peptides: skin penetration ability of copper complexes with peptides. J Cosmet Sci. 2008. PMID 18350235
- Li H, Low YS, Chong HP, Zin MT, Lee CY, Li B, Leolukman M, Kang L. Microneedle-Mediated Delivery of Copper Peptide Through Skin. Pharm Res. 2015. PMID 25690343 DOI 10.1007/s11095-015-1652-z
- Ogórek K, Nowak K, Wadych E, Ruzik L, Timerbaev AR, Matczuk M. Are We Ready to Measure Skin Permeation of Modern Antiaging GHK-Cu Tripeptide Encapsulated in Liposomes? Molecules. 2025. PMID 39795193 DOI 10.3390/molecules30010136
- Wegrowski Y, Maquart FX, Borel JP. Stimulation of sulfated glycosaminoglycan synthesis by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+. Life Sci. 1992. PMID 1522753 DOI 10.1016/0024-3205(92)90504-i
- Gruchlik A, Jurzak M, Chodurek E, Dzierzewicz Z. Effect of Gly-Gly-His, Gly-His-Lys and their copper complexes on TNF-alpha-dependent IL-6 secretion in normal human dermal fibroblasts. Acta Pol Pharm. 2012. PMID 23285694
- Gruchlik A, Chodurek E, Dzierzewicz Z. Effect of GLY-HIS-LYS and its copper complex on TGF-β secretion in normal human dermal fibroblasts. Acta Pol Pharm. 2014. PMID 25745767
- Choi HR, Kang YA, Ryoo SJ, Shin JW, Na JI, Huh CH, Park KC. Stem cell recovering effect of copper-free GHK in skin. J Pept Sci. 2012. PMID 23019153 DOI 10.1002/psc.2455
- Fu SC, Cheuk YC, Chiu WY, Yung SH, Rolf CG, Chan KM. Tripeptide-copper complex GHK-Cu (II) transiently improved healing outcome in a rat model of ACL reconstruction. J Orthop Res. 2015. PMID 25731775 DOI 10.1002/jor.22831
- Bian Y, Deng M, Liu J, Li J, Zhang Q, Wang Z, Liao L, Miao J, Li R, Zhou X, Hou G. The glycyl-l-histidyl-l-lysine-Cu(2+) tripeptide complex attenuates lung inflammation and fibrosis in silicosis by targeting peroxiredoxin 6. Redox Biol. 2024. PMID 38879894 DOI 10.1016/j.redox.2024.103237
- Ma WH, Li M, Ma HF, Li W, Liu L, Yin Y, Zhou XM, Hou G. Protective effects of GHK-Cu in bleomycin-induced pulmonary fibrosis via anti-oxidative stress and anti-inflammation pathways. Life Sci. 2020. PMID 31809714 DOI 10.1016/j.lfs.2019.117139
- Deng M, Zhang Q, Yan L, Bian Y, Li R, Gao J, Wang Y, Miao J, Li J, Zhou X, Hou G. Glycyl-l-histidyl-l-lysine-Cu(2+) rescues cigarette smoking-induced skeletal muscle dysfunction via a sirtuin 1-dependent pathway. J Cachexia Sarcopenia Muscle. 2023. PMID 36905132 DOI 10.1002/jcsm.13213
- Zhang Q, Liu J, Deng MM, Tong R, Hou G. Relief of ovalbumin-induced airway remodeling by the glycyl-l-histidyl-l-lysine-Cu(2+) tripeptide complex via activation of SIRT1 in airway epithelial cells. Biomed Pharmacother. 2023. PMID 37257226 DOI 10.1016/j.biopha.2023.114936
- Wen H, Zhao K, Luo X, Pu J, Li Y, Dou Y, He J, Nie X, Ke Y, Zhou W. The GHK-Cu delays aging in Caenorhabditis elegans via coordinated regulation of mitochondrial function and activation of DAF-16/SKN-1 pathways. Biogerontology. 2026. PMID 42084774 DOI 10.1007/s10522-026-10444-x
- Pickart L, Vasquez-Soltero JM, Margolina A. GHK and DNA: resetting the human genome to health. Biomed Res Int. 2014. PMID 25302294 DOI 10.1155/2014/151479
- Pickart L, Vasquez-Soltero JM, Margolina A. GHK Peptide as a Natural Modulator of Multiple Cellular Pathways in Skin Regeneration. Biomed Res Int. 2015. PMID 26236730 DOI 10.1155/2015/648108
- Pickart L, Vasquez-Soltero JM, Margolina A. The human tripeptide GHK-Cu in prevention of oxidative stress and degenerative conditions of aging: implications for cognitive health. Oxid Med Cell Longev. 2012. PMID 22666519 DOI 10.1155/2012/324832
- Pickart L. The human tri-peptide GHK and tissue remodeling. J Biomater Sci Polym Ed. 2008. PMID 18644225 DOI 10.1163/156856208784909435
- Lee WJ, Sim HB, Jang YH, Lee SJ, Kim do W, Yim SH. Efficacy of a Complex of 5-Aminolevulinic Acid and Glycyl-Histidyl-Lysine Peptide on Hair Growth. Ann Dermatol. 2016. PMID 27489425 DOI 10.5021/ad.2016.28.4.438
- Hudson Biotech. A Phase 2, Randomized, Double-Blind, Vehicle-Controlled, Split-Wound Study of Topical GHK-Cu (Copper(II)-Peptide Complex) Gel to Accelerate Re-Epithelialization of Standardized Acute Skin Wounds in Healthy Adults. Registry record read in full through the ClinicalTrials.gov API v2 on 8 August 2026: recruiting, actual start 2 February 2026, estimated primary completion 14 February 2027, no results posted. ClinicalTrials.gov, NCT07437586. 2026. Source document
- Austin Institute for Clinical Research. A Phase IV Open-label Trial Assessing the Impact on Skin Quality, Hydration, and Barrier of Three (3) Hydrafacial Treatments in Adults of Fitzpatrick Skin Types I-VI. Registry record read in full through the ClinicalTrials.gov API v2 on 8 August 2026: completed 9 October 2024, 27 participants, no results posted. Three interventions, of which one is a drug: a booster serum whose registered description lists the compound among its ingredients, applied to every participant. ClinicalTrials.gov, NCT05932732. 2024. Source document
- US Food and Drug Administration. Bulk Drug Substances Nominated for Use in Compounding Under Section 503A of the Federal Food, Drug, and Cosmetic Act. Document updated 14 May 2026, carrying the category 1 list and the GHK-Cu withdrawal and clarification history. FDA human drug compounding. 2026. Source document
- US Food and Drug Administration. Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks. Category 2 of the bulk substances nominated under sections 503A or 503B, with the table of substances previously in category 2 whose nominations were withdrawn. Page content current 22 April 2026. FDA human drug compounding. 2026. Source document
- US Food and Drug Administration. Questions for PCAC regarding whether FDA should include certain bulk drug substances on the 503A Bulks List, Pharmacy Compounding Advisory Committee, 23 and 24 July 2026. Seven substances are put to a vote across four sessions, two questions each: BPC-157, KPV, TB-500, MOTS-c, emideltide, epitalon and semax. Read in full on 8 August 2026; a case-insensitive search for GHK returns nothing. FDA advisory committee materials. 2026. Source document
- US Food and Drug Administration. FDA Authority Over Cosmetics: How Cosmetics Are Not FDA-Approved, but Are FDA-Regulated. Page content current 18 November 2025. FDA cosmetics laws and regulations. 2025. Source document
- Pickart L, Thaler MM. Tripeptide in human serum which prolongs survival of normal liver cells and stimulates growth in neoplastic liver. Nat New Biol. 1973. PMID 4349963
- LifeWave, Inc. A Two-part Study Investigating the Effect of the X39 Patch on Circulating Blood Levels of GHK and GHK-Cu in a Healthy Adult Population. Registry record read in full through the ClinicalTrials.gov API v2 on 8 August 2026: not yet recruiting, estimated start January 2027, 100 participants estimated. Its four primary outcomes are changes in circulating GHK and GHK-Cu levels from baseline to day 8, so the compound is the quantity measured rather than the intervention. ClinicalTrials.gov, NCT07706361. 2026. Source document