---
slug: ghk-cu
title: GHK-Cu: the copper tripeptide's human evidence, copper risk, and dosing arithmetic
canonical: https://miscsubjects.com/a/ghk-cu
---

GHK-Cu is a chain of three amino acids — glycine, histidine and lysine — holding a single copper(II) ion. It occurs naturally in human blood plasma, where its apparent job is to carry copper to the cells that need it and to signal that tissue has been injured.

One disclosure, because it should change how you read the rest. The operator of this site has a commercial interest in compounds described here. That is a reason to weigh what is on this page against the sources it cites rather than against its tone, and every claim below carries the source that supports it for exactly that reason.
Two facts frame everything else here. The first is that the peptide runs out. Plasma GHK measures about 200 ng/mL at age 20 and falls to about 80 ng/mL by age 60 — a 60% decline across four decades, reported in the same terms in two separate reviews.

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The second is that GHK-Cu is one of the few compounds in this library with a genuine human evidence base, because it spent thirty years as a cosmetic ingredient rather than a research chemical. That evidence is entirely topical. Injected GHK-Cu, which is how most people discussing it online are using it, has no completed human trial of any kind.

## Copper is the cargo, and copper is also the hazard

Strip the peptide away and what GHK-Cu delivers is copper in a form a cell can accept. Copper is a required cofactor for roughly a dozen enzymes. Two of them explain most of the interest in this molecule.

Lysyl oxidase is the enzyme that cross-links collagen and elastin. Newly made collagen is soft, soluble and mechanically useless until lysyl oxidase welds the strands together; without copper the enzyme never activates, and connective tissue never gains tensile strength. Copper-zinc superoxide dismutase is the other — the main enzymatic defence against superoxide inside a cell.

The activation step is physically specific. Lysyl oxidase acquires its copper inside the Golgi apparatus, and a 2026 delivery study built its entire design around that fact, using GHK-Cu as the copper source feeding a Golgi-targeted system. Lysyl oxidase activity rose to 1.78 times control, and collagen alignment improved in a rabbit fascia defect.

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That is the upside. The downside is that copper is a heavy metal with a narrow useful range, and injecting it bypasses the one organ that regulates how much of it enters the body. Dietary copper absorption falls from about 75% when intake is low to about 12% when intake is high — the gut throttles itself. A subcutaneous injection does not.

The arithmetic is worth doing rather than gesturing at. Copper tripeptide-1 has the formula C14H23CuN6O4+ and a molecular weight of 402.92 g/mol. Copper's atomic weight is 63.546. Copper is therefore 63.546 ÷ 402.92 = 15.77% of the mass of the complex.

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| GHK-Cu dose | Elemental copper delivered | Share of the 900 mcg adult RDA | Share of the 10,000 mcg upper limit |
|---|---|---|---|
| 0.5 mg | 79 mcg | 9% | 0.8% |
| 1 mg | 158 mcg | 18% | 1.6% |
| 2 mg | 315 mcg | 35% | 3.2% |
| 3 mg | 473 mcg | 53% | 4.7% |
| 5 mg | 789 mcg | 88% | 7.9% |

The upper limit is an oral figure, set on the basis of liver damage, and it assumes intestinal regulation is working. Read the right-hand column as reassuring and the calculation has been misread. Read the third column instead: 3 mg daily by injection adds roughly half an adult's entire daily copper requirement, unregulated, on top of diet.

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Wilson's disease is a hard stop. It is an autosomal recessive mutation in ATP7B that leaves the body unable to clear copper; untreated it produces cirrhosis, acute hepatitis, haemolytic crisis and neurological damage, and treatment is lifelong copper chelation. Giving a copper delivery vehicle to someone with Wilson's disease means giving them the exact substance their disease cannot handle. Anyone on chelation therapy, anyone with unexplained liver enzyme elevation, and anyone with a family history of Wilson's disease is outside the population every study below describes.

The mirror-image condition, Menkes disease, is copper deficiency caused by defective transport, and it is treated with subcutaneous copper injections in the first weeks of life. Same channel, opposite direction. Parenteral copper is a real intervention with real consequences, not a supplement.

## One laboratory produced most of what is known

GHK was isolated in 1973 from human albumin, identified as the factor that made old human liver tissue synthesise proteins the way young tissue does. The isolation, the naming, the copper hypothesis, the gene-expression work and most of the review literature trace to the same investigator, Loren Pickart, across five decades.

That is not a disqualification. It is also not a footnote. A body of work with one author carries one set of methodological habits and one set of priors, and the independent replications that exist are mostly cell-culture and animal work by other groups on narrow questions — fascia repair, wound dressings, nanoparticle carriers — rather than confirmations of the broad claims. Every figure in the next section inherits that caveat.

## Four steps run from the vial to new collagen, and the last one is the weakest

Step one: the complex delivers copper into the cell. This is the least contested part, and the Golgi work above shows the route in detail.

Step two: copper activates the cuproenzymes, lysyl oxidase among them, so collagen and elastin can be cross-linked into load-bearing tissue.

Step three: the peptide raises production of matrix components directly. In human dermal fibroblast culture at nanomolar concentrations, GHK-Cu increases synthesis of collagen types I, III and IV, elastin, and glycosaminoglycans including dermatan sulphate and chondroitin sulphate. It also modulates matrix metalloproteinases together with their tissue inhibitors — building and controlled demolition at once, which is what remodelling actually requires.

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A pointed test of that step used irradiated human fibroblasts: cells damaged by radiotherapy that had lost the ability to replicate normally. At 1 nanomolar, GHK-Cu brought their doubling time back to approximately that of untreated normal controls, and they secreted significantly more basic fibroblast growth factor and VEGF than untreated controls.

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Step four is the gene-expression claim, and it is the one that travels furthest from its evidence. Using the Broad Institute's Connectivity Map, GHK was reported to change the expression of 31.2% of human genes by 50% or more — 59% of those upward, 41% downward. In absolute counts at the 50% threshold: 1,569 genes stimulated, 583 suppressed. At 100–199% change, 646 and 469. At 1,200% or more, 2 and 4.

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Compressed to a headline, that becomes "GHK-Cu resets more than 4,000 human genes to a healthier state." The compression drops three things. The Connectivity Map is a transcriptional-signature database built from five cancer cell lines exposed to small molecules, not a study of human tissue. The analysis is the same investigator's. And "healthier state" is an interpretation laid over a correlation between two gene-expression signatures. The count is real. The conclusion attached to it in marketing copy is a bet, and it should be labelled one.

## The face creams were tested on 179 women, and that is the controlled human record

Three placebo-controlled cosmetic studies carry the topical case, plus one biopsy study of collagen production. They are small, they are old, two were published as conference proceedings rather than journal papers, and they are still more human data than almost any peptide sold in this category has.

| Study | n | Site and duration | Comparator | Reported result |
|---|---|---|---|---|
| Leyden et al. 2002, facial cream | 71 women with mild to advanced photoageing | Face, 12 weeks | Placebo | Increased skin density and thickness; reduced laxity, fine lines and wrinkle depth; improved clarity |
| Leyden et al. 2002, eye cream | 41 women with mild to advanced photodamage | Around the eye, 12 weeks | Placebo and a vitamin K cream | Beat both; reduced lines and wrinkles, increased skin density and thickness |
| Finkey et al. 2005, facial cream | 67 women aged 50–59 | Face twice daily, 12 weeks | Placebo | Improved laxity, clarity and firmness; reduced coarse wrinkles and mottled pigmentation; strongly increased keratinocyte proliferation on biopsy |
| Abdulghani et al. 1998, thigh biopsy | Pilot, immunohistological scoring | Thigh, 12 weeks | Vitamin C cream and retinoic acid | Collagen production increased in 70% of subjects on GHK-Cu, 50% on vitamin C, 40% on retinoic acid |

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Read the fourth row carefully, because it is the one usually quoted as "GHK-Cu beats retinoic acid." What it reports is the proportion of subjects showing any measurable increase in collagen on biopsy — not the size of the increase — in a pilot study with immunohistological scoring. Suggestive, yes. A head-to-head comparison of how well the two work, no.

A 2025 review of GHK as a topical anti-wrinkle agent lands on the awkward point underneath all of this: the cellular evidence is not in doubt, and there is a surprising absence of clinical studies using GHK-Cu and its palmitoylated derivative in the products actually sold. The same review raises the delivery problem. GHK-Cu is hydrophilic, the stratum corneum is lipophilic, and how much of an applied dose reaches living dermis remains unresolved.

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## The only randomised wound trial found nothing

In 1992 a prospective randomised evaluator-blinded trial in venous stasis ulcers enrolled 86 evaluable patients across three arms: 1% silver sulfadiazine cream, a 0.4% tripeptide-copper complex cream, and an inert vehicle placebo. Silver sulfadiazine statistically reduced ulcer size. The copper tripeptide cream did not differ from placebo.

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That is the largest controlled human wound-healing trial of this compound in the published record. It ran on the indication where the mechanism should be most visible, and it was negative. A page presenting GHK-Cu as an established wound-healing agent without that trial in it has left out the most decision-relevant result available.

One trial now running could change the picture. NCT07437586 is a Phase 2, randomised, quadruple-blind, vehicle-controlled split-wound study: 60 healthy adults each receive two standardised punch-biopsy wounds on the upper arm, one randomised to 0.1% w/w GHK-Cu gel and the other to matching vehicle, roughly 0.5 g applied once daily for 14 days. The primary endpoint is days to complete re-epithelialisation, assessed blind from standardised photography, with a scar-quality follow-up. It started 2 February 2026; estimated primary completion is 14 February 2027.

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The split-wound design is why that trial matters more than its size suggests. Each participant is their own control, which strips out the age, genetics and healing-rate variation that swamps small wound studies.

## Nobody has ever run a human trial on injected GHK-Cu

A search of ClinicalTrials.gov for GHK-Cu returns three studies in total. None of them injects it.

| NCT | Status | n | Route | What it tests |
|---|---|---|---|---|
| NCT07437586 | Recruiting, started Feb 2026 | 60 | Topical gel, 0.1% w/w | Re-epithelialisation of standardised acute wounds against vehicle |
| NCT05932732 | Completed Oct 2024 | 27 | Topical, inside a multi-component facial device treatment | Facial skin quality, hydration and barrier — GHK-Cu is one ingredient of one booster serum, never an isolated variable |
| NCT07706361 | Not yet recruiting, estimated start Jan 2027 | 100 | Transdermal patch | Whether a patch raises circulating GHK and GHK-Cu at all |

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The gap between that table and the practice described on peptide forums is total. Every reported subcutaneous dose, every milligram-per-day protocol, every before-and-after photograph of injected GHK-Cu rests on zero controlled human data. Topical evidence does not carry across: the doses differ by orders of magnitude, the exposure is systemic rather than local, and the copper load is the variable the cosmetic trials never had to think about.

A 2026 narrative review in Sports Medicine covering the unapproved-peptide market — GHK-Cu named alongside BPC-157, TB-500, ipamorelin and the rest — states the position without softening it: favourable tissue-repair outcomes in animal models, scarce rigorous human safety data, potential for serious harm, and a placebo effect amplified by social media.

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## Trace the viral hair number and it belongs to a different molecule

One claim circulates faster than any other. It is specific enough to sound checkable, which is exactly why it spreads.

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The Annals of Dermatology paper is real. It randomised 45 men with pattern hair loss to ALAVAX at 100 mg/mL, ALAVAX at 50 mg/mL, or placebo, once daily for six months. Hair count rose by 52.6 in the high-dose group, 71.5 in the low-dose group and 9.6 on placebo. No adverse events in any group.

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Three problems. ALAVAX is a complex of 5-aminolevulinic acid and GHK — copper-free GHK, not GHK-Cu — so the effect cannot be assigned to either component. Only the low-dose-versus-placebo ratio reached statistical significance, and the higher dose performed worse than the lower one, which is not how a dose-responsive drug behaves. Hair length and hair thickness showed no significant difference between any of the three groups at six months.

A PubMed search across GHK, copper peptide and copper tripeptide against hair and alopecia returns 13 records. Not one is a controlled human trial of GHK-Cu alone for hair. The rest are cell work, mouse work, delivery-vehicle engineering, and multi-ingredient clinic formulations in which copper tripeptide sits among a dozen components alongside minoxidil and finasteride. People report hair effects constantly, and those reports are worth reading as reports:

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## The whole load-bearing-tissue case is one rat knee and a long chain of extrapolation

The connective-tissue case is mechanistically coherent. Collagen and elastin cross-linking is copper-dependent. Ligament, tendon, fascia and disc are collagen structures. A compound that raises collagen synthesis and activates lysyl oxidase is operating on exactly the material a ligament, a tendon and a disc are built from. Three recent orthopaedic reviews list GHK-Cu on that basis, grouped with BPC-157 and TB-500 as wound-healing peptides working through angiogenesis, integrin-mediated matrix remodelling and fibroblast activation.

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The direct musculoskeletal experiment exists. It is one study, in rats, with a mixed result. Seventy-two rats underwent anterior cruciate ligament reconstruction and were randomised to saline, 0.3 mg/mL or 3 mg/mL GHK-Cu, given as intra-articular injections weekly for four weeks starting at week two. At six weeks the GHK-Cu groups had less side-to-side knee laxity than saline (p = 0.009) and the low-dose group had higher graft stiffness (p = 0.026). At twelve weeks neither difference remained. Ultimate load, gait and histology showed no difference at any point, and every graft failed mid-substance on pull-out testing.

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The paper's own title uses the word "transiently." An acceleration of early healing that has vanished by three months is a real finding and a small one, and it is the entire animal case for GHK-Cu in a load-bearing joint.

What follows from that one study, stated plainly:

- Dermal data does not license a musculoskeletal claim. Skin is thin, well vascularised and fast-turning-over; a ligament is none of those. No study has measured GHK-Cu in a human tendon, disc, ligament or fascia.
- The rabbit fascia work is a delivery-system engineering study, not a treatment trial, and its intervention was a nanoparticle-plus-mRNA construct in which GHK-Cu was the copper reservoir.
- The pre-blended recovery stacks pairing GHK-Cu with BPC-157 and TB-500 have no combination study behind them in any species. The pairing exists because the three compounds have adjacent marketing stories, and stacking three unapproved compounds multiplies unknowns rather than averaging them.
- Post-procedure skin recovery — after laser, microneedling or a surgical incision — is the one adjacent use with something resembling human support, and that support is topical.

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## Reconstitution is division, then division again

GHK-Cu ships as a lyophilised powder, usually blue to blue-green, in a sealed glass vial. Vials of 50 mg and 100 mg are the common sizes — an order of magnitude larger than most peptide vials, because the doses discussed are milligrams rather than micrograms. It is reconstituted with bacteriostatic water, which is sterile water containing 0.9% benzyl alcohol; that preservative is what makes it safe to enter the vial repeatedly.

Two divisions produce every number needed.

- **Concentration**: vial strength in mg ÷ water added in mL = mg per mL.
- **Per-unit content**: a U-100 insulin syringe holds 100 units per mL, so mg/mL × 1,000 ÷ 100 = micrograms per unit. In short, mg/mL × 10.
- **Units for a dose**: dose in mcg ÷ micrograms per unit.

| Vial | Bacteriostatic water | Concentration | Per insulin unit | A 2 mg dose |
|---|---|---|---|---|
| 50 mg | 2 mL | 25 mg/mL | 250 mcg | 8 units |
| 50 mg | 5 mL | 10 mg/mL | 100 mcg | 20 units |
| 50 mg | 10 mL | 5 mg/mL | 50 mcg | 40 units |
| 100 mg | 5 mL | 20 mg/mL | 200 mcg | 10 units |
| 100 mg | 10 mL | 10 mg/mL | 100 mcg | 20 units |

At the middle row — 50 mg in 5 mL, giving 10 mg/mL and 100 mcg per unit — the dose-to-units conversion is the simplest available, which is why that dilution is the one most often described.

| Dose | Units at 10 mg/mL | Elemental copper in that dose |
|---|---|---|
| 1 mg | 10 units | 158 mcg |
| 1.5 mg | 15 units | 237 mcg |
| 2 mg | 20 units | 315 mcg |
| 3 mg | 30 units | 473 mcg |
| 5 mg | 50 units | 789 mcg |

Doses in public reports cluster at 1–3 mg daily subcutaneously, with 5 mg at the upper end. There is no established dose, because there is no trial. Continuous daily use running past twelve weeks is common in those reports, and nothing in the evidence base speaks to the cumulative copper load of that pattern.

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Timelines in the same reports are slow and consistent: nothing at two weeks, first skin changes somewhere between four and eight weeks, and the before-and-after photographs that circulate are at six weeks to twelve months.

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## Topical strengths span a factor of a thousand

The concentrations in the literature and the concentrations on shelves are not the same numbers, and neither matches what the safety panel assessed.

| Context | Concentration | Where the figure comes from |
|---|---|---|
| Phase 2 wound gel, NCT07437586 | 0.1% w/w | Trial protocol |
| Venous ulcer trial, 1992 | 0.4% cream | Published methods |
| CIR-assessed typical cosmetic use | under 10 ppm (0.001%) | Panel report |
| Consumer serums described in user threads | 1% | Product labelling quoted by users |

A 1% serum is a thousand times the concentration the safety panel described as typical use. That is not automatically unsafe — the panel's conclusion rested on low use levels plus negative irritation and sensitisation data, not on a hard ceiling — but the gap is where reports of irritation come from, and it explains how two products both labelled "copper peptide" can behave completely differently on the same face.

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## The side effects people report are consistent, local, and absent from the literature

Nothing below is a trial finding. Each is a person describing what happened to them, quoted as written, from a public thread.

Injection-site stinging and welts are the most frequently described physical effect, and the workaround people converge on is technique rather than dose:

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Skin discolouration — described as a golden or tanned tone — comes up repeatedly among people injecting daily, and appears in no published safety assessment:

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Fatigue and histamine-type reactions after injection:

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Systemic symptoms severe enough to stop:

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The topical failure mode has its own name in skincare communities — "copper uglies" — and the pattern described is new fine lines and texture change appearing at around day ten, resolving after stopping:

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Negative results deserve the same space as positive ones. Twelve weeks at 2–3 mg daily made one person's skin measurably worse by their own account, and three months at 2 mg daily produced nothing at all for another:

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The positive reports, at the same evidence tier:

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Read as a body, these reports agree on three things the literature says nothing about: the effect is slow, the injection-site reaction is common, and a visible skin-tone change happens to some people on daily dosing.

## A vial that is not blue may not contain copper

GHK-Cu in solution is blue. The colour is the copper — a d-orbital transition in the Cu(II) ion, not a dye. A reconstituted vial that comes out clear or faintly straw-coloured is a signal worth acting on, and it is a question the forums raise directly, usually in the mistaken belief that bacteriostatic water strips the copper out. It does not. A colourless solution means the powder was plain GHK, or the copper was never complexed at the stated ratio.

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Storage follows from the same chemistry. Lyophilised powder is stable at room temperature in the sealed vial and better refrigerated; once reconstituted it goes to 2–8 °C and stays out of light, because copper complexes are photosensitive and copper is a redox-active catalyst. Light plus dissolved oxygen plus copper is the recipe for degrading the peptide the copper is bound to. Bacteriostatic water gives a multi-dose vial a usable life measured in weeks refrigerated, not months.

Verification is possible and does not require running a laboratory. Copper in a GHK-Cu formulation has been quantified by capillary electrophoresis coupled to inductively coupled plasma tandem mass spectrometry, monitoring copper and phosphorus signals to confirm both the intact complex and its encapsulation.

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## Legal as a face cream, unapproved as an injection

The two regulatory statuses are unrelated, and conflating them is the most common factual error made about this compound.

As a cosmetic ingredient, copper tripeptide-1 is assessed and cleared. The CIR Expert Panel reviewed tripeptide-1, its metal salts including the copper complex, and related derivatives, and concluded that the ingredients are safe in cosmetics in the present practices of use and concentration described in the assessment. Typical use concentrations were reported as under 10 ppm. The panel recorded that low use concentrations plus negative safety test data resolved the question, and noted that when tripeptide-1 is put into a vein it is rapidly broken down to histidyl-lysine and cleared from the blood within minutes.

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As an injectable it has no approval anywhere, and it occupies a specific place on FDA's compounding record. Injectable GHK-Cu was nominated as a bulk drug substance for use in compounding, placed in category 2 — substances that may present significant safety risks — and the nomination was later withdrawn by the nominator. It appears on the withdrawn list with the agency's stated reasoning intact: compounded injectable drugs containing GHK-Cu may pose a risk that the immune system reacts to the drug itself — the agency's word for that is immunogenicity — because the peptide can clump together and because impurities related to the peptide can be present, and there are limited data in humans to inform safety-related considerations. The page carrying that entry is current as of 22 April 2026.

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Withdrawn is not cleared. The substance left the active list because the party who nominated it stopped pursuing it, not because the agency resolved its concern, and the concern is still printed on the page. The practical consequence in the United States is that a compounding pharmacy has no lawful route to supply it as an injectable, so material sold for injection reaches buyers labelled research use only — outside exactly the manufacturing controls that the agency's concern is about.

## Every number above, and the exact call that returns it

Each figure on this page comes from a fetchable record. These are the calls.

| Claim | How to re-derive it |
|---|---|
| Plasma GHK 200 ng/mL at 20, 80 ng/mL at 60 | `curl -s https://pmc.ncbi.nlm.nih.gov/articles/PMC4508379/` — section 1, Introduction |
| 31.2% of genes changed by ≥50%; 1,569 up and 583 down at that threshold | `curl -s https://pmc.ncbi.nlm.nih.gov/articles/PMC6073405/` — section 2, Table 1 |
| Molecular weight 402.92, copper fraction 15.77% | `curl -s 'https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/name/copper%20tripeptide-1/property/MolecularFormula,MolecularWeight/JSON'`, then 63.546 ÷ 402.92 |
| Copper RDA 900 mcg, upper limit 10,000 mcg, Wilson's disease risk | `curl -s https://ods.od.nih.gov/factsheets/Copper-HealthProfessional/` — Tables 1 and 3 |
| Three registered trials, none injectable | `curl -s 'https://clinicaltrials.gov/api/v2/studies?query.term=GHK-Cu&countTotal=true'` |
| 192 PubMed records for GHK-Cu or copper tripeptide | `curl -s 'https://eutils.ncbi.nlm.nih.gov/entrez/eutils/esearch.fcgi?db=pubmed&term=GHK-Cu+OR+%22copper+tripeptide%22&retmode=json&retmax=100'` |
| 13 hair records, none a controlled GHK-Cu trial | `curl -s 'https://eutils.ncbi.nlm.nih.gov/entrez/eutils/esearch.fcgi?db=pubmed&term=(GHK+OR+%22copper+peptide%22+OR+%22copper+tripeptide%22)+AND+(hair+OR+alopecia)&retmode=json&retmax=40'` |
| Negative venous ulcer trial, n = 86 | `curl -s 'https://eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=pubmed&retmode=xml&rettype=abstract&id=1495150'` |
| Rat ACL reconstruction result, n = 72 | `curl -s 'https://eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=pubmed&retmode=xml&rettype=abstract&id=25731775'` |
| FDA withdrawn-nomination entry, verbatim | `curl -s https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks` — second table |
| Every source card on this page, with quote and link | `curl -s https://miscsubjects.com/api/articles/ghk-cu` |

The sibling objects for this page, each one inspectable on its own terms:

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