a scrapbook of the copper tripeptide.

The short version

GHK-Cu is a tiny copper-bound tripeptide — three amino acids (glycine, histidine, lysine) wrapped around a single copper(II) ion. It's naturally present in human plasma, declines with age, and has been studied since 1973. As a topical cosmetic ingredient (Copper Tripeptide-1), it has a long safety record. As a research compound, it's been tested in cell culture, rodent models, and small human skin and hair trials. The evidence is real but mostly preclinical — the strongest human data is in skin and hair, the broader anti-aging claims rest heavily on bioinformatics. It is not FDA-approved as a drug. This site is a binder of the published literature, opened. For reported effects and what communities say about using it, see the effects page.

What GHK-Cu actually is

GHK is a tripeptide: glycine bonded to L-histidine bonded to L-lysine. Cu refers to a single copper(II) ion held in place by three nitrogen donors — the imidazole side chain of histidine, the alpha-amino group of glycine, and the deprotonated amide nitrogen between glycine and histidine ^[1]. The lysine side chain points away from the metal, leaving its terminal amino group free to interact with other molecules.

The molecular weight is 340.39 Da. The CAS number is 49557-75-7. In cosmetic regulation it is listed under the INCI name Copper Tripeptide-1 ^[1][18]. The 1:1 copper-to-peptide stoichiometry in slightly acidic solution is the form that most of the research community has studied, and the form that the in vitro and rodent literature treats as the active complex ^[16].

A few naming conventions are worth holding in mind from the start. GHK refers to the free tripeptide. GHK-Cu refers to the copper-bound complex. Some older papers, including the original 1973 isolation work, called it Liver Cell Growth Factor before the structure was confirmed ^[5]. Most modern literature uses GHK-Cu or Cu(II)-GHK interchangeably.

Why fifty years of researchers kept clipping it in

The hook is biological: endogenous GHK circulates in human plasma at around 200 ng/mL in young adults and falls to roughly 80 ng/mL by the seventh decade of life ^[5][14]. That age-related decline is the quiet fact at the center of most of the modern supplementation hypothesis — if a molecule that is present at hundreds of ng/mL in your twenties is present at tens of ng/mL in your seventies, perhaps restoring some of it has biological meaning.

The other hook is transcriptomic. In cultured human fibroblasts, GHK-Cu at nanomolar concentrations shifts expression of an estimated 4,192 protein-coding genes by 50 percent or more — roughly 31 percent of the genome, with 59 percent of those genes upregulated and 41 percent downregulated ^[5]. Connectivity Map analyses identified GHK as a top reverser of the gene-expression signatures of chronic obstructive pulmonary disease, metastatic colon cancer, and several aging-related programs ^[5].

Those two facts together — endogenous decline plus broad transcriptomic reach — explain why a tripeptide first isolated for a niche liver-cell assay ended up with a thousand-plus paper bibliography.

What the literature actually shows

Most strong-signal data on GHK-Cu is preclinical. Cell culture and rodent studies dominate. The patterns that repeat across that body of work are tissue repair, antioxidant defense, anti-inflammatory signaling, and matrix remodeling ^{[2][3][9][15]}.

In aged mouse lung fibroblasts, GHK reverses age-related fibrosis markers — reducing p21 and p53 expression, increasing the stemness markers p63 and PCNA, and depending on integrin-beta1 signaling at the cell surface ^[3]. In a DSS-induced colitis model in BALB/c mice, oral GHK-Cu at 20 mg/kg for 14 days restored colon length, lowered TNF-alpha and IL-6, and preserved the tight-junction proteins ZO-1 and Occludin through SIRT1 binding and STAT3 deacetylation ^[4].

In a cigarette-smoke-induced emphysema model in C57BL/6J mice, intraperitoneal GHK-Cu at 2 and 20 microg/g/day for 12 weeks reduced histological emphysema and rebalanced the MMP-9 to TIMP-1 ratio through Nrf2 upregulation and NF-kB suppression ^[2]. In Wistar rats given 0.5 microg/kg intraperitoneal GHK, open-arm exploration in the elevated plus maze rose within 12 minutes — a copper-independent anxiolytic-like effect — and inter-male aggression dropped roughly fivefold in a resident-intruder paradigm ^[13].

The human data are narrower and largely topical. A 2024 high-resolution-ultrasound study at McGill University Department of Dermatology tracked 21 subjects on a topical GHK-Cu formulation for three months and reported a 28 percent mean increase in subdermal echogenic density — a proxy for collagen and elastin content — with the top quartile of responders at roughly 51 percent improvement ^[17].

What this site is and is not

GHK-Cu Get is an independent editorial project that summarizes the peer-reviewed research literature on GHK-Cu. It is not a clinic. It does not employ clinicians. It does not provide medical advice. It does not manufacture, sell, or distribute any product, and is not affiliated with any vendor or pharmacy.

The word "get" in the domain is used here as the gerund of the verb to gather — to gather clippings, to collect papers, to assemble a scrapbook of what is known. The hero polaroid, the washi tape, the cork board, the sticky-note caveats — all of this is editorial vocabulary for a researcher's personal binder of the literature, not a call to acquire anything.

If you want to read the underlying papers, the /references page lists every citation used on this site with DOIs and PubMed or PMC links. If you want a quick orientation to the most common questions, /faq is a good entry point. If you want the mechanism in detail, /research is where the bulk of the clippings live. If you want to know what people in skincare and research communities say about using it — and what the literature says to watch for — /effects is where that is pinned.

Where the uncertainty still lives

A few honest caveats belong on the front page rather than buried at the back of the binder.

First, GHK-Cu is not approved by the FDA as a drug for any human indication. Topical Copper Tripeptide-1 is permitted as a cosmetic ingredient ^[19]. Compounded injectable GHK-Cu was removed from FDA compounding Category 2 in April 2026 after the original 503A bulks-list nominations were withdrawn; the legal status of compounded injectable GHK-Cu is currently in flux pending Pharmacy Compounding Advisory Committee review ^[19].

Second, the "reverses 4,000 genes" narrative rests heavily on Connectivity Map and LINCS bioinformatics ^[5]. Those analyses are powerful, but they are inherently indirect — not every predicted gene-level effect has been validated downstream in vivo.

Third, the human evidence base is dominated by small topical cosmetic studies. There are no large randomized controlled trials of systemic GHK-Cu in humans. Online claims about systemic injectable use for hair, joints, or cognition routinely outrun what the published evidence supports.

The scrapbook is honest about what is pinned in and what is missing.