GHK-Cu

GHK is a tripeptide — glycyl-L-histidyl-L-lysine, three amino acids and nothing more — and unlike most of this catalogue it was not designed. Pickart and Thaler isolated it from human serum in 1973, describing an activity in the albumin fraction that changed how old liver tissue behaved in culture (2, 4).

It does not hold steady across a lifetime. The review literature reports a plasma level of about 200 ng/mL at age 20, falling to about 80 ng/mL by age 60 (1). That decline is the reason the peptide is discussed in an ageing context at all, and it is worth being exact about what it is: an observation about a concentration in plasma, not a demonstration that restoring that concentration does anything.

The copper is not an additive. GHK binds copper(II) with a reported binding constant of log K 16.44, above the 16.2 reported for the high-affinity copper site on plasma albumin, and the same review describes GHK taking up copper held at that albumin site (2). The proposal, from the earliest work onward, is that the peptide functions as the complex GHK-Cu rather than as the bare tripeptide, and that the copper's redox activity is silenced while the tripeptide holds it (2). That is why the vial contains a copper complex, and why the molecular weight in the specifications above is the complex's rather than the peptide's.

GHK-Cu holds no marketing authorisation as a medicine. It is a long-standing cosmetic ingredient and a heavily studied research compound, and the controlled human record behind it is small and topical. Every figure on this page describes what a published study measured.

The one controlled human read-out cited here is a multicentre, randomised, evaluator-blinded, vehicle-controlled trial of a topical GHK-Cu gel in diabetic neuropathic ulcers, published in Wound Repair and Regeneration in 1994. Every participant was on the same standardised wound-care protocol — sharp debridement at entry, daily topical application, pressure-relieving footwear and diabetes education — and the gel was compared against its own vehicle inside that protocol (3).

The trial reported a median area percentage closure of 98.5% in plantar ulcers treated with the gel, against 60.8% for vehicle (p < 0.05). The separation was wider in ulcers larger than 100 mm² at entry: a median of 89.2% against −10.3% for vehicle (p < 0.01). Ulcer infection was recorded in 7% of plantar ulcers treated with the gel immediately after debridement, against 34% on vehicle (p < 0.05). The published abstract does not state how many patients were enrolled or across how many centres, so the trial's size is not reproduced here (3).

The rest of the human literature is smaller and cosmetic in endpoint: topical creams tested on facial and periorbital skin over twelve weeks, in groups of 71, 41 and 67 women, against placebo or comparator creams (2). Those are appearance studies of a cream on skin assessed for photodamage. They are reported here as the shape of the literature, and they license no conclusion about anything outside their own endpoint.

GHK's second literature is not clinical at all. Pickart and colleagues have published a series of reviews arguing that GHK shifts the expression of a large number of human genes, drawing on public expression-profiling datasets and grouping the affected pathways under tissue remodelling, antioxidant response, inflammation and DNA repair (1).

That work is reported here without numbers. The gene counts quoted across those reviews differ from one another, and this page does not print a figure it cannot pin to a single stated source. What the reviews describe is a broad expression signature attributed to the peptide in cell-based datasets — not an effect measured in people, and not a result from any of the human studies above.

A sealed vial of lyophilised powder, in a 50 mg or a 100 mg size. Both are the same material; the difference is the mass in the vial, not the concentration — concentration is set later, by how much solvent is added. These two sizes sit an order of magnitude above the 5 mg and 10 mg vials most of this catalogue uses, so a concentration worked out for another product does not carry over to this one.

Each batch is released against a certificate of analysis from an independent issuer, and the batch number printed on the vial matches the number on that certificate. Checking those two against each other is the most useful thing to do with a delivery. The purity, form, storage condition and molecular weight recorded for the current batch are in the specifications above — the molecular weight is the copper complex's, not the free tripeptide's.

Handling is the same as for every other compound in the catalogue. The handling protocol below covers storage temperatures, solvent choice and the concentration calculation.

Every compound Peptio ships arrives as a sealed vial of lyophilised powder. Freeze-drying is what keeps it stable in transit: with the water removed and the vial closed, the peptide keeps far longer than it would in solution. The protocol below applies to all of them, and it is the same protocol whichever compound is in the vial.

The steps that matter most happen in the first few minutes after a vial is opened, and in how the prepared solution is labelled afterwards. A vial with no recorded solvent volume is a vial with no known concentration, and no amount of care later recovers that.