What was Pickart originally studying?

Why plasma from young donors changed protein synthesis in liver tissue from older donors. GHK was the fraction responsible.

Why was it called liver cell growth factor?

It reflected the assay in which the activity was found, not an established function. The name did not survive.

Yes. It was isolated from human plasma, which distinguishes it from compounds whose endogenous status remains unconfirmed.

The Discovery of GHK-Cu in 1973

The short answer

Loren Pickart isolated GHK from the albumin fraction of human plasma in 1973, while investigating why plasma from younger donors caused liver tissue from older donors to synthesise proteins in a pattern more typical of younger tissue. The active component proved to be a tripeptide.

Key facts

Year: 1973
Investigator: Loren Pickart
Source: Human plasma, albumin fraction
Original question: Young plasma altering older liver tissue
Early working name: Liver cell growth factor
Also indexed as: Prezatide

The observation that started it

The experiment was not looking for a peptide. Plasma from young donors was added to liver tissue from older donors, and the older tissue began producing proteins in a pattern more characteristic of younger tissue. Something in young plasma was doing it, and the work that followed was an attempt to find out what.

Why albumin

The activity tracked to the albumin fraction during separation. That is a meaningful detail rather than a procedural one: albumin is the major copper-transport protein in plasma and carries its own amino-terminal copper-binding site of the same class as GHK's. Finding a copper-binding tripeptide in the albumin fraction is consistent rather than coincidental.

Research material referenced

GHK-Cu 100mg, third-party HPLC tested

Buy GHK-Cu · £24.99

The early names

The peptide was described as liver cell growth factor for a period, reflecting the assay it was found in rather than any established function. It is also indexed under the name prezatide. Both names appear in older literature and searching for them surfaces records that a search for GHK misses.

What the original work did and did not establish

It established that a specific tripeptide, isolable from human plasma, altered protein synthesis in a tissue model. It did not establish a receptor, a physiological pathway, or an effect in an organism. Fifty years of subsequent work has substantially expanded the descriptive literature; the mechanistic picture remains built largely on copper delivery rather than on a defined signalling pathway.

Why it stayed interesting

Two features. It is endogenous, present in human plasma, unlike compounds whose endogenous status is asserted rather than demonstrated. And its concentration is reported to decline with age, which gives the observation a natural narrative. Both are real; neither establishes that administering it does anything.

Frequently asked questions

What was Pickart originally studying?: Why plasma from young donors changed protein synthesis in liver tissue from older donors. GHK was the fraction responsible.
Why was it called liver cell growth factor?: It reflected the assay in which the activity was found, not an established function. The name did not survive.
Is GHK endogenous?: Yes. It was isolated from human plasma, which distinguishes it from compounds whose endogenous status remains unconfirmed.

Extended research context

The GHK-Cu (Copper Peptide) deep dive

Deep dive: why the copper ion matters

The GHK tripeptide (Gly-His-Lys) coordinates a Cu²⁺ ion through the imidazole nitrogen of histidine, the terminal α-amino group of glycine, and a deprotonated peptide-bond nitrogen. This near-square-planar geometry is what gives the complex its characteristic deep-blue colour and its redox-modulating chemistry. Uncomplexed GHK is a different molecule pharmacologically. Nearly every peer-reviewed study attributes activity to the copper-bound form, which is why suppliers ship the pre-complexed GHK-Cu rather than plain GHK.

GHK-Cu in the transcriptomic literature

The most-cited modern papers on GHK-Cu come from the Pickart & Margolina group and independent transcriptomic re-analyses. GHK-Cu has been reported to modulate expression of >4,000 human genes at nanomolar concentrations in Broad Institute Connectivity Map re-analyses, including genes involved in DNA repair, antioxidant defence, and ECM remodelling. This gene-signature-level activity is the reason GHK-Cu appears in so many research reviews outside of dermatology.

Analytical fingerprinting of GHK-Cu

On reverse-phase HPLC, GHK-Cu elutes as a well-defined peak; free GHK and copper-free peptide impurities are distinguishable. UV-Vis at ~520 nm confirms the copper d-d transition band. Reputable suppliers publish both HPLC (≥98% area) and mass-spec identity (~340 Da complex, 340.4 free peptide) on the batch CoA.

Research applications

▸In vitro fibroblast and keratinocyte gene-expression studies
▸ECM turnover assays (collagen, elastin, decorin, MMP profiling)
▸Wound-healing scratch assays in cell culture models
▸Antioxidant-mechanism studies (copper redox modulation)
▸Formulation R&D: cosmetic and topical carrier compatibility research

Handling checklist

✓Store lyophilised vial at 2–8 °C, protected from light
✓Reconstitute with bacteriostatic or sterile water; expect a blue-tinted solution
✓Avoid contact with reducing agents (ascorbic acid destabilises Cu²⁺)
✓Aliquot reconstituted solution for freeze/thaw minimisation
✓Verify blue colour and CoA HPLC ≥98% before use

Common research-handling mistakes

Learnt from thousands of researcher orders across our UK labs.

✗ Buying GHK without copper

Fix: Confirm the CoA reads GHK-Cu (copper-bound); free GHK is a different pharmacology.

✗ Mixing with vitamin C in solution

Fix: Ascorbate reduces Cu²⁺ to Cu⁺ and destabilises the complex, keep them separate.

✗ Exposing to sunlight

Fix: Store in amber vial or foil-wrapped container at 2–8 °C.

Continue researching

Peer-reviewed guides, comparators and matched reference materials.

Primary sources & clinical trials

Peer-reviewed research and registered trials from PubMed, ClinicalTrials.gov, PubChem, FDA and NIH. All links open in a new tab and point to the primary source, so every claim can be verified at origin.

UKP

Written and reviewed by

The UK Peptides Editorial Team · Research library, UK Peptides

The editorial team is responsible for supplier selection, batch release decisions and the content published in this research library. Every article here is sourced to primary literature and every product page to a signed third-party certificate. Corrections are made in place and the review date updated.

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How GHK Was Discovered