Skin ⏱ Half-life: Not established in published literature Experimental

AHK-Cu

L-alanyl-L-histidyl-L-lysine copper(II) complex; INCI "Copper Tripeptide-3" is commercial usage, unconfirmed in any official registry

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Evidence at a Glance

Regulatory statusExperimental
Copper tripeptide-3 cosmetic ingredient; used topically, not an approved drug for hair loss.
Human evidenceAnecdotal only
Animal evidenceNone

AHK-Cu stimulated hair-follicle elongation and dermal papilla cell proliferation in a 2007 ex-vivo/in-vitro study, but no controlled in-vivo human trials confirm hair regrowth.

What the research does not support

  • It is not an FDA-approved hair-loss treatment like minoxidil or finasteride.
  • Its supportive evidence is laboratory (ex-vivo follicle and cell-culture) work, not randomized clinical trials showing real-world regrowth.
  • It does not treat the hormonal cause of androgenetic alopecia; any effect is on follicle-cell activity, not DHT.
Half-Life
Not established in published literature
Mol. Weight
Depends on the form supplied: free tripeptide 354.41 g/mol (C15H26N6O4); neutral 1:1 Cu(II) chelate 415.94 g/mol (C15H24CuN6O4, calculated) — see Research Notes
Form
Lyophilized powder

What is AHK-Cu?

AHK-Cu is a synthetic copper(II) coordination complex of the tripeptide alanyl-histidyl-lysine (Ala-His-Lys). It is the position-1 analogue of the far better-known GHK-Cu, differing only in that alanine replaces glycine at the N-terminus. GHK occurs naturally in human plasma, saliva and urine and is a recognized collagen fragment; AHK is not a documented endogenous human peptide but a designed structural variant. It is a genuine three-residue peptide supplied as a metal complex, so its chemistry is dominated by copper coordination.

A single study underpins almost everything written about this compound

The primary record consists of one paper: Pyo and colleagues at Seoul National University, Archives of Pharmacal Research (2007). Using human hair follicles in ex vivo organ culture and cultured human dermal papilla cells, they reported that AHK-Cu at picomolar to nanomolar concentrations stimulated follicle elongation and dermal papilla cell proliferation, with an increased Bcl-2/Bax ratio and reduced cleaved caspase-3 and PARP. The authors noted that the reduction in apoptotic cells measured by flow cytometry was not statistically significant, and framed their conclusion as a proposal rather than a demonstration. A 2026 review of short peptides for hair loss in Biomedicines classifies the evidence status as experimental only, identifying no human clinical trials.

A recurring accuracy problem deserves direct attention. Descriptions of AHK-Cu commonly assert that it raises VEGF, stimulates dermal fibroblast proliferation and suppresses TGF-beta1. Those statements trace to the opening background sentence of the 2007 abstract, which characterizes copper tripeptides as a class — a literature built overwhelmingly on GHK-Cu — and were not experimental findings about AHK-Cu in that paper or elsewhere.

Categorization is a second issue. AHK-Cu is routinely grouped as a skin compound, yet the only published experimental work concerns hair follicles and dermal papilla cells. No study has examined it in wound healing, collagen synthesis, photoaging or dermal remodeling models; the skin association rests on structural similarity to GHK-Cu rather than on direct evidence. Even the coordination geometry usually quoted is read across from GHK-Cu, as no structural study of AHK-Cu itself has been published.

What is missing from the record is as informative as what is present. There are no pharmacokinetic data of any kind — no half-life, bioavailability, ADME characterization or measurement of skin penetration — no animal efficacy studies, no toxicology package and no registered clinical trials. AHK-Cu remains a preclinical research compound with one supporting paper, and it is not approved for human use in any jurisdiction.

How AHK-Cu Works

AHK-Cu is a copper(II) coordination complex of the tripeptide alanyl-histidyl-lysine. Copper is held by the histidine imidazole nitrogen, the N-terminal amine and one deprotonated backbone amide, with the C-terminal carboxylate completing the dianionic ligand. No structural study of AHK-Cu itself exists; this geometry is read across from GHK-Cu, which is dimeric in the solid state and monomeric in solution. Copper tripeptides are hypothesised to carry redox-buffered copper to cells, but copper uptake has never been measured for AHK-Cu. Signalling data come from a single in vitro study: at 10^-12 to 10^-9 M it raised dermal papilla cell viability and the Bcl-2/Bax ratio and lowered cleaved caspase-3 and PARP, though the reduction in apoptotic cells was explicitly not significant. No receptor is known, and claims of VEGF, fibroblast and TGF-beta1 effects describe copper tripeptides as a class, not AHK-Cu.

Research Findings

The published evidence base is extraordinarily thin. PubMed returns one record for AHK-Cu; Europe PMC returns five, only one of which is a primary investigation; ClinicalTrials.gov returns none. That single paper is Pyo HK et al., Archives of Pharmacal Research 2007;30(7):834-9 (PMID 17703734), an ex vivo hair-follicle and dermal papilla cell study. A 2026 Biomedicines review (PMID 42072405) catalogues AHK-Cu as experimental only, with no human clinical trials. Identity is also unsettled. Three CAS numbers circulate commercially: 49557-75-7 in fact belongs to GHK, not AHK; 767286-83-9 resolves only to a malformed database artifact; 682809-81-0 appears in PubChem depositor data for the monohydrochloride but is unconfirmed against a CAS registry. Molecular weight depends on which form is supplied, and the widely repeated 415.12 Da for the neutral chelate is arithmetically wrong (415.94). The INCI name Copper Tripeptide-3 is commercially common but unverified; some sources wrongly use Copper Tripeptide-1, which belongs to GHK-Cu. There are no pharmacokinetic data, no animal efficacy studies, no toxicology package and no published stability study for AHK-Cu. Its common categorisation as a skin compound is extrapolated from GHK-Cu; no AHK-Cu study on wound healing, collagen synthesis, photoaging or dermal remodeling exists.

Dosage & Administration

Published work on AHK-Cu describes no dose administered to an organism. The single primary study (Pyo et al., Archives of Pharmacal Research, 2007) reported bath concentrations in culture medium, not systemic or topical regimens.

  • 10-12 M to 10-9 M (1 pM to 1 nM) — the range across which human hair follicle elongation was reported in ex vivo organ culture and dermal papilla cell proliferation in vitro.
  • 10-9 M (1 nM) — the single concentration at which apoptosis markers (Bcl-2/Bax ratio, cleaved caspase-3, cleaved PARP) were assessed; a 2026 Biomedicines review lists this as the reported working concentration, with no exposure duration specified.
  • 0.05–1% w/w — a formulation convention cited for copper tripeptides as an ingredient class in cosmetic literature, not derived from any AHK-Cu efficacy study.

No dose-response curve in a living animal, effective in vivo concentration, maximum tolerated exposure or adverse-effect threshold has been established, and no injection, oral or topical protocol has been published in any species.

No standardized or validated human dosing exists for AHK-Cu. The figures above are laboratory culture-medium concentrations and cannot be translated into a human dose. AHK-Cu is a research compound intended for research use only; it is not an approved drug and is not approved for human use.

Safety & Side Effects

There is no published safety or toxicology data for AHK-Cu. The one primary study used cultured human dermal papilla cells and ex vivo hair follicle organ culture. No cytotoxicity ceiling, animal toxicology, dermal irritation or sensitization testing, and no human exposure data specific to this compound have been located.

What can be said about the class is indirect. Structural work on the analogue GHK-Cu (Hureau et al., Chemistry, 2011) found the Cu(II) complex inert under moderate redox potentials but reducible to Cu(I) at around -0.62 V, with subsequent release of the copper ion. Free, unchelated copper is a recognized generator of reactive oxygen species and is toxic in excess; whether AHK-Cu releases copper under any physiological condition has not been directly measured.

Reports of transient redness, itching or contact dermatitis that circulate around copper peptides derive from consumer cosmetic use of GHK-Cu formulations and from non-peer-reviewed sources. They are not AHK-Cu findings and should not be presented as a characterized adverse-effect profile for this compound.

The adverse effect profile of AHK-Cu is uncharacterized. Absence of reported adverse effects reflects absence of published study, not evidence of an absence of risk.

Important: All safety information is derived from published research, primarily animal studies. No controlled human clinical trial data exists unless explicitly noted. This compound is sold for research purposes only.

Quick Facts

Sequence Ala-His-Lys (AHK), supplied as a copper(II) coordination complex
Molecular Weight Depends on the form supplied: free tripeptide 354.41 g/mol (C15H26N6O4); neutral 1:1 Cu(II) chelate 415.94 g/mol (C15H24CuN6O4, calculated) — see Research Notes
Half-Life Not established in published literature
Form Lyophilized powder
Available Sizes 100mg
Storage Lyophilized: -20 C, protected from light and moisture (2-8 C acceptable for short working periods). Reconstituted: 2-8 C, used promptly, kept away from reducing agents such as ascorbic acid and from strongly alkaline conditions. No AHK-Cu-specific stability study is published, so a lot-specific certificate of analysis should govern handling.

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