AHK-Cu

Overview

AHK-Cu is a copper(II) complex of the three-amino-acid peptide L-alanyl-L-histidyl-L-lysine: Ala-His-Lys, abbreviated AHK. It is discussed mainly in hair and cosmetic research. The direct published evidence is much narrower than online descriptions suggest: the central paper is a 2007 ex vivo human hair-follicle and in vitro dermal-papilla cell study. That is human-derived tissue research, but it is not a clinical treatment trial.

No completed or ongoing ClinicalTrials.gov intervention record was returned by an exact-name search for AHK-Cu or L-alanyl-L-histidyl-L-lysine on 5 August 2026. The same search boundary located no human pharmacokinetic study and no validated dose. This page therefore reports experimental findings without turning laboratory concentrations into use instructions.

Identity and chemistry

The peptide portion and the copper complex need to be kept separate when a formula or mass is quoted.

PubChem names CID 168431292 [L-alanyl-N-L-histidyl-N,N3-L-lysinato(2-)]copper monohydrochloride. The counterion and charge are part of that exact database record. A vial or cosmetic raw material described only as “AHK-Cu” is not automatically proven to be that same salt, purity, hydration state, or copper-to-peptide form. For that reason, 451.39 g/mol is form-specific rather than a universal AHK-Cu value.

AHK-Cu is not GHK-Cu

AHK-Cu and GHK-Cu are different copper tripeptides:

This one-residue distinction changes the molecule. The 2016 randomized hair study of ALAVAX used 5-aminolevulinic acid linked to GHK, not AHK-Cu. It is therefore not clinical evidence for AHK-Cu.

The PeptideGuide snapshot also assigns AHK-Cu a citation labelled as a 2015 GHK review but links to PMID 6481226. That PMID is a 1984 paper on nasal mucosal changes in scleroderma, unrelated to either AHK-Cu hair research or the claimed GHK review. It is rejected here rather than reproduced.

Proposed mechanism

The direct AHK-Cu study supports a limited cell-biology model:

• At 10^-12 to 10^-9 M, AHK-Cu increased elongation of isolated human scalp follicles during 12-day organ culture and increased proliferation signals in cultured dermal-papilla cells.
• At 10^-9 M, Bcl-2 increased and Bax decreased under the tested culture conditions. Cleaved caspase-3 and PARP cleavage fragments were lower after 72 hours.
• Annexin V/propidium iodide flow cytometry showed 3.48% fewer apoptotic cells, but that result was not statistically significant.

The paper did not test androgen receptors, 5-alpha-reductase, DHT sensitivity, clinical hair density, or hair-loss outcomes in treated people. PeptideGuide’s statement that AHK-Cu “reduces DHT sensitivity” is therefore not supported by the cited record or by the direct 2007 experiment.

Evidence map

The 2007 primary study

The investigators obtained occipital scalp follicles from 10 healthy volunteers aged 20–35 years. The organ-culture experiment analysed 240 hair follicles from three volunteers, with 30 follicles per condition, for 12 days. Cultured dermal-papilla cells were assessed using MTT, flow cytometry, and western blotting.

Follicle elongation was significantly higher at 10^-12 to 10^-9 M than with vehicle. The response was not “more is better”: 10^-8 M inhibited elongation by 14.8 ± 1.2%, and 10^-7 M inhibited it by 81.5 ± 40.8% in that model. The study was partly supported by the Korea Health 21 R&D Project and a research agreement with AmorePacific Corporation.

Human clinical evidence and current registry state

The paper did not apply AHK-Cu to participants. As of the dated search, the exact AHK-Cu terms returned one PubMed record—Pyo et al. 2007—and ClinicalTrials.gov returned zero registered intervention studies. The human ALAVAX trial sometimes cited nearby concerns GHK, not AHK-Cu.

This does not prove that every unpublished, proprietary, regional, or differently indexed experiment is absent. It means that no clinical AHK-Cu treatment evidence was located that can support an efficacy, safety, or dosing claim.

Concentration-response boundary

The strongest practical lesson from the primary paper is not a regimen; it is the biphasic laboratory response. Lower experimental concentrations were associated with follicle elongation, whereas the two highest tested concentrations inhibited elongation.

Molar concentrations in culture medium cannot be converted directly into a percentage serum, scalp application amount, or injectable dose. Skin penetration, formulation, copper speciation, tissue exposure, metabolism, and systemic distribution were not measured. The 2007 values belong in an evidence table, not in instructions for use.

Safety and unknowns

AHK-Cu does not have a clinical safety dataset in the sources located. Specific unknowns include:

• local irritation and sensitisation for a defined topical AHK-Cu formulation;
• systemic absorption and copper exposure;
• pharmacokinetics, metabolism, and half-life;
• interactions with medicines, other cosmetic actives, or copper disorders;
• safety of oral or injectable exposure;
• impurity, counterion, sterility, and concentration differences between marketed raw materials.

The absence of adverse-event reports from a cell/organ-culture paper is not a safety finding in people. The high-concentration inhibition also argues against describing the compound with a generic “green” safety rating.

Regulatory status

As of 5 August 2026, exact-name checks returned no AHK-Cu match in the U.S. Drugs@FDA dataset and no AHK-Cu or alanyl-histidyl-lysine match in the EU Union Register dataset for centrally authorised medicines. Those are bounded database checks, not a claim about every national cosmetic or chemical inventory.

Cosmetic marketing is not medicinal approval. A raw material offered for cosmetic research or labelled “research use only” has not thereby acquired an approved indication, pharmaceutical quality, or a validated human regimen.

Russian literature

A targeted Russian-language search located a 2026 Russian narrative review from authors affiliated with Almea LLC and Reaviz institutions. It discusses AHK-Cu in the context of eyebrow and eyelash cosmetic ingredients and cites Pyo et al. 2007 for the tripeptide. It does not report a new Russian AHK-Cu clinical trial or independent replication.

Importantly, the review concludes that the clinical evidence level for peptides used for hair growth remains low and that further controlled studies are needed. This is useful current regional context, but it is secondary evidence and does not enlarge the underlying AHK-Cu primary dataset.

WADA and sport

A name search of the 2026 WADA Prohibited List and 2026 Monitoring Program did not identify AHK-Cu, alanyl-histidyl-lysine, or copper tripeptide. The Prohibited List is not exhaustive, however, and this page does not infer S0 or any other WADA class from the compound’s lack of medicinal approval.

Absence of a named match is not permission. Athletes remain responsible for the contents of products and should obtain a current case-specific decision from their anti-doping organisation or Global DRO before use.

Common misconceptions

• “AHK-Cu and GHK-Cu are interchangeable.” No. Ala-His-Lys and Gly-His-Lys are distinct sequences, and the GHK human study cannot be transferred to AHK.
• “The study was in humans.” It used human-derived follicles and cells outside the body; participants were donors, not treated study subjects.
• “The paper proves an anti-DHT mechanism.” It did not measure DHT, androgen receptors, or 5-alpha-reductase.
• “The apoptosis reduction was significant.” The reported 3.48% reduction was not statistically significant.
• “The culture concentration gives a topical or injectable dose.” It does not; no human exposure or PK bridge exists.
• “A green safety label means it is clinically safe.” No clinical AHK-Cu safety dataset was located, and higher concentrations inhibited the primary experimental outcome.

Research verdict

AHK-Cu has a defined tripeptide identity and one informative primary study in human-derived hair models. That paper supports further research into concentration-dependent effects on follicle elongation and dermal-papilla cell biology. It does not establish a treatment, dose, clinical benefit, or human safety profile.

The current evidence grade is therefore preclinical, despite the use of human tissue. The most important corrections are to keep AHK-Cu separate from GHK-Cu, reject the unrelated PeptideGuide PMID, preserve the inhibitory high-concentration result, and state plainly that no registered clinical AHK-Cu intervention was located.