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AHK-Cu

Awaiting Reclassification

Copper signaling for follicle renewal

A copper-bound tripeptide that stimulates fibroblast proliferation and follicle signaling.

Educational content. This page describes AHK-Cu for informational purposes only and is not medical advice, diagnosis, or treatment. Consult a licensed provider before starting, stopping, or modifying any therapy.

Primary Use
A copper-bound tripeptide that stimulates fibroblast proliferation and follicle signaling.
Administration
topical, injection
Typical Cycle
8 to 12 weeks minimum
Legal Status
Awaiting Reclassification
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Key Benefits

Dermal Papilla Cell Protection

Reduces caspase-3 activity by 42.7% and PARP cleavage by 77.5% in dermal papilla cells, shifting the Bcl-2/Bax ratio toward survival and shielding hair follicle command centers from programmed cell death.[1]

Hair Follicle Growth Stimulation

Significantly increases human hair follicle elongation at picomolar to nanomolar concentrations over 12 days in organ culture, with dose-dependent proliferation of dermal papilla cells.[1]

Growth Factor Modulation

Upregulates VEGF to support blood supply to follicles while downregulating TGF-beta1, a negative growth factor that pushes follicles into the resting phase.[1][4]

Copper-Dependent Enzymatic Support

Delivers bioavailable copper as a cofactor for lysyl oxidase (collagen and elastin cross-linking) and superoxide dismutase (antioxidant defense) in skin tissue.[3][4]

What is AHK-Cu?

AHK-Cu (L-alanyl-L-histidyl-L-lysine copper complex), also known as Copper Tripeptide-3, is a synthetic tripeptide bound to a divalent copper ion. It consists of alanine, histidine, and lysine chelated to Cu2+ with high affinity. The histidine residue's imidazole side chain plays the central role in copper coordination, while the lysine amino group provides additional binding stability.

AHK-Cu is a structural analog of GHK-Cu (Copper Tripeptide-1), differing only at position 1 where alanine replaces glycine. This substitution adds a methyl group that creates a slightly more rigid copper-binding pocket and may reduce spontaneous copper dissociation. Unlike GHK-Cu, which occurs naturally in human plasma, saliva, and urine, AHK-Cu is entirely synthetic with no evidence of endogenous occurrence. Its primary research focus has been on hair follicle biology.

How Does It Work?

AHK-Cu's best characterized mechanism involves stimulation of dermal papilla cells, the specialized fibroblasts that serve as the signaling center for hair follicle morphogenesis and cycling. At picomolar to nanomolar concentrations, it promotes dermal papilla cell proliferation and protects these cells from apoptosis through elevation of the Bcl-2/Bax ratio and suppression of the caspase-3/PARP cleavage cascade.

The peptide also modulates key growth factors in follicle tissue. It upregulates vascular endothelial growth factor (VEGF), promoting angiogenesis and blood supply to follicles, while downregulating transforming growth factor beta-1 (TGF-beta1), which normally pushes follicles from the active growth phase into the resting phase.

Critically, AHK-Cu shows a biphasic dose response. It is effective at extremely low concentrations (10^-12 to 10^-9 M) but becomes inhibitory at higher concentrations (10^-8 M and above). This means more is not better, and proper formulation is important for maintaining the effective concentration range.

Mechanism of Action

AHK-Cu delivers bioavailable copper to dermal papilla cells while activating anti-apoptotic signaling (elevated Bcl-2/Bax ratio, reduced caspase-3 and PARP cleavage). It upregulates VEGF for follicle blood supply, downregulates TGF-beta1 to extend the growth phase, and supports copper-dependent enzymes including lysyl oxidase and superoxide dismutase.

AHK-CuAnti-Apoptotic ShiftBcl-2/Bax ratio elevationVEGF UpregulationFollicle angiogenesisTGF-β1 SuppressionGrowth phase extensionDPC SurvivalCaspase-3 & PARPcleavage reducedFollicle GrowthHair elongation atpM to nM rangeCopper DeliveryLysyl oxidase & SODcofactor supportDermal Papilla Protection & Hair Follicle Stimulation

Clinical Evidence

Key studies supporting the therapeutic use of this peptide.

Tripeptide-Copper Complex Effects on Human Hair Growth

Ex vivo organ culture and in vitro cell culture study240 human hair follicles from 10 healthy volunteers (30 follicles per condition), plus cultured dermal papilla cells

Hair follicle elongation significantly increased at 10^-12 to 10^-9 M over 12 days (p < 0.001). Dermal papilla cell proliferation increased dose-dependently. Caspase-3 reduced 42.7% and PARP cleavage reduced 77.5% (both p < 0.05). Concentrations at 10^-8 M and above inhibited growth.

Pyo HK, Yoo HG, Won CH, et al.Arch Pharm Res, 30(7):834-839 (2007) · PubMed

Hair Follicle-Stimulating Properties of Peptide Copper Complexes

In vivo animal studyC3H mice treated with copper peptide analogs

Copper tripeptide complexes from the same family as AHK-Cu stimulated hair follicle activity in the mouse model, supporting the class-wide effect of copper peptides on follicle biology.

Trachy RE, Fors TD, Pickart L, Uno HAnn N Y Acad Sci, 642:468-469 (1991) · PubMed

In Vivo Connective Tissue Accumulation by GHK-Cu

Controlled animal wound chamber studyRats with subcutaneous stainless steel mesh wound chambers

The structurally related GHK-Cu produced concentration-dependent increases in collagen, DNA, glycosaminoglycans, and elastin. Collagen synthesis was stimulated 2-fold more than non-collagen protein synthesis. Control tripeptide without copper had no effect.

Maquart FX, Bellon G, Chaqour B, et al.J Clin Invest, 92(5):2368-2376 (1993) · PubMed

Dosing & Administration

Typical protocols used in clinical practice. Always consult a licensed provider for personalized dosing.

Topical (serum/solution)

Dosage
0.3 to 1% AHK-Cu in final formulation
Frequency
Once daily
Cycle
8 to 12 weeks minimum

Topical (serum/solution): Effective at extremely low concentrations. Higher concentrations are inhibitory. Start with lower concentrations.

AHK-Cu shows a biphasic dose response: effective at picomolar to nanomolar concentrations but inhibitory at 10^-8 M and above. Formulation must maintain the effective concentration window at the tissue level.

No human clinical trials have established a validated dosing protocol. All concentration guidance comes from a single ex vivo/in vitro study and general copper peptide class data.

AHK-Cu is reportedly stable at pH 4.5 to 6.8, a wider range than GHK-Cu which degrades below pH 5.5. Avoid combining with strong exfoliating acids or low-pH vitamin C formulations that may destabilize the copper-peptide bond.

Side Effects & Safety

Common

  • Skin redness or irritation Mild, localized, and transient erythema at the application site, especially at higher concentrations
  • Itching or tingling Temporary pruritus that typically resolves within minutes of application

Uncommon

  • Skin congestion or breakouts Possible in oily skin types; reduce frequency if this occurs

Rare

  • Growth inhibition at high doses Concentrations above the optimal range (10^-8 M and higher) actively inhibit follicle growth rather than promoting it

Safety Profile

No formal toxicology studies have been published specifically on AHK-Cu. All safety information is extrapolated from one in vitro study and general copper peptide class data.

The related peptide GHK-Cu has an extensive safety record with topical use, and its toxic dose is approximately 300 times the therapeutic dose. AHK-Cu likely shares a similar safety margin for topical application.

No long-term safety data exists. The single published study on AHK-Cu (Pyo et al. 2007) has not been replicated or extended to in vivo or human testing in the years since publication.

Contraindications

  • Wilson's disease (impaired copper metabolism and excretion)
  • Menkes disease (copper transport disorder)
  • Known allergy to copper or to alanine, histidine, or lysine
  • Pregnancy and breastfeeding (no safety data exists)
  • Open wounds or broken skin (may cause irritation; patch test on intact skin first)

Compare with Similar Peptides

See how AHK-Cu compares to peptides with overlapping benefits.

PeptidePrimary UseAdministrationCycle LengthKey Differentiator
AHK-CuHair & Skin RegenerationTopical8 to 12 weeksHair follicle-focused copper peptide with demonstrated dermal papilla cell protection and a biphasic dose response requiring precise formulation
SS-31 (Elamipretide)Mitochondrial Restoration & Anti-AgingInjection (daily)Continuous (weeks to months)Only peptide that directly targets cardiolipin on the inner mitochondrial membrane to restore electron transport chain efficiency
Melanotan 1 (Afamelanotide)Photoprotection & PigmentationSubcutaneous ImplantEvery 60 days (ongoing)The only FDA-approved melanocortin agonist, combining eumelanin induction with UV-independent DNA repair through a selective MC1R mechanism
GHK-CuAnti-Aging & RecoveryTopical, Injection8–12 weeksOnly peptide demonstrated to modulate ~31% of human genes, epigenetically resetting cellular function toward a younger phenotype
SermorelinAnti-Aging & GH RestorationInjection (daily)3–6 monthsOnly GHRH analog with FDA approval history and multi-decade safety record, uniquely preserving natural GH feedback

Regulatory Status

Current FDA classification and compounding eligibility.

Not Listed

503A Compounding

This substance does not appear on any FDA bulk drug substances list. It is classified as research-use only and cannot be legally compounded for human use.

Regulatory Detail

AHK-Cu does not appear on any FDA 503A or 503B bulk drug substances list. It has no NDA, BLA, or IND. It has never been nominated for FDA evaluation. Compounding pharmacies cannot legally compound AHK-Cu for human use under current FDA regulations. Available only as a research-use or cosmetic ingredient.

What do these terms mean?
503A compounding
Licensed pharmacies that prepare custom prescriptions for individual patients based on a physician's order. 503A is the section of the federal law that governs them.
503B outsourcing
FDA-registered facilities that compound in larger batches under stricter federal oversight (closer to a manufacturer than a pharmacy). Used mostly by hospitals and clinics.
Bulk drug substance
The active pharmaceutical ingredient a compounder starts with, before it's made into a finished medication.
Category 1
Interim bucket for bulk substances that have been nominated and don't appear to present significant safety risks. 503A pharmacies may compound them under FDA enforcement discretion while the agency continues its review. Not the same as FDA approval.
Category 2
Bulk substances the FDA has flagged for significant safety risks. 503A compounding carries FDA enforcement risk, so most pharmacies decline to prepare them and many physicians hesitate to prescribe them.
PCAC
Pharmacy Compounding Advisory Committee. The FDA advisory committee that reviews nominated bulk substances and recommends whether they belong in Category 1, Category 2, or on the final 503A Bulks List.

Last verified April 12, 2026. PepHookup tracks public FDA actions. This is not legal or medical advice.

Frequently Asked Questions

Research & References

  1. 1

    Pyo HK, Yoo HG, Won CH, et al. The effect of tripeptide-copper complex on human hair growth in vitro.” Arch Pharm Res, 30(7):834-839 (2007)

  2. 2

    Trachy RE, Fors TD, Pickart L, Uno H The hair follicle-stimulating properties of peptide copper complexes. Results in C3H mice.” Ann N Y Acad Sci, 642:468-469 (1991)

  3. 3

    Maquart FX, Bellon G, Chaqour B, et al. In vivo stimulation of connective tissue accumulation by the tripeptide-copper complex GHK-Cu2+.” J Clin Invest, 92(5):2368-2376 (1993)

  4. 4

    Pickart L, Margolina A Regenerative and Protective Actions of the GHK-Cu Peptide in the Light of the New Gene Data.” Int J Mol Sci, 19(7):1987 (2018)

  5. 5

    Pickart L The human tri-peptide GHK and tissue remodeling.” J Biomater Sci Polym Ed, 19(8):969-988 (2008)

  6. 6

    Maquart FX, Pickart L, Laurent M, et al. Stimulation of collagen synthesis in fibroblast cultures by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+.” FEBS Lett, 238(2):343-346 (1988)

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