AHK-Cu protocol

Dose ranges reflect commonly studied amounts in published research models. This is not medical advice. For research use only. Not for human consumption.

Protocol Comparison

Research Dose Reference

Available in 50 mg & 100 mg

AHK-Cu

Skin & Hair

Research dose range

0 mg1 mg2 mg3 mg4 mg

Standard research range

1 - 2 mg

Core experimental range for sustained follicle stimulation and VEGF expression.

Research focus

Hair follicle dermal papilla stimulation & microcirculation

Observed window

4-8 week active cycle

Administration

Daily laboratory topical or localized protocol

Primary pathway

Dermal Papilla Cells (DPC) / VEGF / TGF-beta1 suppression

Dosing compiled from copper peptide biological literature. For laboratory research and development only.

PROTOCOL BENEFITS

Engineered Outcomes

Dermal Papilla StimulationVEGF UpregulationHair Follicle Focus

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Directly stimulates dermal papilla cells (DPC) at the base of hair follicles.

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Upregulates VEGF to support capillary microcirculation while suppressing follicle-inhibiting TGF-beta1.

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Engineered by exchanging a single amino acid from GHK-Cu, directing activity specifically to hair follicles.

SCIENCE

How It Works.

AHK-Cu is a copper tripeptide (alanyl-L-histidyl-L-lysine:copper) differing from GHK-Cu by a single amino acid residue. This subtle structural alteration specifically targets the biological microenvironment of hair follicles.

Ex-vivo research at Seoul National University demonstrated that AHK-Cu stimulates dermal papilla fibroblast elongation, boosts VEGF production, suppresses apoptosis-promoting TGF-beta1, and reduces programmed cell death markers by up to 78%.

WHAT TO EXPECT

Because the active anagen growth phase of hair follicles spans years, follicle cycling research is evaluated across active 4–8 week cycles followed by structured resting phases.

PROTOCOL NOTE

Available in 50 mg and 100 mg vials. For laboratory research use only.

FAQ

Protocol Questions

What is the difference between AHK-Cu and GHK-Cu?+

A single amino acid substitution (alanine replacing glycine) shifts AHK-Cu's binding affinity toward hair follicle dermal papilla cells rather than broad systemic collagen synthesis.

Why does the dosage reference draw from GHK-Cu data?+

Because dedicated human clinical pharmacokinetic data for injectable AHK-Cu is limited, dosing models in research communities are extrapolated from its closest structural analog, GHK-Cu.