AHK (Tripeptide-3)

AHK (Tripeptide-3) is a three-amino-acid peptide (Ala-His-Lys) investigated for its effects on hair growth, wound healing, and skin rejuvenation. It activates fibroblasts and modulates VEGF signaling to promote collagen synthesis and angiogenesis.

Overview

AHK Tripeptide-3 is a small peptide consisting of alanine, histidine, and lysine residues. It is frequently complexed with copper to form AHK-Cu, though the uncomplexed peptide retains independent biological activity. The cosmeceutical industry sometimes refers to AHK as a "DNA repair factor." It has been studied extensively in animal and in vitro models for its ability to tighten skin, improve elasticity, reduce photodamage, lessen fine lines and wrinkles, and promote cell turnover in the stratum corneum.

Mechanism of Action

AHK activates fibroblasts, the cells responsible for producing the extracellular matrix in skin and connective tissues. Fibroblast activation leads to increased production of collagen and elastin. Collagen provides structural strength and attracts water to the skin, while elastin confers flexibility and resistance to fine line formation. Both proteins decline in quantity and quality with age.

AHK also modulates two key growth factors: it upregulates vascular endothelial growth factor (VEGF) to stimulate blood vessel growth, and it downregulates transforming growth factor beta-1 (TGF-beta1), which regulates cell growth, differentiation, and apoptosis. This dual modulation promotes angiogenesis in the skin while reducing androgen-mediated follicle regression.

Reconstitution Calculator

Research

Collagen and Elastin Production

In vitro studies on human dermal cells demonstrate that AHK increases collagen type I production by more than 300%. It also stimulates elastin synthesis, contributing to improved skin firmness and reduced wrinkle formation. The combined upregulation of both structural proteins supports its application in anti-aging research (Pollard et al., 2005).

Hair Loss Prevention

Hair follicle death is frequently driven by loss of blood supply. Research in animal models shows that AHK stimulates blood vessel growth around hair follicles through VEGF upregulation, resulting in follicle elongation and proliferation of dermal papilla cells (DPCs). DPCs act as regulators of follicle health, ensuring nutrient access and survival. Studies on human dermal cells confirm that AHK promotes angiogenesis in and around follicles, protecting existing hair and supporting regrowth (Pyo et al., 2007).

Wound Healing and Tissue Regeneration

AHK's ability to activate fibroblasts and promote vascular growth makes it relevant to wound healing research. By increasing extracellular matrix production and improving blood supply to damaged tissue, AHK supports the regenerative processes necessary for tissue repair. Irradiated fibroblast models show that copper tripeptide treatment enhances growth factor expression even in damaged cells (Pollard et al., 2005).

Safety Profile

AHK Tripeptide-3 is generally well-tolerated in topical research applications. As a naturally occurring peptide found in mammalian blood, it has a favorable preclinical safety profile. No significant adverse effects have been reported in animal or in vitro studies. Formal human clinical safety data remains limited, though its widespread use in cosmeceutical formulations suggests a low risk profile.

Pharmacokinetic Profile

AHK (Tripeptide-3) — Pharmacokinetic Curve

Topical
0%25%50%75%100%0m30m1h1.5h2h2.5hTimeConcentration (% peak)T_max 13mT_1/2 30m
Half-life: 30mT_max: 15mDuration shown: 2.5h

Quick Start

Route
Topical

Molecular Structure

Molecular Properties
Weight
354.41 Da
CAS
Not available

Research Protocols

topical

Safety Profile AHK Tripeptide-3 is generally well-tolerated in topical research applications.

Quality Indicators

What to look for

  • Well-established safety profile
  • Naturally occurring compound

Frequently Asked Questions

References (2)

Updated 2026-03-08Reviewed by Tides Research Team2 citationsSources: peptide-wiki-mdx, peptide-wiki-mdx-v2

On this page