GHK-Cu

GHK-Cu is the copper(II) complex of the endogenous tripeptide glycyl-L-histidyl-L-lysine (Gly-His-Lys). Copper coordination occurs through the imidazole nitrogen of the central histidine and the N-terminal glycine amino group, generating the square-planar Cu²⁺ geometry essential to biological activity. The complex modulates an unusually broad transcriptional program — published research describes regulation of approximately 4,000 human genes covering wound healing, collagen synthesis, antioxidant defence, mitochondrial function, and tissue remodelling (Renke et al. 2026, PMID 42123471; Mavrych et al. 2026, PMID 42021992).

Unlike receptor-targeted research peptides, GHK-Cu does not bind a single canonical receptor. Intracellular copper trafficking and direct interaction with chromatin- and transcription-factor-associated proteins are the leading proposed mechanisms (Arciola et al. 2026, PMID 41594073). GHK is also a naturally occurring component of human plasma at roughly 200 ng/mL in young adults, declining with age — a factual basis for the endogenous-tripeptide framing.

A landmark 2026 *Biogerontology* study (Wen et al., PMID 42084774) reported that GHK-Cu extends lifespan in *Caenorhabditis elegans* through coordinated mitochondrial-function preservation (membrane potential, dynamics) and activation of the DAF-16 (FOXO orthologue) and SKN-1 (Nrf2 orthologue) stress-response pathways. Independent zebrafish-larvae work (Hu et al. 2026, PMID 41997403) demonstrates that GHK-Cu reduces neutrophil and macrophage migration, suppresses pro-inflammatory markers, decreases reactive oxygen species, and enhances antioxidant enzyme activity in both CuSO₄ and LPS inflammation models. These are preclinical findings; no human longevity or therapeutic claim is made.

Each Artemis Labs vial ships with a third-party Certificate of Analysis confirming identity (mass spectrometry), purity (≥99% by reverse-phase HPLC), and endotoxin testing (LAL assay, ≤0.5 EU/mg). GHK-Cu is **not** on the FDA 503A Category 2 list and **not** on the WADA Prohibited List. For laboratory research use only — no human dosing, administration, therapeutic, diagnostic, preventative, or longevity claim is made.

Science & Research

## Mechanism of Action

GHK-Cu is the copper(II)-complexed form of the tripeptide Gly-His-Lys (an endogenous human peptide). Copper coordination occurs through the imidazole nitrogen of the central histidine and the N-terminal glycine amino group, generating a square-planar Cu²⁺ geometry essential to biological activity. The complex modulates a broad transcriptional program — published research describes regulation of approximately 4,000 human genes spanning wound healing, collagen synthesis, antioxidant defence, mitochondrial function, and tissue remodelling (Renke 2026, PMID 42123471; Mavrych 2026, PMID 42021992).

The mechanism is fundamentally different from receptor-targeted research peptides: GHK-Cu does not bind a single canonical receptor. Intracellular copper trafficking and direct interaction with chromatin- and transcription-factor-associated proteins are the leading proposed mechanisms (Arciola 2026, PMID 41594073).

## 2024–2026 Mechanism Updates

– **Lifespan extension via mitochondrial / DAF-16 / SKN-1 pathway (Wen et al. 2026, PMID 42084774).** *Biogerontology* report that GHK-Cu extends lifespan in *Caenorhabditis elegans* through coordinated mitochondrial-function preservation (membrane potential, dynamics) and activation of DAF-16 (FOXO orthologue) plus SKN-1 (Nrf2 orthologue) stress-response transcription factors. Most rigorous new mechanism data on GHK-Cu. **Preclinical only — no human longevity claim.**
– **In-vivo anti-inflammatory mechanism (Hu et al. 2026, PMID 41997403).** Zebrafish larvae model: GHK-Cu reduces neutrophil and macrophage migration in both CuSO₄ and LPS inflammation models, suppresses pro-inflammatory markers, upregulates antioxidant enzymes, lowers ROS.
– **Microenvironment-responsive injectable hydrogel for radiation-induced skin injury (Yu et al. 2026, PMID 42058630).** Translational research into GHK-Cu delivery systems.
– **Copper-tripeptide analog synthesis + wound-repair characterisation (Aguilar et al. 2026, PMID 42047624).**
– **Laccase-like enzymatic activity (Chen et al. 2026, PMID 42041438).** Colorimetric phenolic-compound sensing context.
– **Multifunctional wound-repair framing (Arciola et al. 2026, PMID 41594073; Rahman et al. 2026, PMID 41490200).** GHK-Cu reviewed within smart-healing / regenerative-medicine research landscape.

## Regulatory Status

– **Not on FDA 503A Category 2** — unlike CJC-1295, ipamorelin, sermorelin, and BPC-157, GHK-Cu was not placed on the FDA’s interim 503A bulks Category 2 during the 2023–2024 peptide review process.
– **Cosmetic ingredient status** — GHK-Cu is a regulated cosmetic active ingredient. The cosmetic-grade ingredient and the research-grade reagent supplied by Artemis Labs are different supply chains; only the research-grade reagent applies to this product.
– **Endogenous human plasma component** — GHK is naturally present in human plasma at ~200 ng/mL in young adults, declining with age.
– **Not on WADA Prohibited List** — GHK-Cu is not classified as a performance-enhancing compound under WADA.

## Specifications

| Property | Value |
|—|—|
| Tripeptide sequence | Gly-His-Lys (GHK) |
| Coordination | Cu²⁺ chelated via histidine imidazole + N-terminal glycine amino group |
| Tripeptide molecular formula | C₁₄H₂₄N₆O₄ (free tripeptide) |
| Tripeptide MW (free base) | 340.4 g/mol |
| CAS Number — GHK (free) | 49557-75-7 |
| CAS Number — GHK-Cu | 89030-95-5 |
| Endogenous plasma level | ~200 ng/mL in young adults; declines with age |
| Purity Standard | ≥99% by reverse-phase HPLC |
| Storage (lyophilised) | Store at −20 °C, desiccated, protected from light |
| Endotoxin | Tested ≤ 0.5 EU/mg (LAL assay; lot-specific) |
| Form | Lyophilised blue powder, 100 mg/vial |

## Key Citations (selection — full list on research page)

1. Wen H et al. 2026. *Biogerontology* 27(3):100. GHK-Cu delays aging in C. elegans via mitochondrial function + DAF-16/SKN-1. PMID 42084774.
2. Hu J et al. 2026. *Eur J Pharmacol* 1023:178880. GHK-Cu attenuates CuSO₄/LPS inflammation (zebrafish). PMID 41997403.
3. Renke G, Chinellato L. 2026. *Int J Mol Sci.* Therapeutic peptides in aesthetic/metabolic/endocrine conditions. PMID 42123471.
4. Mavrych V et al. 2026. *Front Aging.* Therapeutic peptides in gerontology. PMID 42021992.
5. Arciola CR et al. 2026. *Antibiotics (Basel).* Smart healing for wound repair (regenerative medicine review). PMID 41594073.
6. Mendias CL, Awan TM. 2026. *Sports Med.* Approved + unapproved peptide therapies (musculoskeletal). PMID 41966639.
7. Rahman OF et al. 2026. *J Am Acad Orthop Surg Glob Res Rev.* Therapeutic peptides in orthopaedics. PMID 41490200.
8. Aguilar L et al. 2026. *ChemMedChem.* Copper-tripeptide complexes for wound repair. PMID 42047624.

**No dosing, frequency, route, or human-protocol guidance is supplied. For laboratory research use only.**

Research-Design Pairings

## Research-Design Pairings (Not Human Protocols)

In published research, GHK-Cu is studied alongside other small repair-pathway peptides because its broad gene-expression-modulation profile is mechanistically complementary to the receptor-targeted and cytoskeletal mechanisms of related compounds (Mavrych et al. 2026, PMID 42021992). Pairings below are *research-design rationale*, not human-protocol recommendations.

### GHK-Cu + BPC-157 / TB-500 (regeneration-research stack)

– **GHK-Cu** — Cu²⁺-binding tripeptide; broad gene-expression modulation of collagen, antioxidant, and tissue-remodelling pathways
– **BPC-157** — Pentadecapeptide; VEGFR2-Akt-eNOS angiogenesis + GI/tendon repair literature
– **TB-500** — Tβ4 fragment 17–23; G-actin sequestration; cytoskeletal-repair literature
– **Why studied together** — the four-peptide regeneration-research composition (sometimes called the “Wolverine” stack in popular reporting) combines complementary upstream and downstream repair-pathway mechanisms

### GHK-Cu + KPV (anti-inflammatory pairing)

– **GHK-Cu** — antioxidant-defence + ROS-suppression evidence (Hu 2026)
– **KPV** — α-MSH C-terminal tripeptide; NF-κB pathway inhibition
– **Why studied together** — mechanistically complementary anti-inflammatory pathways at the transcriptional level

### GHK-Cu + MOTS-c (mitochondrial-bioenergetic complement)

– **GHK-Cu** — preserves mitochondrial membrane potential and dynamics (Wen 2026 C. elegans data)
– **MOTS-c** — mitochondrial-derived peptide; AMPK signalling
– **Why studied together** — both target mitochondrial function through different proximal mechanisms; informative comparator pair in longevity research designs

### GHK-Cu Longevity Quartet research context

In gerontology research, GHK-Cu is one of four compounds studied together as a “longevity research” composition (with MOTS-c, SS-31, and Semax). The shared theme is mitochondrial / oxidative-stress / cognitive-protection mechanisms.

**No dosing, frequency, route, or human-protocol guidance is supplied.** All commentary above is research-design rationale per CLAUDE.md content rule #1.

For full mechanism context, see the [GHK-Cu research page](https://artemispeptides.com/product/ghk-cu/) (Science & Research tab + full citation list).