GHK-Cu 100mg

GHK-Cu is a synthetic small-molecule copper-2 tripeptide complex. The peptide portion runs three residues end-to-end — Glycine, Histidine, Lysine — and binds a single Cu(II) ion at a chelation pocket formed by the histidine imidazole nitrogen, the glycine N-terminal amino group, and adjacent backbone amide nitrogens. The compound was first characterised in early-1970s aged-liver research by Loren Pickart, who isolated a serum factor that restored synthetic activity in aged-liver tissue cultures and sequenced it as the three-residue Gly-His-Lys fragment.

The Cu(II) chromophore gives the lyophilized form its characteristic blue-to-blue-violet tint. Reconstituted aqueous solutions retain a visible blue colour at typical research working concentrations, which serves as a useful visual indicator that the copper-bound complex is intact. Loss of colour during storage often signals copper-ligand dissociation and concentration drift; researchers should treat decolourisation as a flag for fresh reconstitution rather than a benign aesthetic change.

The compound is supplied as a lyophilized blue-tinted powder in a sealed amber-glass vial under inert gas. Each vial contains 100 mg of peptide. Reconstitution with bacteriostatic water is required before the peptide can be drawn into an insulin syringe. Reconstitution mechanics are covered in the Reconstitution accordion below.

GHK-Cu has been the subject of an extensive preclinical literature spanning dermal-matrix research, wound-healing models, hair-follicle research, antioxidant chemistry, and gene-expression profiling. A 2015 review in BioMed Research International documented the multiple cellular pathways modulated in skin-regeneration model systems (PMID 26236730). A 2018 review in the International Journal of Molecular Sciences compiled the regenerative-research findings against the backdrop of transcriptomic profiling that flagged thousands of human genes as up- or down-regulated under GHK-Cu exposure (PMID 29986520). A 2020 review in Aging Pathobiology and Therapeutics framed the broader anti-ageing-published literature around the compound (PMID 35083444). Recent 2024–2026 literature continues to add mechanistic findings (PMID 38879894, PMID 41997403).

Across the literature the compound appears under several names — GHK-Cu, GHK-copper, the formal Glycyl-L-Histidyl-L-Lysine copper complex, the cosmetic-industry INCI name Copper Tripeptide-1, and the formal chemistry-context Cu(II)-GHK. CAS registry numbers 89030-95-5 (Cu complex) and 49557-75-7 (free GHK) and PubChem CIDs 11954184 and 73587 anchor the chemical identity.

Regulatory framing for GHK-Cu sits in a different bracket than other peptides Ronin sells. The compound has been approved as a cosmetic ingredient under multiple jurisdictions' cosmetics frameworks (Health Canada cosmetic-ingredient lists, U.S. FDA cosmetic regulation, EU CosIng database), where it appears under the INCI name Copper Tripeptide-1. Cosmetic ingredient approval is regulatorily distinct from drug approval. No major regulatory body has cleared GHK-Cu as a drug for any therapeutic indication. Ronin Peptides ships the compound exclusively as a research-grade reagent for benchwork — the research-grade form is distinct from the cosmetic-grade form embedded in retail skincare formulations. Dosing protocols, treatment regimens, and administration instructions are out of scope and not provided in any form.

The mechanistic anchor for GHK-Cu is its function as a copper-2 carrier and chaperone. The free Gly-His-Lys tripeptide binds Cu(II) at a chelation pocket built from the histidine imidazole, the glycine N-terminal amino group, and adjacent backbone amides. A 2001 study in Biochimica et Biophysica Acta characterised the chemical behaviour of the Cu(II) complex and two synthetic analogues, anchoring the foundational chelation chemistry of the tripeptide-copper system (PMID 11325542). A 2007 study in Talanta applied electrospray ionisation mass spectrometry to clarify the mechanism by which the Cu(II) complex transports across membrane interfaces (PMID 19071668). Together these chemistry-side findings ground later biological-research interpretations.

Antioxidant research forms the second mechanism stream. A 2007 study in Chemical Research in Toxicology observed that the free GHK tripeptide quenched 4-hydroxy-trans-2-nonenal — a cytotoxic lipid-peroxidation aldehyde — via Michael addition at the histidine and lysine side chains, contributing one route to the broader antioxidant profile attributed to the compound (PMID 17672515). A 2012 review in Oxidative Medicine and Cellular Longevity compiled the antioxidant and degenerative-published literature on the parent complex, including superoxide-dismutase-mimetic activity in copper-bound forms (PMID 22666519). A 2024 paper in Redox Biology observed that the Cu(II)-GHK complex attenuated lung inflammation and fibrosis in murine model systems through redox-pathway modulation (PMID 38879894). A 2026 paper in the European Journal of Pharmacology extended the anti-inflammatory mechanism work to LPS-induced and copper-sulphate-induced inflammation models (PMID 41997403).

Dermal-cell mechanism work has compiled findings on integrin expression, p63 keratinocyte-progenitor markers, decorin, and TGF-β1 modulation. A 2009 paper in Archives of Dermatological Research observed that copper-bound GHK increased integrin expression and p63-positive keratinocyte counts in cell-culture experiments, framing one route by which the compound engages the dermal stem-cell compartment (PMID 19319546). A 2012 study in the Journal of Peptide Science compared copper-bound and copper-free forms of the tripeptide in skin stem-cell-recovery models, providing a direct fragment-versus-complex contrast useful for interpreting the broader literature (PMID 23019153).

Gene-expression-profiling research broadens the mechanism picture beyond direct biochemistry. A 2017 paper in Brain Sciences documented gene-expression effects relevant to nervous-system function (PMID 28212278). A 2018 review in the International Journal of Molecular Sciences compiled transcriptome-profiling data showing thousands of human genes flagged as up- or down-regulated under GHK-Cu exposure across multiple cell-type studies, framing the compound's pleiotropy at the regulatory-network level (PMID 29986520). The transcriptome work suggests the dermal, antioxidant, and tissue-remodelling activity streams may share common upstream regulatory drivers.

Dermal-applications form the largest single body of literature on GHK-Cu. A 2008 paper in the Journal of Biomaterials Science Polymer Edition compiled the tissue-remodelling framings then in development (PMID 18644225). The 2015 BioMed Research International review by the originating laboratory catalogued multiple cellular pathways flagged across in vitro and animal-model studies of skin regeneration (PMID 26236730), including collagen, elastin, glycosaminoglycan, and proteoglycan-synthesis stimulation in fibroblast cultures, alongside fibroblast migration and matrix-deposition findings.

Wound-healing research forms a parallel stream tightly connected to the dermal work. A 2025 paper in Biomaterials Research examined a food-derived tripeptide-copper self-healing hydrogel in infected wound-healing models, broadening the application bracket toward biomaterial-integrated delivery (PMID 39902373). A 2023 paper in Acta Biomaterialia investigated photo-crosslinkable hyaluronic-acid-based hydrogel embedded with GHK-peptide nanofibers as a delivery vehicle for skin-applications (PMID 37832839). The biomaterials-integrated literature represents one of the more active translation tracks for the compound.

Hair-follicle research has been compiled in the broader Pickart reviews. The 2008 review touched on hair-follicle work as part of the wider tissue-remodelling discussion (PMID 18644225). Anagen induction, follicular stem-cell signalling, and hair-shaft thickness research feature in the literature, with translation to topical-cosmetic formulations the predominant clinical-research pathway. Several groups have studied dermal papilla cell cultures exposed to copper-bound tripeptide and have observed differentiation-marker shifts; ex vivo human-follicle research has examined the same compound class.

Antioxidant and oxidative-stress research has been compiled across multiple decades. The 2007 Chemical Research in Toxicology aldehyde-quenching paper (PMID 17672515) and the 2012 Oxidative Medicine and Cellular Longevity review (PMID 22666519) provide the foundational and expansion-era anchors. The 2020 Aging Pathobiology and Therapeutics review (PMID 35083444) framed the broader anti-ageing framing under which oxidative-stress findings are typically grouped. The 2024 Redox Biology lung-inflammation paper (PMID 38879894) and the 2026 European Journal of Pharmacology anti-inflammatory paper (PMID 41997403) extend the redox-pathway work into respiratory-research model systems.

Translation to human clinical application has been narrower than the breadth of the preclinical literature would suggest. Topical cosmetic formulations containing Copper Tripeptide-1 are widely marketed, but research-context translation through drug-approval pathways has not produced a marketed therapeutic in any major jurisdiction. The current framing places GHK-Cu in a long-running expansion-era position: continued mechanistic and translational research continues to appear, but with no near-term drug-approval prospect under the current regulatory framing. Independent laboratory groups have studied the compound across multiple cell types and have observed consistent gene-regulatory patterns in regenerative pathways, while contemporary literature has investigated nanoparticle and hydrogel delivery vehicles and has characterised the compound's pharmacokinetic profile across topical and parenteral routes.

One specification note worth flagging: the molecular-weight figure depends on whether the COA reports the copper-bound complex form (~403.93 g/mol) or the free-peptide form (340.38 g/mol). Ronin ships the copper-2 complex; the COA returned for each batch reports the Cu-bound mass against the 403.93 expected value. Researchers integrating this compound into mass-spec-coupled protocols should verify the salt and counterion form against the COA returned for the specific batch in hand.

Unopened lyophilized vials hold up well under dry ambient storage; usable activity persists for several weeks even without refrigeration. The recommended container is the unopened original vial — keep the seal intact until reconstitution. Refrigeration at 2–8 °C is appropriate once the working timeline extends past a month. A standard freezer at −20 °C handles archival storage; ultra-low storage at −80 °C is rarely needed for typical bench-research timescales.

Keep vials shielded from light, ideally in their original outer packaging. The Cu(II) chromophore is photostable in lyophilized form, but reconstituted aqueous solutions show somewhat accelerated degradation under direct UV exposure compared with the dry vial. Repeated temperature cycling accelerates degradation noticeably more than steady storage at any single temperature inside the recommended bands — minimise transitions between cold and ambient.

After reconstitution, refrigerate the solution at 2–8 °C without delay. The typical working window for a reconstituted preparation is four to six weeks at fridge temperature. Past that window, peptide concentration drifts downward through chemical degradation pathways even though the bacteriostatic water's benzyl alcohol still suppresses microbial growth. The 0.9% benzyl alcohol holds back bacterial contamination — the dominant spoilage path — but does not arrest the slower hydrolysis, oxidation, copper-ligand-dissociation, and aggregation processes that accumulate in any aqueous peptide solution.

Loss of the characteristic blue tint in the reconstituted solution is a useful visual signal that the Cu(II) complex has dissociated. Decolourised solutions should be treated as concentration-drifted and discarded; fresh reconstitution from an unopened vial is the appropriate response. The blue colour itself is not a quality indicator at the start of reconstitution — it confirms intact Cu(II) chelation but does not certify peptide purity, which is established at the COA stage.

When a research timeline extends past six weeks, common practice is splitting the reconstituted solution into single-use volumes and freezing them at −20 °C immediately. Ice-crystal formation during each freeze-thaw cycle inflicts mechanical damage on peptide chains, and pre-splitting eliminates the cumulative loss that comes from thawing one vial multiple times. Thaw individual aliquots overnight in a refrigerator — never at room temperature — and use them within a few days of thaw.

The reconstituted product should be visually transparent with a characteristic blue tint, no suspended particulate. Discard any vial showing turbidity, suspended particulate, yellowing, decolourisation, or visible precipitate. The diluent of choice is USP-grade bacteriostatic water containing 0.9% benzyl alcohol — see the bacteriostatic water product page for reconstitution-grade water.

GHK-Cu sits in a distinct mechanism niche from the other tissue-repair compounds Ronin offers. Its Cu(II) carrier role and gene-expression modulation profile differentiate it from the receptor-pathway anchored mechanisms of BPC-157 (VEGFR2) and the actin-cytoskeleton anchor of TB-500. KPV — also a tripeptide — works through a cytokine-modulation pathway tied to the α-MSH sequence rather than a metal-binding mechanism. Researchers planning multi-compound regenerative protocols often examine GHK-Cu alongside one of the other repair-stream compounds.

A 100 mg vial of GHK-Cu reconstituted with 5 mL of bacteriostatic water yields a final concentration of 20 mg/mL, or 20,000 mcg/mL. Other diluent volumes scale linearly: 2.5 mL gives 40 mg/mL, 10 mL gives 10 mg/mL. The choice of reconstitution volume comes down to the working concentration the researcher wants to draw — there is no single "correct" volume.

Reconstitution procedure:

1. Bring both vials — peptide and bacteriostatic water — to room temperature before opening.
2. Sanitise both rubber stoppers with an alcohol swab.
3. Pull the chosen diluent volume into a sterile transfer syringe.
4. Direct the water against the inner wall of the peptide vial as it is injected — never onto the lyophilized cake, since direct impact foams the solution and denatures peptide at the air-water interface.
5. Invert slowly or swirl gently until everything dissolves. Do not vortex; do not shake.
6. Refrigerate at 2–8 °C the moment reconstitution completes.

A finished preparation should be visually transparent with a characteristic blue tint and no suspended particulate. The blue colour confirms intact Cu(II) chelation; loss of colour during storage signals copper-ligand dissociation and concentration drift. If the solution is hazy, contains visible material, or has decolourised, treat it as degraded and discard.

For dose-volume calculations on insulin syringes, use the Ronin peptide reconstitution calculator. The calculator pre-loads GHK-Cu with default reconstitution volumes and converts target doses to U-100 syringe units automatically.

In published preclinical research, GHK-Cu has been examined across in vitro fibroblast and keratinocyte cultures (PMID 19319546, PMID 23019153), murine wound-healing and tissue-remodelling models (PMID 38879894, PMID 39902373), and broader gene-expression-profiling work in cell culture (PMID 28212278, PMID 29986520). Routes documented in the parent literature include topical, subcutaneous, intraperitoneal, and intravenous administration depending on the model. These figures are research-reference only — Ronin Peptides does not provide dosing recommendations or administration instructions for any non-laboratory purpose.

1. Conato C et al. Copper complexes of glycyl-histidyl-lysine and two of its synthetic analogues: chemical behaviour. Biochim Biophys Acta. 2001;1526(2):199-210. PMID: 11325542 | doi:10.1016/s0304-4165(01)00127-1
2. Beretta G et al. Glycyl-histidyl-lysine (GHK) is a quencher of alpha,beta-4-hydroxy-trans-2-nonenal. Chem Res Toxicol. 2007;20(9):1309-1314. PMID: 17672515 | doi:10.1021/tx700185s
3. Mazurowska L et al. ESI-MS study of the mechanism of glycyl-l-histidyl-l-lysine-Cu(II) complex transport. Talanta. 2007;72(3):650-654. PMID: 19071668 | doi:10.1016/j.talanta.2006.11.034
4. Pickart L. The human tri-peptide GHK and tissue remodeling. J Biomater Sci Polym Ed. 2008;19(8):969-988. PMID: 18644225 | doi:10.1163/156856208784909435
5. Kang YA et al. Copper-GHK increases integrin expression and p63 positivity by keratinocytes. Arch Dermatol Res. 2009;301(4):301-306. PMID: 19319546 | doi:10.1007/s00403-009-0942-x
6. Pickart L et al. The human tripeptide GHK-Cu in prevention of oxidative stress and degenerative conditions of aging. Oxid Med Cell Longev. 2012;2012:324832. PMID: 22666519 | doi:10.1155/2012/324832
7. Choi HR et al. Stem cell recovering effect of copper-free GHK in skin. J Pept Sci. 2012;18(11):685-690. PMID: 23019153 | doi:10.1002/psc.2455
8. Pickart L et al. GHK Peptide as a Natural Modulator of Multiple Cellular Pathways in Skin Regeneration. Biomed Res Int. 2015;2015:648108. PMID: 26236730 | doi:10.1155/2015/648108
9. Pickart L et al. The Effect of the Human Peptide GHK on Gene Expression Relevant to Nervous System Function. Brain Sci. 2017;7(2):20. PMID: 28212278 | doi:10.3390/brainsci7020020
10. Pickart L et al. Regenerative and Protective Actions of the GHK-Cu Peptide in the Light of the New Gene Data. Int J Mol Sci. 2018;19(7):1987. PMID: 29986520 | doi:10.3390/ijms19071987
11. Dou Y et al. The potential of GHK as an anti-aging peptide. Aging Pathobiol Ther. 2020;2(1):58-61. PMID: 35083444 | doi:10.31491/apt.2020.03.014
12. Lee S et al. In situ photo-crosslinkable hyaluronic acid-based hydrogel embedded with GHK peptide nanofibers. Acta Biomater. 2023;172:159-174. PMID: 37832839 | doi:10.1016/j.actbio.2023.10.011
13. Bian Y et al. The glycyl-l-histidyl-l-lysine-Cu(2+) tripeptide complex attenuates lung inflammation and fibrosis. Redox Biol. 2024;75:103237. PMID: 38879894 | doi:10.1016/j.redox.2024.103237
14. Chen H et al. Food-Derived Tripeptide-Copper Self-Healing Hydrogel for Infected Wound Healing. Biomater Res. 2025;29:0139. PMID: 39902373 | doi:10.34133/bmr.0139
15. Hu J et al. Glycyl-L-histidyl-L-lysine-Cu2(+) (GHK-Cu) Attenuates CuSO(4) or LPS induced-inflammation. Eur J Pharmacol. 2026. PMID: 41997403 | doi:10.1016/j.ejphar.2026.178880