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Free U.S. shipping on orders over $150Native GHK-Cu peptide is released from the extracellular matrix, cleaved from its parent protein, SPARC (secreted protein, acidic, and rich in cysteine), during extracellular matrix remodelling. Studies find it has vital roles in copper transport, tissue repair, inflammation modulation, and gene regulation [1].
A tripeptide, GHK-Cu is composed of glycine (Gly), histidine (His), and lysine (Lys) [1]. This amino acid complex binds tightly to copper, forming a stable coordination complex [2]. This binding capacity is what gives GHK-Cu its unique biological signalling and regenerative properties [2]. After performing its functions, GHK-Cu is degraded by serum peptidases. Studies show that circulating levels decrease with age, averaging 200 ng/mL at age twenty and declining to 80 ng/mL by age sixty, potentially impacting regenerative capacity [1].
Copper(II) is a redox-active metal required as a cofactor for many enzymes, including cytochrome C oxidase, lysyl oxidase, and superoxide dismutase [2]. GHK binds copper in a bioavailable, non-toxic form, supports shuttling it into cells, and maintains intracellular copper homeostasis [2].
GHK-Cu shows abilities to up- or downregulate over 4,000 genes. These pathways are many, and include those involved in tissue regeneration and repair, anti-inflammatory signalling, antioxidant defenses, and cell growth and differentiation [2].
While scientists are still elucidating some of GHK-Cu peptide’s mechanisms, current research suggests that they include augmenting transcription factors, epigenetic modification (particularly histone and chromatin) and oxidative stress signalling [2].
Research is still emerging on the wide applications of GHK-Cu peptide; however, our current understanding of its actions point towards applications particularly in skin and hair, and regenerative processes.
Research suggests that GHK-Cu peptide may have roles in reprogramming older tissues to act more youthful [2]. When skin gets injured, GHK-Cu is naturally released, acting as an emergency signal to activate skin healing processes [3].
A study using a test tube wound model found that GHK-Cu increases the production of collagen (which gives skin structure), elastin (which keeps skin elastic), and decorin and glycosaminoglycans (key molecules that hydrate and organize skin tissue) [4].
GHK-Cu also supports the balance of enzymes that break down skin proteins, MMPs, and their inhibitors, TIMPs [5],[6]. This prevents the buildup of damaged proteins, and overactive breakdown, which can lead to thinning and sagging skin [2].
One cell-based study found that skin cells exposed to GHK-Cu in combination with red LED light had 12.5x greater cell survival, 230% increase in fibroblast growth factor, and 70% higher collagen production [7].
At the stem cell level, GHK-Cu improved the health and shape of basal cells in the epidermis, increasing markers of stemness, which may help skin regenerate better with age [8].
GHK-Cu peptides show benefits for supporting hair growth, by [9]:
Studies find that GHK-Cu can stimulate fibroblasts, a particular type of skin cell, to produce VEGF (vascular endothelial growth factor), which helps support the growth of new blood vessels surrounding the hair follicle [9]. More blood vessels allow for greater nutrient and oxygen delivery to the area, thus supporting stronger, faster growing hair [9].
It also reduces the production of TGF-beta, a chemical that signals to hair follicles to stop growing and enter the shedding phase of hair growth [9]. With less TGF-beta, hair remains in the growth phase for longer.
By encouraging dermal papilla cells to multiply and protecting them from apoptosis, GHK-Cu supports the development and growth of new hair, by keeping follicles healthy [9].
While more research is needed, our understanding of GHK-Cu points towards potential applications of this peptide in wound healing and repair processes, promotion of antioxidant defenses, angiogenesis, gene modulation, and more [2].
Research Use Only. All findings described above are derived from preclinical studies (animal models and in vitro experiments). GHK-Cu is not approved by the FDA for any diagnostic or therapeutic use in humans. Genesis Peptides makes no claims regarding human clinical efficacy. This product is sold exclusively for laboratory research.
Every lot undergoes six independent assays before release. Results are published in the lot-specific Certificate of Analysis.
GHK-Cu is Glycyl-L-histidyl-L-lysine copper(II), a copper complex of the tripeptide glycyl-L-histidyl-L-lysine (GHK). It is described as the copper-bound form of the human tripeptide glycyl-L-histidyl-L-lysine, with preclinical evidence for tissue regeneration, anti-inflammatory action and antioxidant capacity. A review notes that GHK and GHK-Cu have been studied for matrix remodeling, inflammation, redox regulation, angiogenesis and tissue repair, and that formulation affects coordination state, stability, pharmacokinetics and toxicity. In one in vitro study, GHK-Cu was formulated with Torilis japonica extract (TJE) and examined for anti-atopic and skin-regenerative properties in TNF-α/IFN-γ-stimulated HaCaT cells.
In preclinical animal studies, GHK-Cu reduced inflammation by suppressing the signaling molecules TGF-β and IL-6. A review describes GHK-Cu as an endogenous matricryptin released from collagen Iα2 and SPARC. The review links it to tissue matrix organization, fibrosis reduction and antioxidant defense.
Copper tripeptide-1 is another name for GHK-Cu, which is the copper-bound form of the human tripeptide glycyl-L-histidyl-L-lysine. One source describes GHK-Cu as a human tripeptide derivative, listed as copper tripeptide-1.
Across a group of reviewed peptides that includes GHK-Cu, 67% of identified publications used preclinical animal models, and the review did not report this figure for GHK-Cu separately. For these reviewed peptides, including GHK-Cu, human clinical studies were limited to a handful of investigations. Most of those human investigations lacked robust controls or rigorous study designs, according to the review.
In a human clinical study, GHK-Cu improved patient-reported satisfaction after laser resurfacing and significantly reduced wrinkle volume and depth compared with controls. A separate human clinical study tested GHK-Cu combined with TBFE, not GHK-Cu alone, and found the combination effective in decreasing wrinkles and improving skin barrier conditions. A review covering several peptides, including GHK-Cu, found that human clinical studies were limited to a handful of investigations, most lacking robust controls or rigorous study designs.
In a laboratory study of UV-damaged human skin biopsy samples, Copper Tripeptide-1 (GHK-Cu) combined with ethyl ferulate and cedrol effectively mitigated UV-induced elastic fiber disruption. In a separate laboratory study of human skin explants, a face cream with TBFE and GHK-Cu as its only active ingredients protected the explants from ultraviolet irradiation-induced damage by maintaining skin morphology and decreasing extracellular matrix degradation. Both findings involved GHK-Cu combined with other actives, so they do not show what GHK-Cu alone does against UV damage.
GHK-Cu, a bioactive tripeptide complex known for its anti-aging and tissue repair properties, is described as extensively used in dermatological and hair care formulations. In an animal study, the authors proposed that the dual anti-inflammatory and antioxidant properties of GHK-Cu provide theoretical support for adding it as a functional cosmetic ingredient.
A registered phase 2 study in humans, NCT07437586, is testing GHK-Cu in acute wounds. That study is still recruiting and has no efficacy results. A review lists GHK-Cu among the bioactive peptides it surveys as emerging platforms for wound repair.
In C. elegans worms, GHK-Cu was reported to preserve mitochondrial function, including by increasing mitochondrial membrane potential and promoting ATP biosynthesis. In the same worm studies, GHK-Cu alleviated age-related fragmentation of the mitochondrial network and shifted mitochondrial dynamics toward fusion by regulating drp-1 and fzo-1 expression. GHK-Cu was also reported in C. elegans to activate the DAF-16 and SKN-1 pathways and upregulate sod-3, gst-4, gcs-1, lys-7 and lys-8.
In aged mice, intranasal GHK-Cu induced coordinated suppression of oxidative phosphorylation and MYC target pathways in the hippocampus, with additional attenuation of PI3K-AKT-mTOR signaling in females. The intranasal suppression of oxidative phosphorylation was reported in both males and females, while the attenuation of PI3K-AKT-mTOR signaling was reported only in females and at a false discovery rate of 0.062. In contrast, intraperitoneal GHK-Cu activated oxidative phosphorylation, DNA repair, and MYC targets in the aged mouse hippocampus, which the authors interpreted as engagement of acute stress-response and repair pathways.
In vitro, GHK-Cu was found to have laccase-like catalytic activity. In an in vitro study, a colorimetric method using GHK-Cu's laccase-like activity was used to detect epinephrine, with a linear response range of 20-240 μM and a limit of detection of 9.5 μM.
FOR RESEARCH USE ONLY — Products are sold exclusively for in vitro and preclinical laboratory research. Not for human consumption or administration. Not intended for diagnostic or therapeutic use. These statements have not been evaluated by the FDA.