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ghk-cu-50mg-copper-peptide

GHK-Cu 50mg Copper Peptide

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GHK-Cu 50mg Copper Peptide :

Unit Size 50mg/vial
Unit Quantity 1 vial
Purity (Mass Spectrometry and UV) 99.93%
Sequence Gly-His-Lys.Cu.xHAc
Molecular Formula C14H23CUN604
Appearance Lyophilized Powder
Source Chemical Synthesis
Storage
Lyophilized GHK-Cu 50mg Copper Peptide is stable at room
Temperature for 90 days, however it is best to store
in a freeze below - 8c for any extended period of time.
Terms The products we offer are intended for laboratory
research use only. Please familiarize yourself with
our terms of service prior to ordering.
All content and product information provided on this website are for informational and educational purposes only.
GHK-Cu 50mg Copper Peptide – GHK-Cu, or Glycyl-L-Histidyl-L-Lysine Copper(II), is a synthetic copper peptide created by chelating the GHK peptide with copper ions. Known for a broad range of biological activities, GHK-Cu has been studied in *in vitro* settings for its effects on tissue remodeling, angiogenesis, and anti-inflammatory properties. This product is strictly for in vitro laboratory research and is not approved for human or veterinary use.

Tissue Remodeling and Wound Healing: Studies show that GHK-Cu promotes tissue remodeling by enhancing growth factors like basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF), especially at concentrations around 1 nM.(2-4) These growth factors are essential in angiogenesis, helping support blood vessel formation for tissue repair. Additionally, GHK-Cu has been shown to stimulate endothelial cell proliferation, playing a key role in angiogenesis and wound healing.(5) GHK-Cu also recruits capillary cells, activates macrophages and mast cells, and promotes collagen and elastin production, which are all important in tissue regeneration and wound contraction.(6-8)

Bone Healing and Regeneration: In *in vitro* and animal models, GHK-Cu has demonstrated potential in bone regeneration, primarily through collagen synthesis and improved osteoblast attachment.(9,10) Studies on animal models, such as those for anterior cruciate ligament reconstruction (ACLR), have shown enhanced healing when GHK-Cu is applied, making it relevant for laboratory research focused on bone and tissue repair.(5,11)

Anti-Inflammatory and Antioxidant Properties: GHK-Cu has been examined for its anti-inflammatory and antioxidant effects. Research shows that GHK neutralizes lipid peroxidation end products and lowers reactive oxygen species (ROS) levels in various cell types.(12) In animal models of fibrosis and acute lung injury, both GHK and GHK-Cu reduce inflammation markers like TNF-α and IL-6. Mechanistic studies also demonstrate that GHK-Cu inhibits NF-κB p65 and p38 MAPK signaling pathways, two key regulators of inflammatory responses.(13)

Cognitive Research: Research on aging mice has shown that GHK administration may enhance cognitive function. Treated mice demonstrated improved performance in spatial navigation tasks, while brain tissue analysis indicated reduced inflammation and increased histone deacetylase 2 labeling, suggesting potential epigenetic mechanisms. These findings highlight GHK’s broad biological effects beyond tissue repair and inflammation.(14)

Important Notice: The findings presented are based on in vitro studies and preclinical research. This GHK-Cu product is strictly intended for in vitro laboratory research only and is not suitable for human, veterinary, or therapeutic use. Any use outside of controlled laboratory settings is prohibited.

References

  1. Pickart L. The human tri-peptide GHK and tissue remodeling. J Biomater Sci Polym Ed. 2008;19(8):969-988.
  2. Pollard JD, Quan S, Kang T, Koch RJ. Effects of copper tripeptide on the growth and expression of growth factors by normal and irradiated fibroblasts. Arch Facial Plast Surg. 2005;7(1):27-31.
  3. Steiling H, Werner S. Fibroblast growth factors: key players in epithelial morphogenesis, repair, and cytoprotection. Curr Opin Biotechnol. 2003;14(5):533-537.
  4. Powers CJ, McLeskey SW, Wellstein A. Fibroblast growth factors, their receptors, and signaling. Endocr Relat Cancer. 2000;7(3):165-197.
  5. Wang X, Liu B, Xu Q, et al. GHK-Cu-liposomes accelerate scald wound healing in mice by promoting cell proliferation and angiogenesis. Wound Repair Regen. 2017;25(2):270-278.
  6. Raju KS, Alessandri G, Gullino PM. Characterization of a chemoattractant for endothelium induced by angiogenesis effectors. Cancer Res. 1984;44(4):1579-1584.
  7. Poole TJ, Zetter BR. Stimulation of rat peritoneal mast cell migration by tumor-derived peptides. Cancer Res. 1983;43(12 Pt 1):5857-5861.
  8. Maquart FX, Bellon G, Chaqour B, et al. In vivo stimulation of connective tissue accumulation by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+ in rat experimental wounds. J Clin Invest. 1993;92(5):2368-2376.
  9. Pohunková H, Stehlík J, Váchal J, Cech O, Adam M. Morphological features of bone healing under the effect of collagen-graft-glycosaminoglycan copolymer supplemented with the tripeptide Gly-His-Lys. Biomaterials. 1996;17(16):1567-1574.
  10. Godet D, Marie PJ. Effects of the tripeptide glycyl-L-histidyl-L-lysine copper complex on osteoblastic cell spreading, attachment, and phenotype. Cell Mol Biol (Noisy-le-grand). 1995;41(8):1081-1091.
  11. Fu SC, Cheuk YC, Chiu WY, Yung SH, Rolf CG, Chan KM. Tripeptide-copper complex GHK-Cu (II) transiently improved healing outcome in a rat model of ACL reconstruction. J Orthop Res. 2015;33(7):1024-1033.
  12. Sakuma S, Ishimura M, Yuba Y, Itoh Y, Fujimoto Y. The peptide glycyl-L-histidyl-L-lysine is an endogenous antioxidant in living organisms, possibly by diminishing hydroxyl and peroxyl radicals. Int J Physiol Pathophysiol Pharmacol. 2018;10(3):132-138.
  13. Zhou XM, Wang GL, Wang XB, et al. GHK Peptide Inhibits Bleomycin-Induced Pulmonary Fibrosis in Mice by Suppressing TGFβ1/Smad-Mediated Epithelial-to-Mesenchymal Transition. Front Pharmacol. 2017;8:904.
  14. Mukherjee KK, Lee AY, Zhu L, Darvas M, Ladiges W. Sleep-deprived cognitive impairment in aging mice is alleviated by rapamycin. Aging Pathobiol Ther. 2019;1(1):5-9.