KLOW (BPC-157 + TB-500 + GHK-cu + KPV)

GHK-Cu + TB-500 + BPC-157 + KPV Peptide Blend

This multi-component peptide formulation combines four distinct research peptides—GHK-Cu, TB-500 (Thymosin β4 fragment 17-23), BPC-157, and KPV—each of which has been investigated for its potential to influence cellular repair, tissue remodeling, and inflammatory pathways. The combined blend provides a platform for advanced study of peptide-mediated regenerative and anti-inflammatory mechanisms in experimental biological models.

Overview

Peptide-based signaling plays a critical role in cellular repair and immune modulation. The individual components of this blend have been studied for complementary properties:

GHK-Cu (Copper Tripeptide-1)

GHK-Cu is a naturally occurring copper-binding tripeptide (glycyl-L-histidyl-L-lysine-Cu²⁺) present in human plasma and tissues. It has been reported to upregulate the synthesis of collagen, elastin, and glycosaminoglycans in cultured fibroblasts, while also modulating gene expression linked to tissue regeneration and antioxidant defense. Research indicates that GHK-Cu may also promote angiogenic activity and support wound closure models by influencing metalloproteinase balance.

TB-500 (Thymosin β4 Fragment 17-23)

TB-500 represents a synthetic segment of the Thymosin β4 molecule containing the actin-binding domain (Ac-Ser-Asp-Lys-Pro-Asp-Met-Ala-Glu-Ile-Glu-Lys-Phe-Asp-Lys-OH). In vitro and in vivo experiments have suggested roles in actin cytoskeleton organization, cellular migration, and differentiation. TB-500 has been studied in angiogenesis models, where it may enhance endothelial cell migration and capillary formation.

BPC-157 (Body Protection Compound-157)

BPC-157 is a stable pentadecapeptide fragment derived from a gastric protective protein. Experimental data suggest it modulates nitric-oxide signaling, fibroblast recruitment, and angiogenesis. Rodent studies have associated BPC-157 administration with accelerated wound closure, tendon and ligament regeneration, and gastrointestinal mucosal protection. These effects are believed to be mediated through the activation of growth factor receptors and modulation of the VEGF and FAK-paxillin pathways.

KPV (Lys-Pro-Val)

KPV is a short α-MSH (melanocortin)–derived tripeptide with recognized anti-inflammatory properties. Research indicates KPV can suppress the nuclear translocation of NF-κB and reduce the expression of pro-inflammatory cytokines such as TNF-α and IL-6 in cellular models. It is often utilized in experimental inflammation assays to explore melanocortin receptor signaling (particularly MC1R-mediated responses).

Chemical Makeup

• Total Blend Mass: 80 mg
• Constituents: GHK-Cu, TB-500, BPC-157, KPV (individual ratio proprietary; combined purity ≥ 98 % by HPLC)

Each peptide component is independently characterized by LC-MS to verify molecular identity and purity before formulation. The combined lyophilized blend is provided as a homogeneous powder suitable for reconstitution in sterile water for biochemical research applications.

Research and Experimental Studies

GHK-Cu and Cellular Regeneration

Research demonstrates that GHK-Cu can activate gene networks related to tissue remodeling, stem cell differentiation, and anti-oxidative responses. In dermal fibroblast cultures, GHK-Cu exposure increased collagen and decorin expression and reduced reactive oxygen species.

TB-500 and Cytoskeletal Dynamics

In wound-healing and myocardial injury models, TB-500 has been reported to improve cell migration and capillary tube formation. The fragment’s actin-binding motif enables the stabilization of G-actin monomers, facilitating cellular motility during regeneration.

BPC-157 and Angiogenic Modulation

Studies in tendon, muscle, and gastric tissue models indicate that BPC-157 supports angiogenesis and enhances fibroblast activity, potentially through upregulation of VEGF receptor-2 and nitric-oxide synthase. It has also been linked to reduced pro-inflammatory mediator release in experimental colitis and soft-tissue repair models.

KPV and Inflammatory Regulation

KPV has been shown to exert localized anti-inflammatory effects by downregulating NF-κB activation and cytokine expression in epithelial and macrophage cultures. Its use in experimental dermatologic and intestinal inflammation models continues to provide insight into melanocortin-based immune modulation.

Synergistic Research Potential

The combination of these four peptides offers a multi-pathway model for studying coordinated tissue repair and immune balance. Their distinct receptor targets and signaling pathways—copper-dependent enzymatic activation (GHK-Cu), actin polymerization control (TB-500), growth factor receptor modulation (BPC-157), and melanocortin receptor activity (KPV)—provide a complex but complementary biochemical network suitable for advanced regenerative biology research.

This peptide blend is supplied strictly for research and laboratory use only. Not for human or veterinary application.

References

1. Pickart L, et al. The human tri-peptide GHK and tissue remodeling. J Biomater Sci Polym Ed. 2005;16(6):671-684. https://pubmed.ncbi.nlm.nih.gov/16046853/
   
2. Maquart FX, et al. Stimulation of collagen synthesis by GHK-Cu. FEBS Lett. 1988;238(2):343-346. https://pubmed.ncbi.nlm.nih.gov/3166886/
   
3. Sosne G, et al. Thymosin β4 and its synthetic analogs in cell migration. Ann N Y Acad Sci. 2007;1112:113-122. https://pubmed.ncbi.nlm.nih.gov/17947592/
   
4. Smart N, et al. Thymosin β4 induces adult epicardial progenitor mobilization. Nature. 2007;445(7124):177-182. https://pubmed.ncbi.nlm.nih.gov/17215841/
   
5. Chang CH, et al. Thymosin β4 promotes keratinocyte migration via integrin-linked kinase. J Invest Dermatol. 2010;130(3):658-666. https://pubmed.ncbi.nlm.nih.gov/19812597/
   
6. Sikiric P, et al. The influence of BPC-157 on blood vessel and tissue healing. Curr Pharm Des. 2018;24(18):1974-1989. https://pubmed.ncbi.nlm.nih.gov/29708060/
   
7. Brcic L, et al. BPC-157 modulates VEGFR2 and NO pathways in injured tendon. Muscles Ligaments Tendons J. 2015;5(4):289-298. https://pubmed.ncbi.nlm.nih.gov/26697586/
   
8. Staresinic M, et al. BPC-157 accelerates wound healing in rat skin. J Physiol Pharmacol. 2003;54(3):365-377. https://pubmed.ncbi.nlm.nih.gov/14566078/
   
9. Wikberg JE, et al. Melanocortin peptides and inflammation. Peptides. 2000;21(3):371-375. https://pubmed.ncbi.nlm.nih.gov/10822038/
   
10. 
    Getting SJ, et al. Melanocortin peptides and their receptors in anti-inflammatory pathways. Br J Pharmacol. 2006;149(6):723-732. https://pubmed.ncbi.nlm.nih.gov/17031384/
    
11. Milos PM, et al. KPV tripeptide reduces cytokine-induced NF-κB activation. Inflamm Res. 2001;50(9):500-506. https://pubmed.ncbi.nlm.nih.gov/11605739/
    
12. Pickart L, et al. Gene expression modulation by GHK-Cu. Bioinformatics Biol Insights. 2012;6:1-15. https://pubmed.ncbi.nlm.nih.gov/22399871/
    
13. Hinkel R, et al. Thymosin β4 in cardiovascular regeneration. J Mol Med. 2008;86(7):723-735. https://pubmed.ncbi.nlm.nih.gov/18461361/
    
14. ClinicalTrials.gov. Study of BPC-157 and wound healing. https://clinicaltrials.gov/ct2/show/NCT04173625
    
15. National Center for Biotechnology Information. PubChem Summary for CID 16131225 (GHK-Cu). https://pubchem.ncbi.nlm.nih.gov/compound/16131225

For Research Use Only. Not for human or veterinary use.