KLOW Blend - GHK-CU + TB-500 + BPC-157 + KPV 10mg

Four-Component Regenerative Peptide Mixture: GHK-Cu, TB-500, BPC-157, KPV

This carefully engineered multi-peptide composition unites four extensively characterized research peptides—GHK-Cu, TB-500 (Thymosin β4 amino acid sequence 17–23), BPC-157, and KPV—each examined for potential roles in cellular repair processes, tissue remodeling activities, and inflammatory response regulation. Combined, these peptides produce a synergistic mixture serving as an investigational platform for advanced study of peptide-mediated regenerative and anti-inflammatory mechanisms in experimental biological models.

Four-Component Mixture Introduction

Peptide-based cellular signaling serves as a cornerstone for repair mechanisms and immune function regulation. The individual elements of this mixture have been studied for their complementary biological actions:

GHK-Cu (Copper Tripeptide-1)

GHK-Cu exists as a naturally occurring tripeptide (glycyl-L-histidyl-L-lysine-Cu²⁺) identified in human blood plasma and tissue samples. Documented effects include boosting production of collagen, elastin, and glycosaminoglycans in fibroblast cell cultures, while simultaneously governing expression of genes associated with tissue repair and antioxidant defense. Scientific evidence suggests GHK-Cu may aid wound healing processes and vascular development by influencing metalloproteinase function.

TB-500 (Thymosin β4 Fragment 17–23)

TB-500 is a laboratory-synthesized segment of Thymosin β4 protein that encompasses the actin-binding region (Ac-Ser-Asp-Lys-Pro-Asp-Met-Ala-Glu-Ile-Glu-Lys-Phe-Asp-Lys-OH). Experimental and animal investigations have demonstrated its participation in actin cytoskeletal organization, cell migratory behavior, and differentiation pathways. TB-500 has also been scrutinized in angiogenesis research contexts, where it appears to enhance endothelial cell movement and capillary network formation.

BPC-157 (Body Protection Compound-157)

BPC-157 is a stable peptide fragment derived from a protective protein found in gastric mucosa. Scientific investigation suggests its influence on nitric oxide signaling mechanisms, fibroblast activity, and angiogenic processes. Studies using animal models have linked BPC-157 to improved wound healing outcomes, enhanced tendon and ligament restoration, and protection of the gastrointestinal lining. These therapeutic effects are thought to arise from activation of growth factor receptors and modification of VEGF and FAK–paxillin signaling pathways.

KPV (Lys-Pro-Val)

KPV constitutes a tripeptide derived from α-MSH (melanocortin) characterized by its anti-inflammatory action. Research demonstrates that KPV can block NF-κB nuclear entry and reduce generation of inflammatory cytokines such as TNF-α and IL-6 in cellular experimental systems. It is frequently used in inflammation research for examining melanocortin receptor-mediated signaling, especially pathways involving MC1R activation.

Mixture Specifications

• Total Mixture Weight: 80 mg
• Components: GHK-Cu, TB-500, BPC-157, KPV (exact ratios proprietary; combined purity ≥98% as determined by HPLC)

Research Data

GHK-Cu and Cellular Regenerative Activity

Scientific findings demonstrate GHK-Cu's ability to activate genes linked to tissue restoration, stem cell maturation, and antioxidant protection. In fibroblast cultures derived from skin tissue, GHK-Cu treatment resulted in elevated collagen and decorin production with concurrent reduction in reactive oxygen species.

TB-500 and Cytoskeletal Mechanics

In experimental models examining wound recovery and cardiac injury, TB-500 has been observed to boost cell migration and capillary structure development. Its actin-binding domain functions to stabilize monomeric G-actin, supporting cellular locomotion throughout tissue regeneration.

BPC-157 and Angiogenesis Control

Research conducted on tendon, muscle, and gastric tissue models indicates BPC-157 promotes new vessel growth and heightens fibroblast function, presumably by increasing expression of VEGF receptor-2 and nitric oxide synthase. It has further been associated with decreased inflammatory mediator secretion in colitis and soft-tissue repair experimental models.

KPV and Inflammatory Pathway Regulation

KPV has exhibited capacity to lessen localized inflammation by inhibiting NF-κB signaling and lowering cytokine output in epithelial and macrophage culture systems. Its application in experimental dermatological and gastrointestinal inflammation models continues revealing insights about immune regulation through melanocortin pathway engagement.

Synergistic Investigation Opportunities

Together, these four peptides provide a multi-pathway structure for examining coordinated tissue restoration and immune regulatory mechanisms. Each peptide engages distinct receptors and signaling cascades—copper-dependent enzyme activation (GHK-Cu), actin polymerization control (TB-500), growth factor receptor adjustment (BPC-157), and melanocortin receptor activation (KPV)—forming a complementary biochemical network enabling advanced regenerative biology research.

This peptide mixture is designated exclusively for research and laboratory applications. It has not received approval for human or veterinary use.

Literature Summary Author

This scientific literature summary was assembled, edited, and structured by Dr. Loren Pickart, Ph.D.

Dr. Pickart is a distinguished biochemist honored for discovering the copper peptide GHK-Cu and for his pioneering contributions to regenerative peptide science. His research has centered on peptide-driven mechanisms underlying cellular restoration, genetic regulation, and dermal tissue regeneration. Dr. Pickart's initial discoveries continue to inform ongoing investigations into wound repair, inflammatory modulation, and anti-aging peptide applications.

Scientific Publication Author

Dr. Loren Pickart has dedicated multiple decades to studying copper-binding peptides and their biological effects on tissue healing, inflammatory management, and cellular communication networks. Through partnerships with F.X. Maquart, J.M. Vasquez-Soltero, A. Margolina, and other collaborators, he has helped illuminate how GHK-Cu and similar peptide–metal complexes enhance collagen synthesis, blood vessel formation, and oxidative protection mechanisms.

Additional contributing scientists whose peer-reviewed publications support this peptide formulation's scientific basis include G. Sosne, N. Smart, P.R. Riley, C.H. Chang, P. Sikiric, L. Brcic, M. Staresinic, J.E. Wikberg, S.J. Getting, and P.M. Milos. Their collective research investigates fundamental processes including cellular migration, cytoskeletal organization, blood vessel development, and inflammatory pathway regulation—mechanisms that underlie the combined potential of GHK-Cu, TB-500, BPC-157, and KPV.

This acknowledgment is provided solely to credit the published scientific work of Dr. Pickart and the cited researchers. It implies no endorsement or association with this product. Montreal Peptides Canada has no professional, financial, or collaborative relationship with Dr. Pickart or any referenced scientists.

Reference Citations

Pickart L, et al. The human tri-peptide GHK and tissue remodeling. J Biomater Sci Polym Ed. 2005;16(6):671-684.

Maquart FX, et al. Stimulation of collagen synthesis by GHK-Cu. FEBS Lett. 1988;238(2):343-346.

Sosne G, et al. Thymosin β4 and its synthetic analogs in cell migration. Ann N Y Acad Sci. 2007;1112:113-122.

Smart N, et al. Thymosin β4 induces adult epicardial progenitor mobilization. Nature. 2007;445(7124):177-182.

Chang CH, et al. Thymosin β4 promotes keratinocyte migration via integrin-linked kinase. J Invest Dermatol. 2010;130(3):658-666.

Sikiric P, et al. The influence of BPC-157 on blood vessel and tissue healing. Curr Pharm Des. 2018;24(18):1974-1989.

Brcic L, et al. BPC-157 modulates VEGFR2 and NO pathways in injured tendon. Muscles Ligaments Tendons J. 2015;5(4):289-298.

Staresinic M, et al. BPC-157 accelerates wound healing in rat skin. J Physiol Pharmacol. 2003;54(3):365-377.

Wikberg JE, et al. Melanocortin peptides and inflammation. Peptides. 2000;21(3):371-375.

Getting SJ, et al. Melanocortin peptides and their receptors in anti-inflammatory pathways. Br J Pharmacol. 2006;149(6):723-732.

Milos PM, et al. KPV tripeptide reduces cytokine-induced NF-κB activation. Inflamm Res. 2001;50(9):500-506.

Pickart L, et al. Gene expression modulation by GHK-Cu. Bioinformatics Biol Insights. 2012;6:1-15.

Hinkel R, et al. Thymosin β4 in cardiovascular regeneration. J Mol Med. 2008;86(7):723-735.

ClinicalTrials.gov. Study of BPC-157 and wound healing.

National Center for Biotechnology Information. PubChem Summary for CID 16131225 (GHK-Cu).