Klow Blend (TB-500/10MG-BPC-157/10MG-GHK/50MG-KPV/10MG)

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Product Overview

KLOW Peptide Blend Evidence

KLOW is a precision-formulated peptide blend combining GHK-Cu, KPV, BPC-157, and TB500, designed to synergistically support cellular repair, inflammation control, and tissue regeneration.

Cellular Repair & Tissue Regeneration

  • GHK-Cu: Stimulates collagen, elastin, and GAG synthesis; promotes angiogenesis and fibroblast activation; accelerates wound healing in skin, bone, GI mucosa, and other tissues; upregulates pro-repair genes and downregulates pro-inflammatory/tissue-destructive genes.[1–6]
  • BPC-157: Pleiotropic healing across skin, muscle, tendon, ligament, nerve, and GI tissue; supports angiogenesis, modulates growth-factor pathways, and facilitates rapid resolution of vessel constriction/clot formation; broad wound-healing gene modulation.[7–8]
  • TB500 (thymosin β4): Actin sequestration, cell migration, and angiogenesis to accelerate repair and reduce fibrosis (established in preclinical/translational literature).

Inflammation Control

  • GHK-Cu: Suppresses TNF-α/IL-6, inhibits NF-κB and p38 MAPK, reduces oxidative stress; restores MMP/TIMP balance; mitigates inflammatory cell infiltration and supports mucosal/epithelial healing via SIRT1/STAT3 and TGFβ1/Smad2/3 pathways in colitis and pulmonary fibrosis models.[3,9–12]
  • BPC-157: Anti-inflammatory and cytoprotective across multiple organs with favorable safety in preclinical work; supports tissue homeostasis during injury/repair.[7–8]
  • KPV (Lys-Pro-Val): Melanocortin-derived tripeptide that inhibits pro-inflammatory cytokines and supports epithelial barrier function (established in literature).

Synergistic Mechanisms

  • GHK-Cu: Drives tissue remodeling, angiogenesis, and anti-inflammatory gene programs.[1–6,9–12]
  • BPC-157: Accelerates wound closure, supports angiogenesis, modulates inflammation.[7–8]
  • KPV: Targets cytokine suppression and epithelial barrier integrity (mechanism established).
  • TB500: Enhances cell migration/angiogenesis and reduces fibrosis (mechanism established).

References

  1. Pickart L, Margolina A. Int J Mol Sci. 2018;19(7):E1987.
  2. Pickart L. J Biomater Sci Polym Ed. 2008;19(8):969-988.
  3. Pickart L, Vasquez-Soltero JM, Margolina A. Biomed Res Int. 2015;2015:648108.
  4. Pickart L, Vasquez-Soltero JM, Margolina A. Biomed Res Int. 2014;2014:151479.
  5. Wang X, Liu B, Xu Q, et al. Wound Repair Regen. 2017;25(2):270-278.
  6. Lee S, Lee SM, Lee SH, et al. Acta Biomater. 2023;172:159-174.
  7. Seiwerth S, Milavic M, Vukojevic J, et al. Front Pharmacol. 2021;12:627533.
  8. Józwiak M, Bauer M, Kamysz W, Kleczkowska P. Pharmaceuticals. 2025;18(2):185.
  9. Ma WH, Li M, Ma HF, et al. Life Sci. 2020;241:117139.
  10. Park JR, Lee H, Kim SI, Yang SR. Oncotarget. 2016;7(36):58405-58417.
  11. Pickart L, Vasquez-Soltero JM, Margolina A. Oxid Med Cell Longev. 2012;2012:324832.
  12. Mao S, Huang J, Li J, et al. Front Pharmacol. 2025;16:1551843.

All information provided is for research purposes only.

ALL ARTICLES AND PRODUCT INFORMATION PROVIDED ON THIS WEBSITE ARE FOR INFORMATIONAL AND EDUCATIONAL PURPOSES ONLY. The products offered on this website are furnished for in-vitro studies only. In-vitro studies (Latin: in glass) are performed outside of the body. These products are not medicines or drugs and have not been approved by the FDA to prevent, treat or cure any medical condition, ailment or disease. Bodily introduction of any kind into humans or animals is strictly forbidden by law.