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GHK-Cu + TB + BPC + KPV 80mg

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GHK-Cu + TB + BPC + KPV

80mg · Single vial · Lyophilized powder

Single vial89.99CAD

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Sender: Vennori Biosciences · orders@vennori.com

Dose
80mg
Pack size
Single vial
Form
Lyophilized powder
Storage
2–8°C

In vitro laboratory research use only · Not for human or veterinary use · Batch documented · Third-party tested · Ships from Canada

§ Verification — Batch 2026-05

Certivos verified

Janoshik Analytical

Independent Analysis

Test date
2026-06-11

Certificates are issued and hosted by Certivos.

§ Research

Research · GHK-Cu + TB + BPC + KPV

Overview

GHK-Cu + TB + BPC + KPV is a four-component research combination of independently studied compounds. GHK-Cu is the copper(II) complex of the endogenous Gly-His-Lys sequence; TB (TB-500) is a synthetic analog derived from the actin-binding region of thymosin beta-4; BPC-157 is a synthetic 15-residue sequence derived from a gastric juice protein fraction; and KPV is the Lys-Pro-Val C-terminal fragment (residues 11 to 13) of alpha-melanocyte-stimulating hormone. The blend is supplied for laboratory investigation of tissue-repair, cytoskeletal, and inflammatory-signaling pathways.

Mechanism of action

Each component acts through a distinct pathway. GHK-Cu binds copper(II) with high affinity and is proposed to function as a copper-delivery and signaling complex, with gene-expression data indicating modulation of extracellular matrix and antioxidant transcripts. Thymosin beta-4 sequesters monomeric G-actin, regulating cell motility, and activates integrin-linked kinase and downstream Akt signaling. BPC-157 has been reported to interact with the nitric oxide system and to modulate VEGFR2 and FAK-paxillin signaling in endothelial and fibroblast models. KPV retains the anti-inflammatory activity of the alpha-MSH C-terminus, inhibiting NF-kB activation and pro-inflammatory cytokine release, and is transported into intestinal epithelium via PepT1.

Key research findings

  1. 01

    Gene-expression and cell-culture studies of GHK-Cu characterize modulation of collagen synthesis and broad transcript-level changes in human cell lines.

  2. 02

    Murine cardiac injury models of thymosin beta-4 and rodent injury models of BPC-157 characterize effects on cell migration, angiogenesis, and tissue-repair endpoints.

  3. 03

    In vitro keratinocyte assays and murine colitis models characterize KPV-associated suppression of NF-kB signaling and inflammatory markers.

  4. 04

    The combination itself has not been characterized as a single entity in peer-reviewed studies; available data derive from investigations of each component individually.

Published references

  • GHK and DNA: resetting the human genome to health

    Pickart L et al. — Biomed Res Int, 2014 · PMID: 25302294

  • BPC 157 and Standard Angiogenic Growth Factors. Gastrointestinal Tract Healing, Lessons from Tendon, Ligament, Muscle and Bone Healing

    Seiwerth S et al. — Curr Pharm Des, 2018 · PMID: 29998800

  • Thymosin beta4 activates integrin-linked kinase and promotes cardiac cell migration, survival and cardiac repair

    Bock-Marquette I et al. — Nature, 2004 · PMID: 15565145

  • alpha-Melanocyte-stimulating hormone, MSH 11-13 KPV and adrenocorticotropic hormone signalling in human keratinocyte cells

    Elliott RJ et al. — J Invest Dermatol, 2004 · PMID: 15102092

The information above is derived from published preclinical and clinical research. It is provided for educational purposes only and does not constitute medical advice, diagnosis, or treatment recommendations.