Janoshik Analytical
Independent Analysis
- Test date
- 2026-06-11
This site supplies research compounds and laboratory materials for in vitro research only. Not for human or veterinary use.
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80mg · Single vial · Lyophilized powder
In vitro laboratory research use only · Not for human or veterinary use · Batch documented · Third-party tested · Ships from Canada
§ Verification — Batch 2026-05
Janoshik Analytical
Independent Analysis
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§ Research
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.
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.
Gene-expression and cell-culture studies of GHK-Cu characterize modulation of collagen synthesis and broad transcript-level changes in human cell lines.
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.
In vitro keratinocyte assays and murine colitis models characterize KPV-associated suppression of NF-kB signaling and inflammatory markers.
The combination itself has not been characterized as a single entity in peer-reviewed studies; available data derive from investigations of each component individually.
GHK and DNA: resetting the human genome to health
BPC 157 and Standard Angiogenic Growth Factors. Gastrointestinal Tract Healing, Lessons from Tendon, Ligament, Muscle and Bone Healing
Thymosin beta4 activates integrin-linked kinase and promotes cardiac cell migration, survival and cardiac repair
alpha-Melanocyte-stimulating hormone, MSH 11-13 KPV and adrenocorticotropic hormone signalling in human keratinocyte cells
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.