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70mg · Single vial · Lyophilized powder
- Dose
- 70mg
- 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
§ Research
Research · BPC + GHK-Cu + TB-500
Overview
BPC + GHK-Cu + TB-500 is a research combination of three independently studied compounds. BPC-157 is a synthetic 15-residue sequence derived from a protein fraction originally isolated from human gastric juice. GHK-Cu is the copper(II) complex of the endogenous Gly-His-Lys sequence, first identified in human plasma. TB-500 is a synthetic analog derived from thymosin beta-4, a 43-residue actin-sequestering protein expressed in most nucleated cells, and is commonly described as incorporating its actin-binding region. The blend is supplied for laboratory investigation of tissue-repair, angiogenesis, and cell-migration pathways.
Mechanism of action
Each component acts through a distinct pathway. BPC-157 has been reported to interact with the nitric oxide system and to modulate VEGFR2 expression and FAK-paxillin signaling in endothelial and fibroblast models. GHK-Cu binds copper(II) with high affinity and is proposed to act as a copper-delivery and signaling complex, with gene-expression analyses indicating modulation of transcripts governing extracellular matrix synthesis and remodeling. Thymosin beta-4 sequesters monomeric G-actin, regulating cytoskeletal dynamics and cell motility, and has been shown to form a complex with PINCH and integrin-linked kinase, activating Akt survival signaling in cardiac and endothelial cells.
Key research findings
- 01
Preclinical rodent studies of BPC-157 characterize effects on angiogenesis, vascular collateral recruitment, and tissue-repair endpoints in gastrointestinal, tendon, and vascular injury models.
- 02
In vitro and gene-expression studies of GHK-Cu document modulation of collagen and glycosaminoglycan synthesis and broad shifts in transcript profiles in human cell lines.
- 03
Murine myocardial infarction studies of thymosin beta-4 (2004) characterized integrin-linked kinase activation, cardiomyocyte migration and survival, and effects on cardiac function endpoints.
- 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
BPC 157 and blood vessels
GHK and DNA: resetting the human genome to health
Thymosin beta4 activates integrin-linked kinase and promotes cardiac cell migration, survival and cardiac repair
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.