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PEG MGF
PEG MGF

PEG MGF

PEG-MGF (Pegylated Mechano Growth Factor) is a synthetic, pegylated version of Mechano Growth Factor (MGF), an IGF-1Ec splice variant. Pegylation — the covalent attachment of polyethylene glycol (PEG) — increases molecular stability and significantly prolongs circulation time in experimental systems.
This modification extends the peptide’s half-life from approximately 5–7 minutes to several hours or days in published research, enhancing exposure in laboratory models. Regulatory Status:
Not FDA-approved. Not intended for human administration, therapeutic use, or clinical applications.

Mechanism of Action
(Mechanistic descriptions based on published research models; NOT effects of this product.)

  • Activates satellite cells (muscle stem cells) in response to mechanical stress or injury in preclinical studies.
  • Acts via autocrine/paracrine–type signaling pathways rather than systemic endocrine mechanisms.
  • Stimulates cellular proliferation, differentiation, and migration in skeletal muscle, cardiac tissue, cartilage, bone, and neural tissue.
  • Pegylation shields the peptide from rapid enzymatic degradation while maintaining biological activity in in-vitro or in-vivo research systems.


Tissue Specificity

  • Skeletal Muscle: Investigated for involvement in muscle repair, hypertrophy signaling, and satellite-cell activation.
  • Cardiac Tissue: Studied in relation to cardiomyocyte signaling, apoptosis pathways, and post-injury remodeling in experimental models.
  • Bone & Cartilage: Associated with osteoblast proliferation and cartilage regeneration pathways.
  • Neural Tissue: Examined in neuroprotection and motor-neuron survival models.

Clinical References

  1. Kandalla, P.K., et al. (2011). Mechano Growth Factor E peptide increases human muscle progenitor cells and induces an increase in fusion potential at different ages. Mechanisms of Ageing and Development, 132(3–4), 154–162.
  2. Riddoch-Contreras, J., et al. (2009). Mechano-growth factor, an IGF-I splice variant, rescues motor neurons and improves muscle function in SOD1G93A mice. Experimental Neurology, 215(2), 281–289.
  3. Dluzniewska, J., et al. (2005). A strong neuroprotective effect of the autonomous C-terminal peptide of IGF-1Ec (MGF) in brain ischemia. FASEB Journal, 19(13), 1896–1898.
  4. Xue, S., et al. (2019). Mechano growth factor attenuates mechanical overload-induced bone deterioration via MAPK pathway inhibition. Frontiers in Endocrinology, 10, 573.
  5. Philippou, A., et al. (2018). Expression of Mechano-Growth Factor modulates inflammatory cytokine responses during macrophage activation in skeletal muscle injury. Frontiers in Physiology, 9, 999

*These findings are from published literature on MGF/PEG-MGF analogs and do not represent effects of this research-use product.

  • Satellite Cell Signaling: Studies show increased activation and proliferative capacity of satellite cells following mechanical stress (Kandalla et al., 2011; Riddoch-Contreras et al., 2009).
  • Inflammatory Pathways: Research reports modulation of inflammatory cytokines and post-injury molecular responses (Philippou et al., 2018).
  • Cardiac Signaling: Experimental models note reduced cardiomyocyte apoptosis and improved cardiac recovery signals (Riddoch-Contreras et al., 2009).
  • Neurobiology: Studies report protective effects in brain ischemia models and enhanced motor neuron survival (Dluzniewska et al., 2005).
  • Bone & Cartilage Models: Literature describes osteoblast signaling and mechanical-overload recovery pathways (Xue et al., 2019).
  • Tissue Remodeling: Research demonstrates reduced fibrosis markers and accelerated remodeling in tissue-injury models.
  • Neurodegeneration Studies: Preclinical ALS models show improved motor-neuron survival and functional recovery in association with MGF variants

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