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PEG-MGF

Growth Hormone & IGF

PEG-MGF

A PEGylated synthetic form of mechano growth factor (the IGF-1Ec splice variant), studied preclinically for muscle satellite cell activation, cardioprotection, and...

Full research profile

What it is

PEG-MGF is the polyethylene glycol (PEG)-conjugated form of Mechano Growth Factor (MGF), itself the IGF-1Ec splice variant of insulin-like growth factor 1 (IGF-1). MGF is produced in skeletal muscle, cardiac tissue, and other tissues in response to mechanical stretch and injury; it was first characterised by Geoffrey Goldspink's group in 1999 as the splice variant containing a 52 base-pair insert in exon 5 that causes a reading-frame shift, producing a distinct C-terminal Eb/Ec peptide structurally unrelated to any other IGF-1 isoform. Native endogenous MGF has very short local half-life, functioning as an autocrine/paracrine signal at sites of mechanical stress. PEGylation — attachment of polyethylene glycol chains — is a well-established pharmaceutical strategy to extend peptide half-life; applied to the 24-amino acid synthetic MGF E-domain peptide, it converts the molecule from one with minutes of systemic availability to a form with an estimated half-life of approximately 24–72 hours following subcutaneous injection, substantially increasing systemic exposure. All published research on MGF and PEG-MGF is preclinical: rodent and in vitro models demonstrating muscle satellite cell activation, cardiac protection after myocardial infarction, ALS motor neuron rescue, and age-related neurogenesis promotion. No human clinical trial has been published evaluating PEG-MGF for any indication. PEG-MGF is prohibited in competitive sport by WADA (banned since 2005 under growth factors affecting muscle regeneration). Illicit synthetic preparations have been confirmed in black-market products by mass spectrometry. All human use occurs without regulatory oversight. This is a research compound only.

Highlights

  • Activates muscle satellite (stem) cells to proliferate after mechanical injury, via IGF-1R-independent ERK signaling
  • Reduces cardiac cell apoptosis and preserves contractile function in rodent myocardial infarction models
  • Rescues motor neurons and improves hindlimb muscle strength in ALS (SOD1 G93A) mouse models
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For research use only. Not medical advice.