Research summary
PEG-MGF
MGF conjugated to polyethylene glycol to extend its otherwise very short systemic half-life.
Evidence at a glance
What the research says about PEG-MGF
The PEG-MGF evidence base cited here is 6 sources — 1 clinical, 4 preclinical, 1 review. Its strongest evidence is human — a clinical study, most recently 2016 ("Effects of resistance training on expression of IGF-I splice variants in…"). Regulatory status: Not FDA-approved.
Key findings
What the literature shows
- PEGylation of the MGF E-domain peptide extends its half-life by creating a hydrophilic polymer shield that reduces renal clearance and protease degradation, converting a peptide that degrades in minutes into one with a half-life measured in hours — enabling systemic rather than purely local delivery.
- A sheep model of myocardial infarction found that intravenous administration of the MGF E-domain reduced the area of compromised cardiac muscle by 35% compared to controls and preserved systolic function, suggesting that when delivered systemically at sufficient concentrations the peptide reaches ischemic tissue and is cardioprotective.
- Controlled sustained release of MGF from mesoporous silica scaffolds on titanium prosthetics promoted genuine muscle regeneration into the implant via Akt/mTOR signaling, underscoring the importance of delivery format (slow local release vs. rapid bolus) in translating MGF's bioactivity into functional tissue outcomes.
Citations
6 peer-reviewed sources
All citations link to the original source (PubMed, journal site, or regulatory filing). Independent research database — no vendor influence on what's cited.
Clinical1 source
Preclinical4 sources
Mechano-growth factor reduces loss of cardiac function in acute myocardial infarction
Improved Muscle Regeneration into a Joint Prosthesis with MGF Loaded within Mesoporous Silica on Porous Titanium Alloy
MGF E peptide activates human muscle progenitor cells and induces an increase in their fusion potential at different ages
Mechano-growth factor peptide has no apparent effect on myoblasts or primary muscle stem cells
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