MGF (Mechano Growth Factor)
Locally acting splice variant of IGF-1 (human IGF-1Ec) upregulated by mechanical stress and tissue injury to prime regeneration by activating muscle satellite cells.
⚡ Executive Summary
MGF (Mechano Growth Factor) is an IGF-1 splice variant (IGF-1Ec) that rises locally after mechanical stress to “prime” tissue regeneration by expanding progenitor cells, especially muscle satellite cells. In humans, MGF increases within hours after resistance exercise — an effect blunted with aging. It differs mechanistically and temporally from systemic IGF-1. Evidence remains preclinical and mixed. WADA prohibited (S2).
WADA Prohibited: MGF and IGF-1 (and analogs) are on the WADA Prohibited List (S2). Athletes subject to anti-doping rules should not use MGF in any form.
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Overview
💪 What is MGF?
MGF is an alternative splice variant of the IGF-1 gene that encodes a distinct C-terminal E-domain (Ec in humans, Eb in rodents).
Mechanical overload and injury shift IGF-1 splicing toward this variant in the affected tissue, creating a local, rapid response to stress.
🎯 Key Actions
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Progenitor expansion — activates satellite cells
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Rapid response — rises within 2–3 hours
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Local action — autocrine/paracrine signaling
⏱️ Prime-Then-Build Model
MGF acts as an early, local “primer” for regeneration. It expands the progenitor cell pool (more cells to repair) while delaying differentiation. This “prime-then-build” sequence aligns with observed kinetics: early MGF → later IGF-1Ea for differentiation and tissue rebuilding.
MGF Surge
Rapid local response
Proliferation
Satellite cell expansion
IGF-1Ea Rise
Differentiation begins
Research only: MGF is a research peptide with no approved human therapeutic indications. Evidence is preclinical and mixed — some studies report null effects of synthetic MGF on muscle cells.
Entity Properties
| Aliases | Mechano Growth Factor (MGF), IGF-1Ec (human), IGF-1Eb (rodent) |
|---|---|
| E-Domain Sequence |
YQPPSTNKNTKSQRRKGSTFEEHK
|
| Length | 24 amino acids (E-domain peptide) |
| Molecular Weight | ~2,847 Da |
| CAS Number | Not assigned for 24-aa research peptide |
| Family | Alternative splice variant of IGF-1; GH/IGF axis |
| Diluent(s) | Sterile saline or buffered saline |
| In Vitro Conc. | 10–100 nM (typical range for E-peptide studies) |
| In Vivo Dose | ~4.5 mg/kg/day continuous infusion (mouse MI models) |
| Storage | Lyophilized: cold & dry, protected from light. Solutions: minimize bench time, aliquot |
| Half-Life | ~20 min in media (E-peptide is labile) |
Naming note: You may see “IGF-1Eb/Ec,” “MGF-E,” or “MGF-24aa-E.” We use MGF (IGF-1Ec) for human and MGF E-domain peptide for the 24-amino-acid synthetic research fragment.
Mechanism of Action
🧠 How does MGF work?
MGF acts as an early, local signal that cooperates with (not replaces) IGF-1. It amplifies pro-proliferative cascades early so differentiation and tissue rebuilding can proceed later.
The MGF E-domain peptide increases proliferation and delays differentiation of human muscle progenitors in vitro — conceptually supplying more building blocks for later regeneration.
🔄 Progenitor Expansion
Activates satellite cells and other progenitors; delays differentiation to expand the repair cell pool
📡 MAPK/ERK Signaling
E-peptide activity often modulates IGF-1R toward MAPK/ERK (not AKT) in myoblasts
📍 Local Action
Produced and acts locally (autocrine/paracrine) after load/injury — distinct from systemic IGF-1
Receptor debate: MGF’s receptor story is mixed. Some studies show E-peptide actions require or modulate IGF-1R; others describe IGF-1R-independent effects in neural models. Full-length IGF-1Ec can activate IGF-1R at higher concentrations.
Research Evidence
🔬 Key Preclinical Findings
Skeletal Muscle (Human)
MGF mRNA rises ~2.5h post-exercise in young adults; blunted response in older adults — a factor in age-related recovery
Cell Studies
MGF E-peptide increases proliferation and fusion potential of human muscle progenitors in vitro
Cardiac (Mouse MI)
Stabilized MGF E-peptide preserved cardiac function and delayed decompensation after myocardial infarction
Neuroprotection
MGF C-terminal peptide showed strong neuroprotection in ischemia models without classical IGF-1 behavior
Regeneration Timing
IGF-1 isoforms change over time: MGF/Ec early phases → IGF-1Ea later as fibers mature
Mixed Results
Some studies found no effect of synthetic MGF on myoblast proliferation — model/peptide sensitivity matters
Evidence grade: Most results are preclinical (cells/rodents/large animals). Human therapeutic evidence is absent, and synthetic peptides used can differ (sequence length, modifications), affecting outcomes. Balance enthusiasm with skepticism.
Research Handling
Research use only. Design around MGF’s short-lived, local biology: choose models, dosing windows, and endpoints that capture early proliferative effects and later differentiation separately.
📊 Dosing Reference
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In vitro: 10–100 nM E-peptide range
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In vivo: ~4.5 mg/kg/day continuous infusion
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Timing: Sample early (hours) for proliferation
⚗️ Stability Considerations
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⏳
Half-life: ~20 min in media (E-peptide is labile)
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❄️
Storage: Lyophilized cold/dry; fresh aliquots
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Modifications: D-Arg substitutions may stabilize
📋 Research Checklist
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✓
Verify sequence (YQPPSTNKNTKSQRRKGSTFEEHK) and purity (HPLC/MS)
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Choose form: full-length pro-IGF-1Ec vs 24-aa E-domain peptide
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Include vehicle and IGF-1 comparator controls
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Time sampling to capture early proliferation AND later differentiation
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Plan readouts: Ki-67, satellite cell counts, MAPK/ERK, Myogenin, MyHC
Comparison
MGF is a local, short-window primer; IGF-1 is a systemic builder; PEG-MGF seeks longer exposure via chemistry, but direct clinical data are lacking.
MGF
Early, local response to load/injury. Expands progenitor pools. Short-lived (~20 min half-life). Receptor behavior mixed.
IGF-1
Endocrine/paracrine growth factor. Drives differentiation and anabolic signaling broadly. Well-characterized IGF-1R binding.
PEG-MGF
Designed to prolong MGF exposure via PEGylation. Preclinical rationale. No standardized human PK/efficacy data.
Key distinction: MGF “primes” regeneration with a short, local signal that likely cooperates with IGF-1 — amplifying pro-proliferative cascades early so differentiation can proceed later.
FAQ
Bottom line: MGF appears to “prime” regeneration (especially in muscle) with a short, local signal that cooperates with IGF-1 — amplifying pro-proliferative cascades early so differentiation and tissue rebuilding can proceed later. Evidence is preclinical and mixed; translating this into therapy will require standardized peptides, delivery methods, and human trials.