MGF / PEG-MGF (Mechano Growth Factor, IGF-1Ec)
MGF / PEG-MGF — the mechano-growth-factor muscle peptide: real splice biology, thin human evidence

Class: peptide
Synonyms: MGF
Mechano Growth Factor
IGF-1Ec (human; IGF-1Eb in rodents)
the IGF-1 E-peptide (Ec)
PEG-MGF / PEGylated MGF (the long-acting form). INCI: none
Function tags: muscle growth / repair
satellite-cell (stem-cell) activation
tissue repair
(IGF-1 axis, early proliferative phase)
Overall evidence grade: D
WADA prohibited: yes
WADA note: Sport as an IGF-1/growth-factor agent, it falls in WADA-prohibited growth-factor territory.
Last updated: 2026-07-13

In brief: MGF (Mechano Growth Factor, IGF-1Ec) is a splice variant of IGF-1 produced locally in muscle in response to mechanical stress or damage. Its distinctive part is a 24-amino-acid E-peptide that acts as an early "first responder" repair signal — it wakes up quiescent satellite cells (muscle stem cells) and makes them proliferate, a job the ordinary circulating IGF-1 doesn't do well. In the natural repair cascade, this MGF pulse comes first (within hours), expanding the stem-cell pool, and is followed by a switch to IGF-1Ea, which drives the actual fiber growth. The biology is elegant and real — but it's overwhelmingly preclinical. Native MGF has an extremely short half-life (~5-7 minutes) by design (it's meant to be a local, transient signal), which is why the gray market sells PEG-MGF (PEGylated, longer-acting) — a form that carries batch-to-batch inconsistency and still lacks meaningful human trials. Add no long-term safety data on artificially activating muscle stem cells, and the honest read is: interesting mechanism, minimal human proof.

## Identity MGF is a **splice variant of the IGF-1 gene** (chromosome 12q23). The IGF-1 gene splices exons 4-6 into several isoforms that share the *same* mature IGF-1 sequence but differ in a **C-terminal "E-peptide."** MGF's distinguishing feature is its unique **24-amino-acid E-peptide** (from a reading-frame shift in exon 5), which has **biological activity of its own**, independent of the mature IGF-1 domain. The synthetic "MGF" sold for research is typically just this **E-peptide**. **PEG-MGF** attaches polyethylene-glycol chains to it to extend its very short half-life. ## Mechanism (as proposed) the **IGF-1 gene** produces multiple isoforms by alternative splicing. Two matter for muscle: **IGF-1Ea** (the liver-derived, circulating, *systemic* anabolic form — "tonic" growth signal) and **IGF-1Ec = MGF** (the *local*, mechano-responsive form). When muscle is loaded or damaged, it transiently makes **MGF within hours**; MGF's **E-peptide** then **activates satellite cells** (muscle stem cells sitting dormant between fibers), driving them to **proliferate** — critically, **without forcing early differentiation**, so the stem-cell pool expands first. The muscle then **switches to IGF-1Ea**, whose mature IGF-1 acts via **IGF-1R → PI3K/Akt/mTOR** to drive **myoblast fusion, protein synthesis and fiber hypertrophy**. So MGF is the **early proliferative trigger**; classic IGF-1 is the **later growth executor**. MGF biology is therefore **not simply "more IGF-1"** — the E-peptide works through partly different pathways to achieve a different early outcome (proliferation vs differentiation).

Evidence grades by outcome:
outcome: Satellite-cell (muscle stem-cell) activation / proliferation
grade: D
base: Well-characterised in cell/animal models — MGF E-peptide activates quiescent satellite cells where mature IGF-1 barely does
caveat: Genuinely distinct, reproducible preclinical biology — but not demonstrated as a human therapy
outcome: Muscle repair / hypertrophy (the marketed use)
grade: F
base: Animal / model data on the MGF→IGF-1Ea repair cascade
caveat: Very limited human data; no controlled human hypertrophy/repair trials establishing efficacy
outcome: Aged-muscle / regeneration
grade: F
base: Observation: aged muscle shows a blunted MGF response to loading vs young
caveat: Interesting rationale (maybe why older muscle repairs slower) — but human interventional data absent
outcome: PEG-MGF as a practical agent
base: PK: PEGylation extends half-life from ~minutes to ~hours/≈24 h
caveat: Solves the half-life problem mechanically, but subcutaneous kinetics not formally characterised, and unregulated PEG products vary widely batch-to-batch
outcome: Safety
base: Little formal human data
caveat: Injection-site pain/swelling common; no long-term data on chronically/artificially activating muscle stem cells; theoretical concerns (scar tissue, unregulated growth signalling) unquantified

Legal status:
region: EU
status: Not FDA-approved (gray-market)
note: not approved anywhere; investigational research peptide. Not a cosmetic; no compounding pathway.

Cosmetic claims:

Note: The "first responder" of muscle repair — elegant splice-variant biology, almost entirely preclinical. Three points define this entry: (1) it's a genuinely distinct piece of biology — an IGF-1 splice variant whose unique E-peptide activates muscle stem (satellite) cells, a different job from ordinary IGF-1; (2) native MGF has a ~5-7 minute half-life by design, so the gray market sells PEG-MGF (PEGylated) to extend it — introducing its own quality-control problem; (3) despite rich mechanism, human data are very limited and the "artificially switching on muscle stem cells" question has no long-term safety data.
Status note: watch for any controlled human data — the field is preclinical-heavy; that would move the grades

Sources:
Goldspink G, et al. — characterization of MGF/IGF-1Ec as the mechano-responsive IGF-1 splice variant (UCL, mid-1990s onward); E-peptide autonomous activity.
Reviews of IGF-1 splice isoforms and the MGF→IGF-1Ea repair cascade / satellite-cell activation (Hill & Goldspink and successors).
PEGylation pharmacology for MGF (half-life extension; note un-formalised SC kinetics and batch variability in unregulated products).
Observations of blunted MGF response in aged skeletal muscle after loading/injury.
(Note: as of 2026, human interventional efficacy/safety data for exogenous MGF/PEG-MGF remain very limited.)