MGF is the 24-amino-acid C-terminal E-peptide of the IGF-1Ec splice variant. Almost every page about it repeats a 2002 finding that satellite cells proliferate in response to the peptide; in 2014 two pharmaceutical companies tried to reproduce that finding across four cell systems and could not, while IGF-1 worked in the same assays. This guide covers what the record actually supports, a half-life figure we previously published and have now withdrawn, and how to read a certificate of analysis. PEG-MGF, the PEGylated form, has its own guide. Research-use educational reference only.
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MGF Guide: Available Now
Educational use only — not medical advice. This guide summarizes information reported in published research and community practice for educational purposes. It is not medical advice and not a recommendation to use any compound. Any doses, schedules, or combinations shown are examples of what has been reported, not instructions for you. Many peptides described here are research compounds that are not FDA-approved for the uses discussed and may be investigational or restricted. Effects, risks, and legal status vary; individual needs and results vary. Consult a qualified, licensed healthcare professional before making any decision. Do not use this content to diagnose, treat, or dose yourself.
MGF at a glance
What it is
The 24-amino-acid C-terminal E-domain peptide of IGF-1Ec, a splice variant of IGF-1 upregulated in muscle after loading or injury. Named 'mechano growth factor' by Goldspink and Yang after the stimulus that induces the transcript.
Researched for
Satellite-cell activation and local muscle repair in the original work. The largest current body of research on this exact peptide is oncology, where it is studied as a tumour-associated marker and drug target rather than a repair agent.
The replication problem
Fornaro et al. 2014, working at Novartis and GSK, tested synthetic MGF peptide up to 500 ng/mL in C2C12 cells, primary human myoblasts, primary mouse muscle stem cells and cardiac myocytes. It failed to increase proliferation, failed to delay differentiation and failed to activate p-ERK, while IGF-1 and full-length IGF-1Eb worked in the same assays.
Plasma half-life
Never measured. No published pharmacokinetic study reports a half-life for the MGF E-peptide in any species. A figure of '5-7 minutes' previously appeared on this page and has been withdrawn — see the half-life section.
Regulatory status
Not FDA-approved. Prohibited in sport at all times by WADA under class S2. Research use only.
Not the same as PEG-MGF
PEG-MGF is this peptide with polyethylene glycol chains attached. It is covered in a separate guide; dosage, half-life claims and the anti-PEG immunogenicity question belong there.
Educational reference. This page does not publish dose ranges or reconstitution arithmetic.
What it is / mechanism
MGF is not a separate gene product. The IGF-1 gene is alternatively spliced, and one of its variants — IGF-1Ec in humans, IGF-1Eb in rodents — is preferentially transcribed in skeletal muscle after mechanical loading or damage. A reading-frame shift in the E-domain of that transcript produces a distinct C-terminal sequence. When the precursor is processed, the mature 70-amino-acid IGF-1 protein is cleaved from a 24-amino-acid C-terminal peptide, and it is that C-terminal fragment, not the whole splice variant, that is sold as 'MGF'.
The original proposal, from Goldspink and Yang's work in the early 2000s, was that this E-peptide has activity of its own, separate from IGF-1: that it drives quiescent satellite cells into the cell cycle and delays their fusion into myotubes, expanding the pool of muscle stem cells available for repair, and that it does so through some receptor other than IGF-1R, since the effect was reported not to be blocked by IGF-1 receptor antibodies. That model — MGF expands the satellite pool, systemic IGF-1 later drives differentiation — is the mechanism every commercial page describes.
It is important to be clear about the status of that model. The receptor was never identified. In more than two decades since the peptide was named, no binding partner has been characterised, which is unusual for a signalling peptide with an ascribed physiological role. And the central cell-biology claim did not survive an independent replication attempt, described in the next section. The mechanism above is what was proposed; it is not settled biology.
Researched effects
In the original literature and in the animal and cell-culture work that followed it, the MGF E-peptide has been associated with satellite-cell proliferation, protection against apoptosis, stem-cell recruitment and local repair signalling in muscle, cardiac tissue, nerve, cartilage and bone. That literature is substantial in volume — several hundred indexed papers reference mechano growth factor — and much of it is genuine cell and tissue work.
What it does not contain is a human trial. No controlled study has tested injected MGF peptide in people for muscle growth, recovery or anything else. Community reports of faster perceived recovery or a localised pump after injection are uncontrolled self-reports of a peptide whose in vitro activity has itself been contested. They are not evidence of effect, and they should not be presented as such.
One strand of that literature deserves to be stated because it is systematically omitted from pages selling this peptide. The IGF-1Ec E-peptide is under active study as a cancer-associated factor: expression has been reported to rise with colonic polyp dysplasia and colorectal cancer, in endometrial carcinoma, and in prostate tumours, where IL-6 has been associated with IGF-1Ec upregulation and Ec peptide secretion. In 2024 a monoclonal antibody against the Ec peptide was developed and tested specifically to block it — anti-PEc reduced prostate cancer cell proliferation, migration and invasion, and reduced tumour size and metastasis rate in mice. That is the most active present-day research direction for this exact peptide, and its logic runs opposite to the one used to sell it: the peptide is the thing being targeted, not the therapy.
Evidence & regulatory status
The independent replication failed, at two companies, across four systems. Fornaro M et al., Am J Physiol Endocrinol Metab 2014;306(2):E150-6 (PMID 24253050), titled 'Mechano-growth factor peptide, the COOH terminus of unprocessed insulin-like growth factor 1, has no apparent effect on myoblasts or primary muscle stem cells'. Concentrations up to 500 ng/ml failed to increase proliferation of C2C12 cells or primary human skeletal muscle myoblasts; MGF failed to inhibit myoblast differentiation into myotubes; primary mouse skeletal muscle stem cells showed no significant effect; and neither native nor stabilised MGF peptide activated p-ERK in cardiac myocytes, an effect previously documented for the peptide. Mature IGF-1 and full-length IGF-1Eb produced robust responses in the same cells. The authors' conclusion: 'These results call in to question whether there is a physiological role for MGF.'
The replication attempt is unusually strong evidence, and it is worth saying why. It was industrial rather than academic — the author list spans Novartis Institutes for Biomedical Research and GSK, and includes David Glass, a senior figure in skeletal muscle biology. Two pharmaceutical companies do not run a negative replication of a muscle-growth target because they want it to fail; they run it because they wanted it to work.
No pharmacokinetic study exists. A targeted PubMed search for half-life, pharmacokinetics or clearance of the MGF peptide returns no study reporting a measured value in any species. The closest published statement is Goldspink and Yang's own remark (PMID 11915923) that MGF 'has a shorter half-life in the unbound state than the systemic liver type IGF-1' — a qualitative comparison, with no figure attached.
Part of the supporting literature has been retracted. A 2019 paper reporting that MGF attenuates mechanical overload-induced nucleus pulposus cell apoptosis (Biosci Rep 2019;39(3):BSR20182462) was retracted by the journal in August 2024 (retraction notice PMID 39171815). One retraction does not invalidate a field, and it is noted here for completeness rather than as an argument.
The peptide is an oncology target in current research. Anti-PEc, a monoclonal antibody raised against the Ec peptide, was reported in Br J Cancer 2024;131(3):551-564 (PMID 38902531) to reduce prostate cancer cell proliferation, migration and invasion (p<0.0005 in every case) and to reduce tumour size and metastasis rate in SCID mice. Related expression work covers colorectal cancer (PMID 32772171), endometrial carcinoma (PMID 33193855) and prostate tumours (PMID 30134795).
Regulatory and sport status: not approved by the FDA or any regulator for any indication. Prohibited at all times under WADA class S2 (peptide hormones, growth factors, related substances and mimetics). Material sold as MGF is for laboratory research only.
Research timeline
Dated milestones taken from the primary records: the molecule's discovery, its first registered human study, the trials that shaped the evidence and the regulatory decisions. Each entry links to the record it comes from.
At the Royal Free Hospital School of Medicine in London, Goldspink's group clones an IGF-1 splice variant that appears in rabbit muscle forced to grow by stretch and is barely detectable in resting muscle; the human equivalent is the Ec form. PMID 8884603
Goldspink and Yang give the variant its name, mechano growth factor, because its expression was detectable only after mechanical stimulation, and describe it as a local repair signal in muscle. PMID 11915923
In cultured myoblasts, Yang and Goldspink report that the peptide made from the variant's distinct end increases proliferation and delays differentiation through a receptor other than the IGF-1 receptor; this is the finding most later claims repeat. PMID 12095637
In muscle biopsies from eight young and seven older adults, a bout of heavy knee-extensor exercise raises the variant's messenger RNA in the young but not in the older group; the study measured the body's own gene expression, not a supplied peptide. PMID 12562960
Researchers at the Polish Academy of Sciences, with Goldspink as co-author, report that the synthetic end peptide protected vulnerable neurons in gerbils after a temporary interruption of blood flow to the brain. PMID 16144956
Scientists at two pharmaceutical companies, Novartis among them, try to reproduce the 2002 effect in mouse and human myoblasts and primary muscle stem cells and find none, while mature IGF-1 worked in the same assays. PMID 24253050
Bioscience Reports retracts a 2019 paper claiming that the peptide protected spinal-disc cells from overload-induced cell death. PMID 39171815
Records checked Oct 4, 2026
Claims at a glance
The claims most often made about this compound, each with the strongest kind of evidence we found for it. The grade says what was studied, not whether the claim is true; the line beside it says what that study showed.
Activates muscle stem cellsCell or tissue studies only. Earlier cell studies reported more muscle-cell growth; an independent replication in four cell systems, including human muscle cells, found no effect while IGF-1 controls worked. PMID 24253050
Builds muscle size and strengthNo study found. A PubMed search for the peptide with muscle-size or strength terms in people returned 35 records, exercise and gene-expression studies, reviews and lab work; none gave the peptide to anyone. PubMed search, Oct 7, 2026
Speeds muscle repairAnimal studies only. In mice it helped transplanted human muscle precursor cells take hold, a cell-therapy model; no study tested recovery from injury or training. PMID 17845560
Protects the heartAnimal studies only. Given to mice at the time of a heart attack, it preserved heart contractility; the cell-signalling effect thought to explain this did not replicate. PMID 23712705
Aids recovery after brain injuryAnimal studies only. Rats injected after a traumatic brain injury resumed eating sooner and showed less bleeding in the brain; no person has been given it. PMID 27863093
The reasoning behind each grade, study by study, is in this guide's Benefit & Outcome Review.
Grades checked Oct 7, 2026
A printable reference sheet with the compound's key facts, storage guidance and a vial record comes with All-Access Lifetime.
Half-life & pharmacokinetics
No half-life has ever been measured for the MGF E-peptide, and a figure that previously appeared on this page has been withdrawn.
This page formerly stated a native MGF half-life of 'about 5-7 minutes'. On re-checking that figure against the primary literature we could not trace it to any published measurement, so it has been removed rather than softened. A targeted search for pharmacokinetic, half-life or clearance data on the MGF peptide returns no study reporting a value in any species. The nearest published statement is from Goldspink and Yang themselves (PMID 11915923), who wrote that MGF 'has a shorter half-life in the unbound state than the systemic liver type IGF-1' — a comparative claim with no number attached, and one made about the endogenously expressed peptide rather than an injected synthetic version.
We are stating the retraction rather than quietly correcting it because the number had been live on this page and had been read. If you find a specific half-life for MGF quoted elsewhere, the useful question is which study produced it. As far as the indexed literature goes, none did.
The practical consequence is that the standard argument for PEGylation — that the native peptide is cleared too fast to be useful, so a PEG chain is required — rests on an unmeasured premise on both sides. That question is taken up in full on the PEG-MGF guide, where the PEGylated form's own half-life claim is examined.
Reported side effects & toxicology
No systematic safety data exist for injected MGF peptide in humans. Community reports describe injection-site soreness and localised swelling, which is unremarkable for an intramuscular injection of a reconstituted powder.
The consideration that deserves more weight than injection-site reactions is the oncology literature described above. A peptide whose expression is associated with tumour progression in prostate, colorectal and endometrial tissue, and against which a therapeutic antibody is being developed precisely to block it, is not a compound whose long-term administration has a benign prior. That is not a claim that injecting MGF causes cancer — no study has tested that, in either direction. It is a statement that the relevant literature exists, points the way it points, and is absent from every commercial description of this peptide. Nothing here is medical advice.
Storage & handling
Lyophilized vials are described as stored refrigerated at 2-8 C and protected from light; frozen storage is described for longer holding of the sealed powder.
After reconstitution, refrigerate at about 2-8 C, protect from light, do not freeze and do not shake. No published stability study covers this peptide in bacteriostatic water, so any 'use within X weeks' figure is handling practice rather than data.
Bacteriostatic water is the diluent assumed throughout this page; its benzyl alcohol is what allows a reconstituted vial to be entered more than once.
References
Primary sources for this guide, last verified 2026-08-13. Replication failure: Fornaro M, Hinken AC, Needle S, et al. Mechano-growth factor peptide, the COOH terminus of unprocessed insulin-like growth factor 1, has no apparent effect on myoblasts or primary muscle stem cells. Am J Physiol Endocrinol Metab. 2014;306(2):E150-6. PMID 24253050. Original characterisation and the only published statement bearing on clearance: Goldspink G, Yang SY. Effects of activity on growth factor expression. Int J Sport Nutr Exerc Metab. 2001;11 Suppl:S21-7. PMID 11915923. Oncology: Armakolas A, Alevizopoulos N, Stathaki M, et al. Anti-PEc: development of a novel monoclonal antibody against prostate cancer. Br J Cancer. 2024;131(3):551-564. PMID 38902531; with expression studies PMID 32772171 (colorectal), PMID 33193855 (endometrial) and PMID 30134795 (prostate, IL-6 association). Retraction notice: Biosci Rep. 2024;44(8), PMID 39171815, retracting Biosci Rep 2019;39(3):BSR20182462. Withdrawn figure: a native half-life of 5-7 minutes previously published on this page was removed on 2026-08-13 because a targeted search of the pharmacokinetic literature returned no study reporting a measured value.
Evidence File
The MGF Evidence File
The free guide gives the verdict; this module is the audit trail underneath it. Six ClinicalTrials.gov searches and the PubMed queries behind every absence claim are named verbatim, so the finding can be re-run rather than taken on trust. The 2014 replication is read for what its design forecloses rather than for its headline. Each circulating figure is followed back to the document it actually came from, the retraction notice is read in machine-readable full text for its stated reason, and the positive literature is named and weighted rather than omitted.
6 registry searches, 0 studies administering it
4 cell systems, 2 companies, 0 responses
1 retailer blog behind a peer-reviewed dosing table
25 papers in the batch that swept up the MGF retraction
Six Registry Searches, Named So They Can Be Re-Run
NCT07151807: The Only Registry Record That Names the Compound
Reading Fornaro 2014 for What Its Design Forecloses
The 2002 Letter Everything Traces To, and the Erratum on Its Record
A 2026 Review Grades the Family Tier D, and Its Dosing Citation Is a Retailer Blog
The Replication Failure Is Not in That Review's Reference List
The Supporting Literature, Audited: Three Positives, One Retraction, One Lineage
Two Hundred Papers, and What They Are Actually About
8 more sections in the Evidence File for MGF
Unlock the Evidence File, Sourcing File and Benefit & Outcome Review for MGF for $14 — or every compound in the library, plus the printable reference sheets, for $99.
The sections above this one stay free to read without an account.
Sourcing File
The MGF Sourcing File
This compound removes the check most peptide buyers rely on. The public chemistry database record that normally supplies a canonical formula and mass does not exist for it, and the federal substance register carries more than one entry under this compound's name. This module works through what is left to verify identity with: the sequence and the three authorities that agree on it, the mass arithmetic computed from that sequence with every basis stated, the substitution and degradation species that would actually be seen here, the salt arithmetic behind a labelled milligram, and a certificate read field by field with a verdict on each line.
0 PubChem CIDs, 2 FDA UNIIs, 1 checkable sequence
0.98 Da between two substances both named MGF
8 basic sites on a 24-residue peptide
871 mcg/mL where the label implies 1,000
There Is No CID, So the Sequence Is the Only Anchor
One Molecule, Three Masses, and a Public Record That Disagrees With Itself
Two Registered Substances Share This Name, 0.98 Daltons Apart
What This Sequence Cannot Do, and the Certificate Fields That Follow From It
189 Daltons: the Species Trap Nobody Prints
Eight Basic Sites, and What a Labelled 2 mg Vial Actually Contains
A Certificate Read Line by Line, With the Verdicts
7 more sections in the Sourcing File for MGF
Unlock the Evidence File, Sourcing File and Benefit & Outcome Review for MGF for $14 — or every compound in the library, plus the printable reference sheets, for $99.
The sections above this one stay free to read without an account.
Benefit & Outcome Review
The MGF Benefit and Outcome Review
Ten claims circulate commercially for this peptide. Each is taken here on its own, and for each the review states the species it was measured in, the design that produced the measurement, what the comparator did in the same experiment, and who generated the material and the data. Species and design come first every time, because those are the details the marketing omits most often. Where a claim was tested and failed, it is recorded as a failure rather than as an absence; where nothing was measured, the searches establishing that are named. The register closes with what the peptide has actually been shown to do.
10 marketed claims reviewed, 0 rated supported
2 contradicted, 5 with no study of the peptide being given
3 plausible-unproven, none in a marketed context
0 human studies of the administered peptide, at any tier
The Scoreboard: Ten Claims, and Why None Reaches Supported
Satellite-Cell Activation: Contradicted, and by Exactly What
Muscle Growth and the Post-Injection Pump: Two Claims With Empty Columns
Muscle Repair: the One Real In Vivo Positive, and What It Measured
Cardiac Protection and the Isolated Preclinical Models: Plausible in Contexts Nobody Markets
The Human Studies Cited Here Measured a Transcript, Not a Treatment
Three Claims Resting on Nothing: IGF-1 Superiority, Fat Loss, and the Half-Life Rationale
What Exogenous Synthetic MGF E Peptide Has Actually Been Shown to Do
8 more sections in the Benefit & Outcome Review for MGF
Unlock the Evidence File, Sourcing File and Benefit & Outcome Review for MGF for $14 — or every compound in the library, plus the printable reference sheets, for $99.
Quick answers about guide scope, access, and educational use context.
What is MGF?
MGF is the 24-amino-acid C-terminal E-domain peptide of IGF-1Ec, a splice variant of the IGF-1 gene that is preferentially transcribed in skeletal muscle after mechanical loading or damage. It was named 'mechano growth factor' after that stimulus. The material sold under the name is the cleaved C-terminal fragment, not the full splice variant.
Does MGF actually work?
The central claim has failed independent replication. In 2014 researchers at Novartis and GSK tested synthetic MGF peptide at up to 500 ng/ml in C2C12 cells, primary human myoblasts, primary mouse muscle stem cells and cardiac myocytes. It did not increase proliferation, did not delay differentiation and did not activate p-ERK, while IGF-1 and full-length IGF-1Eb worked in the same assays. Their published conclusion was that the results call into question whether MGF has a physiological role at all (PMID 24253050). No human trial has ever been run.
What is MGF's half-life?
It has never been measured. No published pharmacokinetic study reports a half-life for this peptide in any species. This page previously stated 'about 5-7 minutes' and that figure has been withdrawn because it could not be traced to a source. The only published statement is Goldspink and Yang's qualitative one that MGF is cleared faster than systemic IGF-1, with no number given.
What is the difference between MGF and PEG-MGF?
PEG-MGF is this same E-peptide with one or more polyethylene glycol chains covalently attached, intended to slow clearance. The underlying biology is identical, which means the replication failure applies to both. The PEGylated form has its own additional issues — no direct study record of its own, vendor-to-vendor non-standardisation of the PEG chain, and anti-PEG antibody questions — and those are covered on the separate PEG-MGF guide.
Why is MGF injected into a specific muscle?
Because the proposed mechanism is autocrine and paracrine rather than endocrine — the native transcript is induced locally by loading and is supposed to act where it is produced. That is the stated rationale for local intramuscular placement in community protocols. It follows from the model rather than from any study of injected peptide distribution.
Is MGF studied for anything other than muscle?
Yes, and the largest current strand is oncology. The IGF-1Ec E-peptide is studied as a tumour-associated factor in prostate, colorectal and endometrial cancer, and in 2024 a monoclonal antibody against it (anti-PEc) was developed and shown to reduce prostate cancer proliferation, migration, invasion and metastasis in mice (PMID 38902531). That research treats the peptide as a target to be blocked.
Was any MGF research retracted?
One paper was. A 2019 study reporting that MGF attenuates mechanical overload-induced nucleus pulposus cell apoptosis was retracted by Bioscience Reports in August 2024 (PMID 39171815). It is noted for completeness; a single retraction is not by itself an argument about the field.
Is MGF banned in sport?
Yes. Growth factors of this class are prohibited at all times under WADA class S2, which covers peptide hormones, growth factors, related substances and mimetics. It is also not approved by the FDA or any other regulator for any use.
Can I buy MGF for personal use?
Material sold under this name is supplied for laboratory research use only and is not a medicine. Nothing on this page is a recommendation to use it in humans, and no dose stated here is a personal dose.
Compliance and trust notes
Educational content only; no personalized health or outcome claims.
No personalized use recommendation outputs.
Use this material for general learning and research-context literacy.
A certificate of analysis (COA) is a laboratory’s report on one sample of one batch. The single most useful thing to know about it is that purity and identity are two separate results that fail in different ways. A high purity figure says the sample was mostly one substance; it does not say that substance was MGF. Identity — normally a mass-spectrometry result matching the expected molecular weight — is what establishes what the material actually is, and a certificate reporting purity alone has not answered that question.
Two further limits are worth holding onto. Mass per vial is its own test: a vial can be 99% pure and still contain less material than the label claims. And sterility, endotoxin, heavy metals and residual solvent screening are separately commissioned tests, usually priced individually — so a “third-party tested” badge asserts none of them unless the certificate names them. Check that the batch or lot number on the document matches the vial in front of you; an unmatched certificate describes someone else’s material.
Medibact does not test, endorse or resell peptides, and publishes no rating of any laboratory. How to read a peptide certificate of analysis walks through the document section by section, and what each COA field establishes covers the field-by-field detail and the laboratories that publish their methods.
You’ll need bacteriostatic water
The diluent for reconstituting MGF
Reconstitution is volume arithmetic — it assumes a lyophilized vial is dissolved in bacteriostatic water, which is sterile water preserved with 0.9% benzyl alcohol. The preservative is what allows a vial to be entered more than once; plain sterile water carries none and is single-entry by design. Medibact supplies USP-grade Bacteriostatic Water for Injection in a 30 mL multi-dose vial, made in the United States and shipped from the United States, for research use only. One 30 mL vial covers 30 reconstitutions at 1 mL each, 15 at 2 mL, or 10 at 3 mL — division only, not a dosing recommendation.
Educational use only — not medical advice. This guide summarizes information reported in published research and community practice for educational purposes. It is not medical advice and not a recommendation to use any compound. Any doses, schedules, or combinations shown are examples of what has been reported, not instructions for you. Many peptides described here are research compounds that are not FDA-approved for the uses discussed and may be investigational or restricted. Effects, risks, and legal status vary; individual needs and results vary. Consult a qualified, licensed healthcare professional before making any decision. Do not use this content to diagnose, treat, or dose yourself.
