Growth hormone axis

PEG-MGF

Name: PEG-MGF: What the Research Actually Shows
Creator: Peptide Health Lab

FOR RESEARCH PURPOSES ONLY

Also known as: PEGylated MGF, PEGylated mechano growth factor

Regulatory status: Research only
Evidence grade: Animal studies only

Last reviewed September 1, 2026 · 15 sources

What PEG-MGF is and how it works

PEG-MGF is a name for a commercial preparation, and the shortest honest description of this page is that the name and the science do not refer to the same thing. Three separate molecules travel under overlapping labels here, and keeping them apart is the only way the evidence below means anything.

The first is MGF itself, also called IGF-1Ec. The IGF-1 gene is alternatively spliced, and one of its products is an isoform whose E domain carries a 49-base-pair insert in humans — 52 in rodents, where the equivalent isoform is IGF-1Eb. The insert causes a reading-frame shift, producing a distinct mature isoform.^[1] That isoform was identified in the 1990s as responding to mechanical loading, which is where the name mechano growth factor came from, and it was subsequently tied to the growth hormone axis: in growth-hormone-deficient lit/lit mice, muscle MGF was preferentially induced by growth hormone.^[5] Human tissue work confirms that the Ec peptide is produced alongside its precursor protein in muscle, liver, heart and other tissues, with proprotein convertase furin capable of cleaving the pro-peptide to release the free peptide.^[8]

The second is the synthetic E peptide — a 24-amino-acid analogue corresponding to the C-terminal end of the IGF-1Ec E domain, made to probe what that fragment does on its own.^[7] Almost every promising result associated with the name MGF was generated with this synthetic fragment applied to cells in a dish. It is not the full splice variant, and it is not what the body makes.

The third is the PEGylated preparation that carries the commercial name. Polyethylene glycol conjugation is a real and well-understood strategy for extending a protein's circulating half-life, and it comes with a well-understood cost: attaching PEG frequently reduces the protein's bioactivity, and getting around that trade-off is an active engineering problem. For PEGylated IGF-I — a related but different protein — one published solution was to attach the polymer through a protease-sensitive linker so the active protein could be released at the target site rather than remaining permanently conjugated.^[13] No equivalent characterization has been published for a PEGylated MGF preparation. Whether the PEG group on a commercial preparation preserves activity, abolishes it, or changes what the peptide binds is simply not known, because nobody has measured it.

So the mechanism claimed for PEG-MGF — a longer-lasting version of the muscle repair signal — is a plausible-sounding chain of inferences in which every link after the first is unsupported. The splice variant is real. The synthetic fragment does things in culture. The PEGylated preparation has never been studied.

What the research actually shows

The synthetic E peptide activates human muscle progenitor cells in vitro. This is the strongest result in the literature and it deserves to be stated accurately. Applied to primary human muscle cell cultures, the MGF 24-amino-acid E peptide significantly increased the proliferative lifespan and delayed senescence of satellite cells isolated from neonatal and young adult muscle — but not from old adult muscle — and increased fusion potential across all cultures.^[1] A separate group showed the same synthetic peptide acts as a motogenic factor for human myogenic precursor cells in vitro and in vivo, modulating u-PA, u-PAR, MMP-7 and PAI-1 in a direction that favours cell migration, and presented evidence that it does so through a mechanism not involving the IGF-1 receptor.^[2] The therapeutic idea behind both was Duchenne muscular dystrophy cell transplantation, not athletic performance.

Animal work is disease-model work. A synthetic MGF E peptide improved the success of myogenic precursor cell transplantation in mice.^[3] Mechano-growth factor rescued motoneurons and improved muscle function in SOD1(G93A) mice, a model of amyotrophic lateral sclerosis.^[4] Reviews of growth factors and muscle ageing treat the isoform as a candidate for sarcopenia and muscle-wasting conditions.^[14] The consistent setting is a damaged or diseased muscle in a rodent, or a transplantation procedure, not a healthy trained adult.

The activity is species-specific in a way that undercuts the usual extrapolation. In paired culture experiments, the synthetic human Ec peptide stimulated the growth of human PC-3 cells within a narrow 5–50 nanomolar window in serum-rich medium, and had no effect at all on mouse C2C12 myoblasts under any condition tested. The synthetic mouse Ec was inactive in the human cells while stimulating the mouse ones. Blocking the human IGF-1 receptor did not abolish the activity, while a neutralizing anti-IGF-1Ec antibody did, and the active core was localized to the last four amino acids of the C-terminal end.^[6] A peptide whose activity does not survive a change of species between mouse and human cells is a poor candidate for confident reasoning from rodent studies to people.

The strongest human-relevant data is analytical, and it is unflattering. When a doping-control laboratory characterized a preparation offered as "full-length MGF" — reported as circulating among athletes in 2014 and believed at the time to be undetectable — top-down and bottom-up sequencing identified a 12,264.9-dalton protein closely related to IGF-1Ec but lacking the signal and propeptide moieties, with the terminal lysine eliminated and an arginine-to-histidine substitution at position 109. Once characterized, it was detectable at 0.25 nanograms per millilitre by adapted routine methods.^[11] The point for a reader is not the detection limit. It is that the actual contents of a preparation carrying this name, when someone finally looked, were a modified protein that differs from the published sequence.

Where the evidence is weak

PEGylation is the defining feature of the marketed compound and the part with no literature at all. Every finding above was generated with the unmodified splice variant or the unmodified synthetic E peptide. Nothing has been published about a PEGylated MGF preparation: not its potency, not its half-life, not its receptor interaction, not its immunogenicity, not its behavior in any organism. The general PEGylation literature says the modification extends half-life and frequently reduces bioactivity — a real trade-off, demonstrated for a related protein, that engineers work specifically to circumvent.^[13] Which side of that trade-off a commercial PEG-MGF preparation lands on is unknown. Assuming it inherits the E peptide's culture-dish activity is the central unexamined assumption of the entire compound.

No human has ever been given any MGF preparation in a published study. Not the splice variant, not the synthetic peptide, not the PEGylated form. There is no trial, no dose-finding study, no case series, and no adverse-event record. A review of performance-enhancing peptides acting on this axis names PEG-MGF directly, describes self-administration of these compounds running well ahead of the clinical evidence, and places PEG-MGF in the tier defined by a complete absence of human studies.^[15]

In vitro concentrations are not doses, and this peptide's window is narrow. The human Ec peptide stimulated growth only between roughly 5 and 50 nanomolar, and only in serum-rich medium; outside that range and in serum-poor medium it did nothing.^[6] A compound with a narrow, condition-dependent effective window in a controlled dish is a compound whose behavior in a whole organism is especially unpredictable — and no study has measured what concentration any systemic administration would produce.

The species-specificity finding cuts both ways. If rodent efficacy data does not transfer to humans, rodent safety data does not either. The mouse studies that report benign muscle effects cannot be read as reassurance about a peptide whose human activity runs through a different, partly uncharacterized pathway.^[6]

There is a cancer-biology signal, and it is specific rather than generic. The MGF transcript is preferentially expressed in human prostate cancer and prostatic intraepithelial neoplasia tissue, and not expressed at all by normal prostate epithelial cells. Exogenous synthetic MGF E peptide stimulated the growth of PC-3 and LNCaP cells and activated ERK1/2, and silencing both the IGF-1 receptor and the insulin receptor failed to abolish that mitogenicity.^[9] A review of IGF-1Ec in the myoskeletal system covers its involvement in osteosarcoma pathophysiology.^[10] These are cell-line and tissue-expression findings, not a measured human risk, but they concern this specific peptide rather than the IGF-1 axis in the abstract, and they belong in a clinical conversation.

Identity is genuinely unresolved. The one preparation that was formally characterized turned out to be a modified protein.^[11] Separately, when a doping-control laboratory analyzed seventeen products labeled as a different muscle-targeting protein, several contained growth-promoting peptides that were not what the label claimed, MGF among them.^[12] With no approved manufacturer there is no assay standard and no release specification behind anything carrying this name.

Legal and regulatory status

PEG-MGF is not approved by the FDA for any indication, and no MGF preparation has been approved by any regulator anywhere. A search of approved drug products returns no application for mechano growth factor in any form. Material carrying the name is distributed for laboratory research use, which is why every mention of it on this site carries research-only framing. Its history is that of a preclinical drug candidate for neuromuscular disorders whose misuse potential in sport was identified shortly after the preclinical results appeared.^[11]

In tested sport the status is long-settled. MGF peptides have been prohibited under World Anti-Doping Agency regulations since 2005, and the class has been discussed in the doping-control literature as a growth-factor doping agent for just as long.^[11] Detection is not theoretical: immunoaffinity purification followed by nanoscale liquid chromatography and high-resolution mass spectrometry identifies the full-length variant at 0.25 nanograms per millilitre.^[11]

What the regulatory status means for a reader is narrower and more useful than any argument about enforcement: there is no label, no approved manufacturer, no assigned indication, and no regulated quality standard behind anything carrying this name — and in the one documented case where someone sequenced such a preparation, the contents did not match the published molecule. PHL does not sell peptides and takes no position on how unapproved material reaches anyone.

Questions to bring to a provider

The useful conversation is not "how would I run PEG-MGF." Given that no MGF preparation has ever been administered to a person in a published study, and that the PEGylated form specifically has no literature in any species, the honest question comes earlier. Questions worth raising:

What is the underlying problem — a healing injury, age-related muscle loss, a training plateau — and is there any evidence that a growth-factor intervention addresses it in humans?^[14]
Given that no human has received this compound in any published study, what would count as evidence that it did anything, and what would count as evidence that it was safe?^[15]
The published biology is about a splice variant the body makes and a synthetic fragment applied to cells. What is the reasoning that connects either of those to an injected PEGylated preparation, and does that reasoning hold up?^[7]
Does a personal or family history of prostate cancer or another malignancy change the calculus, given that the MGF E peptide is mitogenic for prostate cancer cells through a receptor-independent mechanism?^[9]
If a study in mice is being cited as reassurance, does the species-specificity finding undermine it?^[6]
If competing in a tested sport, what does the current prohibited list say, and what are the consequences of a positive finding?^[11]

A clinician who answers "what was studied and what is sold are not the same molecule" has understood this compound correctly.

Evidence by claim

Grades describe how strong the evidence is; the line under each grade describes what kind of studies it is. How we grade evidence.

Muscle growth, strength, or recovery in humans from a PEGylated MGF preparation

Anecdotal reports only review

No human evidence exists, and no evidence of any kind exists for the PEGylated preparation specifically. No published trial, controlled study, open-label series, or case report has administered MGF, the MGF E peptide, or a PEGylated version of either to a person and measured muscle mass, strength, or recovery. A review of this field describes self-administration of these compounds running well ahead of any clinical evidence, and assigns PEG-MGF to the tier defined by a complete absence of human studies.

[15]

Activation of muscle progenitor cells by the unmodified E peptide

Animal studies only in vitro

This is the parent peptide's genuine finding, and it is in vitro. The synthetic 24-amino-acid C-terminal E peptide of IGF-1Ec increased the proliferative lifespan of primary human satellite cells isolated from neonatal and young adult muscle — but not from old adult muscle — and increased their fusion potential. The same synthetic peptide acted as a motogenic factor for human myogenic precursor cells, modulating the fibrinolytic and metalloproteinase systems, apparently through a mechanism that does not involve the IGF-1 receptor. Both studies used the unmodified peptide added to cells in culture. Neither used a PEGylated preparation, and neither administered anything to an intact human.

[1] [2]

Functional benefit in animal disease models

Animal studies only animal

In SOD1(G93A) transgenic mice, a model of amyotrophic lateral sclerosis, mechano-growth factor rescued motoneurons and improved muscle function. In mouse myogenic precursor cell transplantation, a synthetic MGF E peptide improved graft success. In growth-hormone-deficient lit/lit mice, muscle MGF was preferentially induced by growth hormone, which is what tied the splice variant to the GH axis in the first place. Each of these is a rodent disease or deficiency model using the unmodified peptide or the endogenous splice variant. None is a study of a healthy adult, and none is a study of a PEGylated preparation.

[4] [3] [5]

Endogenous MGF/IGF-1Ec as an exercise-responsive splice variant in humans

Anecdotal reports only human observational · review

Human observational work confirms that the Ec peptide is produced alongside its precursor protein in a wide range of human tissues, and provides initial evidence that it is differentially regulated during muscle regeneration after exercise-induced damage. This is evidence that the body's own splice variant participates in repair. It is not evidence that injecting a synthetic or PEGylated version reproduces, amplifies, or improves on that process — a distinction that is the entire content of this page's argument.

[8] [7]

Transfer of animal findings to humans

Anecdotal reports only in vitro

The usual assumption that rodent muscle results probably indicate human muscle results is specifically contradicted for this peptide. In paired experiments, the human Ec peptide stimulated human prostate cancer cells but had no effect on mouse C2C12 myoblasts under any culture condition, and the synthetic mouse Ec was inactive in human cells while stimulating mouse cells. The authors located the active core in the last four amino acids of the C-terminus and described the mode of action as species-specific. Rodent MGF data therefore has a weaker claim on human relevance than rodent data usually does.

[6]

Effect of PEGylation on the molecule's behavior

Anecdotal reports only in vitro

Unstudied for this compound. PEGylation of a protein ligand extends its half-life and frequently reduces its bioactivity — a trade-off demonstrated directly for PEGylated IGF-I, a related but different protein, where the solution required engineering a protease-sensitive linker to release the active protein at the target site. No published work reports what PEGylation does to the MGF E peptide's potency, clearance, receptor interaction, or immunogenicity. The modification that gives the marketed preparation its name is the part with no literature behind it at all.

[13]

Long-term safety in humans

Anecdotal reports only in vitro

Nothing is known. No human has been followed on any MGF preparation in any published study. What exists instead is a cell-line signal pointing the wrong way: the MGF E peptide is mitogenic for human prostate cancer cells through an IGF-1-receptor-independent mechanism, and the transcript is preferentially expressed in cancerous rather than normal prostate tissue. That is a reason for caution, not a measured risk.

[9]

Claim area	Evidence & sources	What the research shows
Muscle growth, strength, or recovery in humans from a PEGylated MGF preparation	Anecdotal reports only review [15]	No human evidence exists, and no evidence of any kind exists for the PEGylated preparation specifically. No published trial, controlled study, open-label series, or case report has administered MGF, the MGF E peptide, or a PEGylated version of either to a person and measured muscle mass, strength, or recovery. A review of this field describes self-administration of these compounds running well ahead of any clinical evidence, and assigns PEG-MGF to the tier defined by a complete absence of human studies.
Activation of muscle progenitor cells by the unmodified E peptide	Animal studies only in vitro [1] [2]	This is the parent peptide's genuine finding, and it is in vitro. The synthetic 24-amino-acid C-terminal E peptide of IGF-1Ec increased the proliferative lifespan of primary human satellite cells isolated from neonatal and young adult muscle — but not from old adult muscle — and increased their fusion potential. The same synthetic peptide acted as a motogenic factor for human myogenic precursor cells, modulating the fibrinolytic and metalloproteinase systems, apparently through a mechanism that does not involve the IGF-1 receptor. Both studies used the unmodified peptide added to cells in culture. Neither used a PEGylated preparation, and neither administered anything to an intact human.
Functional benefit in animal disease models	Animal studies only animal [4] [3] [5]	In SOD1(G93A) transgenic mice, a model of amyotrophic lateral sclerosis, mechano-growth factor rescued motoneurons and improved muscle function. In mouse myogenic precursor cell transplantation, a synthetic MGF E peptide improved graft success. In growth-hormone-deficient lit/lit mice, muscle MGF was preferentially induced by growth hormone, which is what tied the splice variant to the GH axis in the first place. Each of these is a rodent disease or deficiency model using the unmodified peptide or the endogenous splice variant. None is a study of a healthy adult, and none is a study of a PEGylated preparation.
Endogenous MGF/IGF-1Ec as an exercise-responsive splice variant in humans	Anecdotal reports only human observational · review [8] [7]	Human observational work confirms that the Ec peptide is produced alongside its precursor protein in a wide range of human tissues, and provides initial evidence that it is differentially regulated during muscle regeneration after exercise-induced damage. This is evidence that the body's own splice variant participates in repair. It is not evidence that injecting a synthetic or PEGylated version reproduces, amplifies, or improves on that process — a distinction that is the entire content of this page's argument.
Transfer of animal findings to humans	Anecdotal reports only in vitro [6]	The usual assumption that rodent muscle results probably indicate human muscle results is specifically contradicted for this peptide. In paired experiments, the human Ec peptide stimulated human prostate cancer cells but had no effect on mouse C2C12 myoblasts under any culture condition, and the synthetic mouse Ec was inactive in human cells while stimulating mouse cells. The authors located the active core in the last four amino acids of the C-terminus and described the mode of action as species-specific. Rodent MGF data therefore has a weaker claim on human relevance than rodent data usually does.
Effect of PEGylation on the molecule's behavior	Anecdotal reports only in vitro [13]	Unstudied for this compound. PEGylation of a protein ligand extends its half-life and frequently reduces its bioactivity — a trade-off demonstrated directly for PEGylated IGF-I, a related but different protein, where the solution required engineering a protease-sensitive linker to release the active protein at the target site. No published work reports what PEGylation does to the MGF E peptide's potency, clearance, receptor interaction, or immunogenicity. The modification that gives the marketed preparation its name is the part with no literature behind it at all.
Long-term safety in humans	Anecdotal reports only in vitro [9]	Nothing is known. No human has been followed on any MGF preparation in any published study. What exists instead is a cell-line signal pointing the wrong way: the MGF E peptide is mitogenic for human prostate cancer cells through an IGF-1-receptor-independent mechanism, and the transcript is preferentially expressed in cancerous rather than normal prostate tissue. That is a reason for caution, not a measured risk.

FOR RESEARCH PURPOSES ONLY

Typical protocol range in the research

In vitro proliferation assays in human PC-3 prostate cancer cells, using the synthetic 24-amino-acid human Ec peptide — the unmodified peptide, not a PEGylated preparation

A narrow window of 5 to 50 nanomolar stimulated growth in serum-rich medium; outside that window, and in serum-poor medium, no stimulation was observed at all [6]
Cell-culture work on primary human muscle progenitor cells and myogenic precursor cells, again with the unmodified synthetic MGF C-terminal 24-amino-acid E peptide added to culture medium

Concentrations applied directly to cells in a dish. No systemic dose is derivable from an in vitro concentration, and none of these studies administered anything to an intact organism [1] [2]

No published study of any species has administered a PEGylated MGF preparation at any dose. The figures above are culture-medium concentrations of the unmodified peptide, reported for context rather than as anything that could be converted into a dose. The microgram figures that circulate in community discussion have no published study behind them and are therefore not reported here.

Ranges are what published research reports, not a recommendation. PHL does not prescribe, and nothing here is personalized to you.

Side effects & safety signals

No human safety data for any MGF preparation

Not established · No published clinical trial, case series, or registry has administered MGF or a PEGylated MGF preparation to a person. There is no adverse-event profile to describe. A 2026 review of performance-enhancing peptides acting on the growth-hormone/IGF-1 axis names PEG-MGF directly and places it in its lowest evidence tier — a complete absence of human studies — while describing the gap between online self-administration protocols and any clinical evidence.

[15]
Mitogenic activity in human cancer cells

Reported in prostate cancer cell lines · The MGF transcript is overexpressed in human prostate cancer tissue and in PC-3 and LNCaP cell lines, while normal prostate epithelial cells did not express it. Exogenous synthetic MGF E peptide stimulated the growth of those cancer cells and activated ERK1/2 phosphorylation, and silencing the IGF-1 receptor and the insulin receptor did not abolish the effect — meaning the mitogenic activity runs through a pathway that is not the IGF-1 receptor. A separate review places IGF-1Ec in osteosarcoma pathophysiology as well. These are cell-line observations, not a demonstrated cancer risk in a person, but they are a signal in the unwelcome direction and they are specific to this peptide rather than inherited from the IGF-1 axis generally.

[9] [10]
Species-specific activity that does not transfer between organisms

Demonstrated in paired cell-culture experiments · This is a safety-relevant finding as much as an efficacy one. The human Ec peptide stimulated human PC-3 cells but had no effect on mouse C2C12 myoblasts under any culture condition, and the synthetic mouse Ec peptide was inactive in human cells while stimulating mouse cells. If the peptide's activity does not transfer between species in a dish, then rodent safety observations do not transfer to humans either — in either direction.

[6]
Unverified identity of material carrying this name

Not quantified · A doping-control laboratory that characterized a preparation offered as full-length MGF identified a protein of 12,264.9 daltons whose sequence was closely related to IGF-1Ec but modified: the terminal lysine had been eliminated and an arginine-to-histidine substitution was present at position 109. That is a different molecule from the one in the published biology. Separately, when a laboratory analyzed preparations labeled as a different muscle-targeting protein, MGF was among the growth-promoting peptides found inside products labeled as something else entirely. With no approved manufacturer, nothing guarantees that a vial holds the molecule its label names.

[11] [12]
PEGylation as an uncharacterized modification

Never studied for this preparation · Attaching polyethylene glycol to a protein reliably extends its half-life, and it frequently does so at the cost of reduced bioactivity — that trade-off is the central problem the PEGylation literature works on, and it has been demonstrated directly for PEGylated IGF-I, a related but different protein. Nobody has published what PEGylation does to the MGF E peptide's potency, its receptor interaction, its clearance, or its immunogenicity. The modification that defines the marketed preparation is the part of it that has never been measured.

[13]
Prohibited in tested sport

Standing status since 2005 · MGF peptides have been prohibited under World Anti-Doping Agency regulations since 2005, and detection methods reach concentrations of 0.25 nanograms per millilitre for the full-length variant using immunoaffinity purification and high-resolution mass spectrometry. This is an enforceable status rather than a theoretical one. Any athlete in a tested sport should confirm the current year's prohibited list rather than rely on this page.

[11]

Published lists are never exhaustive, so report anything unexpected to a licensed provider.

Storage, handling & reconstitution

Lyophilized storage: Lyophilized peptide preparations of this class are conventionally kept refrigerated at 2–8 °C and protected from light, with freezing used for long-term holding. That convention comes from general lyophilized-peptide practice. No published stability study addresses this preparation, and the polyethylene glycol conjugation is itself an unquantified variable: no published work characterizes how the PEG moiety on a commercial MGF preparation behaves on storage.
Reconstituted storage: Once in solution, peptides are conventionally refrigerated at 2–8 °C, protected from light, and treated as short-dated rather than indefinitely stable. No published study establishes a solution shelf life for any PEGylated MGF preparation.
Reconstitution diluent: The conventional diluent for lyophilized research peptides is bacteriostatic water: sterile water preserved with 0.9% benzyl alcohol. Sterile water without a preservative is used where a preservative is contraindicated and is treated as single-use.
Reconstitution & handling: Conventional handling: sanitize the stopper before piercing it, add the diluent slowly down the inside wall of the vial rather than directly onto the powder, and let it dissolve on its own. Swirl gently if needed; never shake. A properly reconstituted solution is clear; anything cloudy, discolored, or carrying visible particulate is discarded. PHL does not publish volume or unit calculations, because those are dosing decisions and dosing decisions belong with a licensed clinician.
Handling notes: There is no approved manufacturer, so there is no label, no assigned beyond-use date, and no lot-level stability testing behind any storage claim. When a doping-control laboratory characterized a preparation offered as full-length MGF, the protein it identified carried a C-terminal lysine elimination and an amino-acid substitution relative to the published sequence — so even the assumption that a vial holds the molecule its label names is an assumption. Treat everything above as convention, not specification.

The how-to guides cover the conventions behind these fields, and what the published stability data does and does not establish: Storage, Reconstitution, Handling.

Questions for your provider

Bring this page to a licensed provider. A provider can order labs, review your medications and history, and tell you whether anything here is relevant to your situation. This page can't. Peptide Health Lab does not prescribe and does not sell peptides.

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Citations

15 sources · every identifier checked against PubMed

[1] Mechano Growth Factor E peptide (MGF-E), derived from an isoform of IGF-1, activates human muscle progenitor cells and induces an increase in their fusion potential at different ages · Mechanisms of Ageing and Development, 2011. In vitro study
[2] A new pro-migratory activity on human myogenic precursor cells for a synthetic peptide within the E domain of the mechano growth factor · Experimental Cell Research, 2007. In vitro study
[3] A synthetic mechano growth factor E peptide enhances myogenic precursor cell transplantation success · American Journal of Transplantation, 2007. Animal study
[4] Mechano-growth factor, an IGF-I splice variant, rescues motoneurons and improves muscle function in SOD1(G93A) mice · Experimental Neurology, 2009. Animal study
[5] Muscle mechano growth factor is preferentially induced by growth hormone in growth hormone-deficient lit/lit mice · The Journal of Physiology, 2004. Animal study
[6] The human Ec peptide: the active core of a progression growth factor with species-specific mode of action · Hormones (Athens), 2016. In vitro study
[7] Biological activity of the e domain of the IGF-1Ec as addressed by synthetic peptides · Hormones (Athens), 2014. Review
[8] Identification of the IGF-1 processing product human Ec/rodent Eb peptide in various tissues: Evidence for its differential regulation after exercise-induced muscle damage in humans · Growth Hormone & IGF Research, 2017. Human observational study
[9] Preferential expression of IGF-1Ec (MGF) transcript in cancerous tissues of human prostate: evidence for a novel and autonomous growth factor activity of MGF E peptide in human prostate cancer cells · The Prostate, 2010. In vitro study
[10] The role of the IGF-1 Ec in myoskeletal system and osteosarcoma pathophysiology · Critical Reviews in Oncology/Hematology, 2016. Review
[11] Mass spectrometric characterization of a biotechnologically produced full-length mechano growth factor (MGF) relevant for doping controls · Growth Hormone & IGF Research, 2014. In vitro study
[12] Detection of black market follistatin 344 · Drug Testing and Analysis, 2019. In vitro study
[13] Bioresponsive release of insulin-like growth factor-I from its PEGylated conjugate · Journal of Controlled Release, 2018. In vitro study
[14] Growth factors and muscle ageing · Experimental Gerontology, 2004. Review
[15] The emerging landscape of performance-enhancing peptides modulating GH-IGF1 axis: bridging the gap between clinical evidence and patient self-administration · Frontiers in Endocrinology, 2026. Review

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