BRAK LABS Peptide research, plainly written

group

Muscle and performance compounds

Compounds that act on the two signalling systems governing muscle size: the growth factor pathway and the myostatin brake. Each entry names the molecule that was studied, separates it from the one it is confused with, and cites the record.

Last Reviewed Editorial policy Methodology

Muscle size is governed by two opposing signals, and everything on this page acts on one of them. The first is a growth signal: growth hormone prompts the liver to release insulin-like growth factor 1, usually written IGF-1, and IGF-1 tells muscle cells to build. The second is a brake called myostatin, a protein muscle makes to limit its own growth. Cattle born with a broken myostatin gene grow visibly larger muscles, which is the observation that started the whole field [13].

Two of the four entries here push on the growth signal and two release the brake. IGF-1 LR3 is a modified copy of the growth factor itself, engineered so that the carrier proteins that normally hold IGF-1 inactive cannot bind it. Follistatin-344 and ACE-031 both intercept myostatin before it reaches its receptor, by different means. The fourth entry covers the myostatin-inhibitor class as a whole, because two of its members have gone further in people than anything sold in the gray market.

The evidence question on this page is unusual, and it is worth naming before the entries. For three of the four, a large and often impressive body of human work exists for a closely related molecule, and almost none for the thing being sold. Sorting out which molecule each study tested is most of the job here, and every entry below does it explicitly, with the study design, the species and the numbered source stated each time.

Not medical advice

This page reports what has been documented about a compound. It is not medical advice, not a diagnosis, not a dosing protocol, and not a recommendation to obtain or use anything described here. Talk to a licensed clinician about anything concerning your health. Read the full disclaimer.

Reviewed against editorial standards Updated

The compounds in this group

Each row names what the compound is and what its published work covers. The evidence level is the strongest tier of evidence about that compound for the use it is sold for. It is a single figure for a whole entry rather than a claim by claim grading, so an entry may also describe work that is weaker, or that tested a different route or a different molecule, and each of those carries its own citation in the text. Where a compound's own review has been run, its page grades every claim area separately.

Compounds covered on this page, what each one is, and what the published record on it covers
CompoundAlso known asWhat the published work coversWhere it standsEvidence level
IGF-1 LR3Long R3 IGF-1, IGF-1 Long Arg3Infusion studies in pigs, guinea pigs and cattle; no human trial of this modified form on any registryUnapproved. The native molecule is an approved drug with its own record[Animal]
Follistatin-344FS-344, FST-344A published case series of eye harm in eleven men who injected it; the human muscle results people cite belong to a gene therapyUnapproved. No registered trial of the injected protein[Anecdote]
ACE-031Ramatercept, ActRIIB-FcA 48 participant randomised phase 1 measuring lean mass, and a phase 2 in boys with Duchenne muscular dystrophy stopped on preliminary safety dataNever approved. Both phase 2 registrations terminated in 2011[Human RCT]
Myostatin inhibitors (class)GDF-8 antagonistsRandomised trials of four different molecules in muscular dystrophy, spinal muscular atrophy and obesity, with mixed and often negative functional resultsNo myostatin inhibitor is approved for any indication anywhere[Human RCT]

The two signals everything here acts on

The growth arm is straightforward to describe. Growth hormone acts largely by prompting the liver to release IGF-1, and IGF-1 binds a receptor on muscle cells that switches on the machinery for building protein. In the bloodstream, almost all IGF-1 is bound up by a family of carrier proteins called IGF-binding proteins, which keep it inactive until it is released at a tissue. That binding is the natural throttle on the signal, and it is precisely the thing IGF-1 LR3 was engineered to escape.

The brake arm works the other way. Muscle cells release myostatin, also called GDF-8, which binds a receptor called activin receptor type IIB and instructs the muscle to stop growing. Block that signal and the brake comes off. Follistatin is a natural myostatin-binding protein, so injecting more of it is one way to block it; ACE-031 takes the other route, using a soluble decoy version of the receptor to soak up myostatin before it reaches the real receptor.

Both routes have the same design hazard, and it has already produced harm in a trial. Myostatin belongs to a large family of related signalling proteins, the transforming growth factor beta superfamily, and a molecule built to catch myostatin frequently catches its relatives too. The ACE-031 entry below is the worked example: the phase 2 in boys with Duchenne muscular dystrophy was stopped on preliminary safety data, and the reported findings were bleeding-related rather than muscle-related [11].

Which molecule a study tested, and why it is the whole question here

Three of the four entries on this page are routinely credited with a record that belongs to something else. IGF-1 LR3 is credited with the trials of native recombinant IGF-1, an approved drug with a substantial clinical file. Follistatin-344 sold as an injectable protein is credited with the functional results of a follistatin gene therapy, which is a virus-delivered construct given directly into a specific muscle under a hospital trial protocol [8]. The gray-market ACE-031 supply has been shown, in an anti-doping laboratory study, to contain a different protein from the one the trials used [12].

This site's rule on that is fixed and it is in EVIDENCE-TIERS.md: evidence about a different molecule never sets a compound's tier. A fragment does not inherit its parent's trials, an analog does not inherit the original's, and a protein does not inherit the record of a gene therapy that makes the same protein by a different route. The related work is reported here, labelled as being about the other molecule, and the tier on each entry reflects only what tested that entry's own compound.

In sport, all of these fall under the annual Prohibited List published by the World Anti-Doping Agency, whose 2026 edition took effect on 1 January 2026 [18]. That is a separate question from regulatory approval, and an athlete subject to testing has a different set of consequences to consider than a reader who is not.

The four entries, one at a time

IGF-1 LR3

Also known as Long R3 IGF-1, IGF-1 Long Arg3

Plain-English version: An 83 amino acid modified version of a natural growth factor, altered so that it evades the proteins that normally hold it inactive.

Strongest evidence, and what it covers [Animal] Muscle growth with a binding-protein-resistant IGF-1 analog [1] [2] [3] [4] [5] [6]

IGF-1 LR3 is native human IGF-1 with one amino acid swapped at position 3 and a thirteen amino acid extension added to the front, so that the IGF-binding proteins cannot hold it. It stays free in circulation far longer than the natural molecule.

The published work on the modified form is in farm and laboratory animals. A four-day infusion in finisher pigs, at a daily rate of 180 micrograms per kilogram of body weight, decreased average daily weight gain and feed intake [1]. In guinea pigs, seven days of infusion raised the fractional weights of the adrenals, gut, kidneys and spleen without raising overall growth [2], and in beef heifers it conserved muscle protein while lowering circulating amino acids and glucose [3].

The native molecule is a different molecule with a different record. Recombinant human IGF-1, marketed as mecasermin, is approved for severe primary IGF-1 deficiency, and its label reports hypoglycaemia in 30 of 71 children across five clinical studies, or 42 percent, with four experiencing seizures or loss of consciousness [4]. LR3 is longer acting, and nothing has measured what that means for blood sugar in a person.

Higher circulating IGF-1 was associated with higher incidence of colorectal, breast, prostate and thyroid cancer in a prospective UK Biobank analysis, an observational finding about the body's own level rather than about anything taken [5]. A 2026 review covers what clinicians see in people self-administering compounds on this axis [6]. A registry search for IGF-1 LR3 returned nothing on 2 August 2026.

Where it stands IGF-1 LR3 is not an approved drug anywhere and no trial of it is registered on ClinicalTrials.gov, searched on 2 August 2026. The native molecule mecasermin is FDA-approved for severe primary IGF-1 deficiency and carries the prescribing information cited here [4].

Our takeTwo facts sit oddly beside each other. The approved native molecule carries a documented rate of one specific adverse event in the population it was tested in, and the modified version has never been given to anyone in a study. This site does not read the first as a prediction about the second, for the same reason it refuses to read the native molecule's efficacy record as one: they are different molecules, and that rule is not suspended when the read-across happens to sound cautious. What can be said is that the question has never been put.

Follistatin-344

Also known as FS-344, FST-344, Follistatin

Plain-English version: Not a peptide. A 344 amino acid glycoprotein that blocks a growth-limiting signal in muscle.

Strongest evidence, and what it covers [Anecdote] Muscle growth from injected follistatin protein [7] [8] [9] [13] [18] [19]

Follistatin is a natural protein that binds myostatin and several relatives, taking the brake off muscle growth. FS-344 is one of its two forms, and at 344 amino acids it is not a peptide.

The human results people cite belong to a gene therapy. In a published trial in sporadic inclusion body myositis, a virus carrying the follistatin gene was delivered to the quadriceps muscles of six participants alongside an exercise regimen, and six-minute walk distance improved against matched untreated comparators [8]. That is a different product from an injected protein.

The one published human record of the injected protein is a harm report: a retrospective case series of eleven male bodybuilding athletes who developed central serous chorioretinopathy, in which fluid collects under the retina and vision drops, after high-dose subcutaneous follistatin-344. In the eight with one previous injection the fluid cleared over an average of 2.3 months; all three with multiple previous injections had a recurrence [7].

A registry search for follistatin as an intervention on 2 August 2026 returned fourteen studies, and those that deliver it to a person deliver a gene therapy rather than a protein; a broader term search returns 78, most measuring follistatin in blood as a marker in other research [9]. The muscle-growth claim therefore rests on the biology of the brake [13], on a gene therapy [8], on a 2026 review of self-administration [19], and on community reports. Nothing has measured muscle in a person given the injected protein.

Where it stands Follistatin-344 is not an approved drug or biological product in any country, and no registered trial delivers it as an injected recombinant protein [9]. Follistatin acts on myostatin, and agents modifying myostatin function fall within the annual World Anti-Doping Agency Prohibited List, whose 2026 edition took effect on 1 January 2026 [18].

Our takeThe single most misattributed evidence base in the catalog: a gene therapy's walking-test result, quoted for a protein injection, alongside a published case series of vision loss in the exact population that buys it.

ACE-031

Also known as Ramatercept, ActRIIB-Fc

Plain-English version: Not a peptide. An engineered protein that traps the signals limiting muscle growth, whose trial program was stopped for safety.

Strongest evidence, and what it covers [Human RCT] Lean mass and muscle volume with a soluble activin receptor decoy [10] [11] [12] [20]

ACE-031 is a fusion protein: the outside portion of activin receptor type IIB stitched to the tail of a human antibody. In the bloodstream it acts as a decoy, catching myostatin and related proteins before they reach the real receptor. It is not a peptide.

The phase 1 was double-blind and placebo-controlled, in 48 healthy postmenopausal women randomised three to one to a single subcutaneous injection across a range from 0.02 to 3 mg per kilogram of body weight. In the 3 mg per kilogram group, total body lean mass by DXA was 3.3 percent higher and thigh muscle volume by MRI was 5.1 percent higher at day 29 [10].

The phase 2, in ambulatory boys with Duchenne muscular dystrophy, was stopped after the second regimen on preliminary safety data, with nosebleeds and telangiectasias, meaning small dilated blood vessels visible in the skin, given as the reason. Trends toward higher lean mass and maintained six-minute walk distance were reported, none statistically significant [11]. Both phase 2 registrations, covering 24 and 11 participants, are recorded as terminated in 2011 [20].

The third piece is about the supply. An anti-doping laboratory examined fourteen products sold as ACE-031 outside the regulated market. Two contained no protein the assay recognised. In the other twelve, mass spectrometry and immunoblotting identified full-length human activin receptor IIB rather than ACE-031, and a protease that cleaves antibody fusions confirmed the antibody portion was absent [12].

Where it stands ACE-031 has never been approved anywhere. Its two phase 2 registrations on ClinicalTrials.gov are both recorded as terminated, with the registry's stated reason given as preliminary safety data and completion dates in mid-2011 [20].

Our takeA rare case where the human evidence is real, the harm signal is real, and the product on the gray market has been shown in a laboratory to be a different protein from the one that produced either.

Myostatin inhibitors

Also known as GDF-8 antagonists, Myostatin, GDF-8

Plain-English version: Not peptides. A family of antibodies and engineered proteins that block the signal limiting muscle growth, none of which has been approved anywhere.

Strongest evidence, and what it covers [Human RCT] Blocking the myostatin brake to increase muscle mass in people [13] [14] [15] [16] [17] [18]

Myostatin, also known as GDF-8, is a protein muscle makes to limit its own growth. The founding observation is genetic: cattle breeds with visibly enlarged muscles carry mutations in the myostatin gene [13]. Blocking that signal has been attempted in people with antibodies, with decoy receptors, and with molecules that block the receptor. None is a peptide, and none has been approved anywhere.

The class has a longer human record than the gray market suggests, and most of it reads the same way: the muscle gets bigger and the person does not get better. MYO-029, an antibody against myostatin, was tested in 116 adults with three muscular dystrophies. Skin hypersensitivity appeared at the two highest levels. No improvement in strength or function was seen, though the trial was not powered to find one, and a trend toward increased muscle size was reported [14].

ACE-083 was designed to act locally rather than through the bloodstream. In a randomised phase 2 in facioscapulohumeral muscular dystrophy, 58 participants received it into either the biceps or the tibialis anterior against placebo. Total muscle volume rose by 16.4 percent in the biceps group and 9.5 percent in the tibialis anterior group, both statistically significant, with no consistent improvements in functional or patient-reported measures over as much as twelve months [15]. That is the cleanest published demonstration in the class that muscle volume and muscle function are separate things.

The two programmes still in serious development are the exceptions, and neither is available outside a trial. Bimagrumab, an antibody against the activin type II receptor, was tested in a 48-week phase 2 in 75 adults with type 2 diabetes and obesity; fat mass fell by 20.5 percent against 0.5 percent on placebo, and lean mass rose by 3.6 percent against a 0.8 percent fall [16]. Apitegromab met its primary endpoint in SAPPHIRE, a phase 3 in 188 people with non-ambulatory spinal muscular atrophy already on standard therapy, by 1.8 points on a motor-function scale with a confidence interval of 0.30 to 3.32 [17].

Two things belong on the record together. The class has produced genuine randomised human measurements of increased muscle, so the mechanism does something in people. And the two that went furthest before this generation, ACE-031 and MYO-029, both produced off-target effects consistent with catching relatives of myostatin rather than myostatin alone. Neither of the two furthest along today is what a gray-market vendor sells.

Where it stands No myostatin inhibitor has been approved for any indication in any country. Neither bimagrumab nor apitegromab appears in the National Library of Medicine's database of FDA-approved labels, checked on 2 August 2026. Agents modifying myostatin function fall within the annual World Anti-Doping Agency Prohibited List, whose 2026 edition took effect on 1 January 2026 [18].

Our takeThirty years of work on this target has produced repeatable increases in muscle size and almost no repeatable improvement in what people can do, and that gap is the most useful thing on this page.

What we do not know about this group

No human study has given IGF-1 LR3 to anyone under observation. Nothing is known about what it does to blood sugar, to muscle, or to anything else in a person, at any exposure, by any route.

No human study has given injected recombinant follistatin-344 protein to anyone in order to measure muscle. The one published human record of that exposure describes eye harm, and it is a retrospective case series rather than a trial.

Where a myostatin inhibitor did increase muscle volume in a randomised trial, function generally did not follow. Why the two came apart has not been settled, and it is the open question the whole class turns on.

The long-term consequences of holding IGF-1 signalling high, or of holding the myostatin brake off, have not been characterised in any published human study of any of these compounds. The observational association between higher circulating IGF-1 and several cancers is a reason the question is being asked; it is not an answer to it.

For ACE-031 and for follistatin, what is sold under the name has been shown or is likely to differ from what the trials tested, so even the trial evidence that exists may not describe the substance in question.

None of these compounds has a published toxicology package covering repeated exposure in a person. The safety records that exist belong to short trials in patient populations, or to related molecules.

What this evidence can and cannot show

These results come from pigs, guinea pigs and cattle in infusion and growth studies in farm and laboratory animals, not from people. An animal model is a deliberate simplification: the injury is created on purpose, the animal is young and healthy, the dose is scaled to body weight in a way that does not translate directly, and the outcome is measured at a fixed point rather than lived with. Cell and tissue work is a further step removed, because the concentrations that produce an effect in a dish are often far above anything a body reaches. Mechanism is a reason to run a trial. It is not a substitute for one, and compounds that looked mechanistically convincing have failed in people many times.

Frequently asked questions

Is IGF-1 LR3 the same as the approved IGF-1 drug?

No. The approved drug, mecasermin, is native recombinant human IGF-1. LR3 has one amino acid swapped and a thirteen amino acid extension added so that binding proteins cannot hold it, which makes it longer acting. The approved drug's trials tested the native molecule, and its label reports hypoglycaemia in 42 percent of 71 children across five studies. None of that record is about LR3.

Why do people say follistatin has dozens of trials?

Because a registry search on the word returns 78 studies, and most of them measure follistatin in blood as a marker in research about something else. Searching for follistatin as an intervention returns fourteen, and the ones that actually deliver it deliver a gene therapy rather than an injected protein.

What is the difference between follistatin gene therapy and injecting follistatin?

They are different products. The gene therapy delivers a gene into a specific muscle, once, using a virus, in a hospital trial, and the muscle then makes the protein locally. Injecting a recombinant protein delivers the protein itself into the body repeatedly. The published functional result belongs to the first, and nothing tested the second for muscle.

Why was the ACE-031 programme stopped?

The phase 2 in boys with Duchenne muscular dystrophy was halted after the second regimen on preliminary safety data, with nosebleeds and small dilated skin vessels reported. Both phase 2 registrations are recorded as terminated with the same stated reason and completion dates in 2011.

Has any myostatin inhibitor ever been approved?

No. Not for muscular dystrophy, not for spinal muscular atrophy, not for obesity, and not anywhere in the world. Two programmes are still active, bimagrumab and apitegromab, and neither has an FDA-approved label.

If the muscle gets bigger, does that mean it works better?

The trials say those are separate questions. In the phase 2 of ACE-083, total muscle volume rose significantly against placebo in both muscles tested, and there were no consistent improvements in functional or patient-reported measures over as much as twelve months. Muscle volume is a measurement, not an outcome.

Is what is sold as ACE-031 actually ACE-031?

In one published laboratory examination of fourteen gray-market products, two contained no protein the assay recognised, and the other twelve contained full-length human activin receptor IIB rather than the antibody-fusion protein the trials used. That is one study of one sample set, and it is the only published check of its kind on this compound.

Are these prohibited in sport?

Compounds acting on the growth factor axis and on myostatin fall within the annual Prohibited List published by the World Anti-Doping Agency, whose 2026 edition took effect on 1 January 2026. The list itself is the governing document, and it is reissued every year, so a summary of it goes out of date.

Why is there so much animal data and so little human data here?

Because most of these molecules were developed for muscle-wasting diseases and either stopped early or never entered human testing under the modified form that is sold. IGF-1 LR3 in particular has been used for decades as a laboratory and livestock research reagent, which is where its animal literature comes from.

References

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  20. US National Library of Medicine, ClinicalTrials.gov. Registry search for ACE-031 as an intervention, run 2 August 2026. Four studies returned: two completed phase 1 studies, and two phase 2 studies in Duchenne muscular dystrophy (NCT01099761, 24 participants, and NCT01239758, 11 participants) both recorded as terminated with completion dates in 2011 and the stated reason given as preliminary safety data. ClinicalTrials.gov. 2026. Registry search