ACE-083
Localized myostatin inhibitor
ACE-083 (Localized myostatin inhibitor) is a gh & growth research compound. A follistatin-based ligand trap injected directly into a specific muscle. It sequesters myostatin and related TGF-beta ligands locally, so hypertrophy is confined to the injected muscle rather than being systemic.
ACE-083 quick facts
| Reported research dose | 150–200mg per muscle (trial doses) |
| Route | Intramuscular (local) |
| Frequency | Every 3 weeks in trials |
| Half-life | Local depot effect; dosed every 3 weeks in trials |
| Forms | Injectable |
| Evidence level | Phase 2 trials — muscle volume increased, but strength and function did not follow |
The trial result is the honest headline and it's a disappointment: in facioscapulohumeral muscular dystrophy and Charcot-Marie-Tooth, ACE-083 increased muscle volume but produced no improvement in function or strength, and development was discontinued. Bigger muscle that doesn't do more. Anyone selling this as localized growth should be quoting that finding.
How ACE-083 works
A follistatin-based ligand trap injected directly into a specific muscle. It sequesters myostatin and related TGF-beta ligands locally, so hypertrophy is confined to the injected muscle rather than being systemic.
Proposed benefits
Researched for lean-mass support, recovery, sleep depth, connective-tissue repair and improved body composition via the GH/IGF-1 axis.
Where to get ACE-083
Buy ACE-083 at Disguised Alpha →Bacteriostatic water is the diluent — sterile water with 0.9% benzyl alcohol, which is what lets a vial be drawn from more than once. It does not come with the vial, and unlike the compound it is bought again every time.
Need bacteriostatic water? Get it at AminoWell USA (my company) → Code CAMERON.
The evidence for ACE-083
Graded by what exists behind each claim.
✅ Clinically validated
- A real pharmaceutical program with a real result. Acceleron ran phase 2 trials of ACE-083 in facioscapulohumeral muscular dystrophy and Charcot-Marie-Tooth disease. It reliably increased muscle volume in the injected muscle — that part worked — but did not produce corresponding improvements in strength or function, and development was discontinued.
- That dissociation is the finding worth carrying: bigger muscle and stronger muscle are not the same endpoint, and this is one of the cleanest demonstrations of it in the literature.
📊 Correlative data
- Essentially no community use, and that absence is itself informative — it was never widely available after Acceleron shut the program, so unlike most compounds here there is no anecdotal record to weigh against the trial. What you see is what there is: a well-run phase 2 that produced measurable hypertrophy and no functional gain.
🧪 Theoretical / extrapolated
- A locally-acting myostatin/activin ligand trap, designed for intramuscular injection so the effect stays where it is put rather than acting systemically.
- The local design is what made it interesting and what the trial result complicates: hypertrophy without functional gain suggests the added tissue was not contributing normally, which is a caution for every myostatin-targeting approach.
How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →
What ACE-083 actually does
ACE-083 is the rarest thing in this catalog: a compound with two completed randomized human trials, both of which met their primary endpoint and failed anyway. That sentence is the page, and almost nowhere selling this molecule says it.
What the molecule is. It is not a peptide. It is a locally-acting follistatin-based fusion protein, and the engineering has two halves that pull in opposite directions Pearsall 2019. The first half is the ligand trap: surface plasmon resonance and cell-based assays confirmed that it binds and potently neutralizes myostatin, activin A, activin B and growth differentiation factor 11. Four ligands, not one. Anything sold as a clean myostatin inhibitor is being described by its intent rather than by its binding data, and the whole class shares that problem Rodgers 2022.
The second half is the interesting one, and it is a pharmacokinetic trick rather than a pharmacological one. ACE-083 was characterized as having high affinity for heparin and for extracellular matrix Pearsall 2019. That is the entire localization mechanism. Follistatin itself comes in isoforms that differ in exactly this property — the cell-surface-binding form sticks to heparan-sulfate proteoglycans while the soluble form circulates Schneyer 2004 — and ACE-083 was built to sit at the sticky end of that spectrum on purpose. Inject it into a muscle and the matrix holds it there. That is why the trials dosed one named muscle rather than a person.
Where the brake it releases actually sits. Myostatin and activins signal through the activin type II receptors, and blocking that signal — with the myostatin propeptide, with follistatin, or with a dominant-negative activin receptor — produces muscle mass increases in transgenic mice comparable to deleting myostatin altogether Lee 2001. The target is real, the direction is not in doubt, and that is precisely why the human result on this page is so instructive: the pathway did what it was supposed to do and the patients did not get better.
One structural consequence follows from the design and is worth stating before the trial data. A protein held in the extracellular matrix of one injected muscle cannot act as a systemic anabolic. In mice, intramuscular ACE-083 produced localized, dose-dependent hypertrophy with no evidence of systemic muscle effects or endocrine perturbation Pearsall 2019. Read as a benefit that is elegant. Read as a limit it means the compound can only ever change the muscles somebody is willing to put a needle into.
Cell, rodent, human — and where it stops
Step one, in mice, and the rodent result is genuinely positive. Intramuscular ACE-083 caused localized, dose-dependent hypertrophy of the injected muscle in wild-type mice and in mouse models of Charcot-Marie-Tooth disease and Duchenne muscular dystrophy Pearsall 2019. Critically, it did not stop at size: the injected tibialis anterior produced more isometric contractile force in situ, in wild-type animals and in the disease models, and CMT mice gained ankle dorsiflexion torque. So in the mouse, volume and force moved together. Hold that, because it is the step that did not transfer.
Step two, in healthy humans, and the dissociation is already visible here in 2018. A phase 1 randomized, double-blind, placebo-controlled dose-ranging study enrolled 58 healthy postmenopausal women, 42 on ACE-083 and 16 on placebo, with 50 to 200 mg injected unilaterally into either rectus femoris or tibialis anterior as 1 or 2 doses 3 weeks apart Glasser 2018. Maximum mean increases in muscle volume were 14.5% plus or minus 4.5% in rectus femoris and 8.9% plus or minus 4.7% in tibialis anterior. There were no serious adverse events, no dose-limiting toxicities and no discontinuations for adverse events. And there were no significant changes in mean muscle strength. That is the whole problem, in healthy people, four years before the phase 2 results.
Step three, in facioscapulohumeral muscular dystrophy. Part 1 enrolled 37 participants in an open-label ascending-dose safety arm; Part 2 randomized 58 to 240 mg per muscle or placebo, injected bilaterally every 3 weeks into biceps brachii or tibialis anterior for 6 months, followed by 6 months open-label Statland 2022. Among 55 evaluable participants the treatment difference in total muscle volume was 16.4%, with a 90% confidence interval of 9.8% to 23.0% and P less than 0.0001, in the biceps group, and 9.5%, confidence interval 3.2% to 15.9%, P equal to 0.01, in the tibialis group. Contractile muscle volume rose significantly in both groups and fat fraction fell in the tibialis group. There were no consistent improvements in functional or patient-reported measures in either group, across up to 12 months of treatment.
Step four, in Charcot-Marie-Tooth disease, where the result is slightly better and still negative. 63 adults with CMT1 or CMTX entered; Part 1 dosed 18 open-label; Part 2 randomized 45 with 44 treated to 240 mg per muscle bilaterally in tibialis anterior for 6 months plus a 6-month open-label extension Thomas 2022. Total muscle volume rose 13.5% against placebo, p equal to 0.0096, and there were significant differences in contractile muscle volume and in change in ankle dorsiflexion strength. Fat fraction and all other functional outcomes were not significantly improved. The trial is graded Class II evidence that intramuscular ACE-083 is safe and increases muscle volume, and the authors state plainly that patients did not demonstrate greater functional improvement than placebo. A strength measure moved. Walking did not.
The obstacles, and they are specific rather than generic. (1) In situ force in an anesthetized mouse and a 6-minute walk test in a person are not the same measurement. The mouse endpoint isolates the injected muscle; the human endpoints are whole-body tasks that recruit dozens of muscles, only two of which were injected. (2) The added tissue was contractile by imaging and still did not produce function — contractile muscle volume rose in both phase 2 trials, so the easy explanation, that the drug added fat or fibrous tissue, is ruled out by the trials' own data. (3) In CMT the limiting lesion is the motor nerve, and adding sarcomeres to a muscle whose motor units are being lost cannot restore what the innervation no longer delivers. (4) In FSHD the disease is patchy and asymmetric across many muscles, so two injected muscles cannot rescue a task. (5) Nothing in the research market is this molecule at this dose. The trials used a clinician-administered recombinant fusion protein at 240 mg per muscle, injected bilaterally, every 3 weeks, under a protocol. This site's own dose field, 150 to 200 mg per muscle, does not match either the 50-to-200 mg phase 1 range or the 240 mg phase 2 dose.
And the honest place to put it in the class. An independent 2021 review of antimyostatin treatment across 20 years is subtitled the story of great expectations and limited success, and its conclusion is that preclinical promise has repeatedly failed to translate into patient populations Nielsen 2021. ACE-083 is not an exception to that pattern. It is one of the cleanest examples of it, because the pharmacodynamic endpoint was hit hard and the clinical one was not touched.
ACE-083 pharmacokinetics — how much of it actually gets in
The catalog says ‘local depot effect, dosed every 3 weeks in trials’. That is correct and it is worth unpacking, because the pharmacokinetics of this compound are the design rather than an afterthought.
What holds it in place. ACE-083 binds heparin and extracellular matrix with high affinity Pearsall 2019. Its residence in the injected muscle is therefore governed by matrix binding and by local proteolysis rather than by renal or hepatic clearance, which is why the dosing interval is 3 weeks rather than daily, and why the phase 1 protocol could give as few as 1 or 2 doses and still measure a 14.5% volume change Glasser 2018.
What degrades it. It is a protein, so it is degraded by tissue proteases and taken up by cells rather than filtered intact. There is no published human half-life for it in this site's data and no figure in the trial abstracts, so the honest number is the dosing interval that worked: 240 mg per muscle every 3 weeks sustained a 16.4% volume difference over 6 months Statland 2022.
The oral barrier, which is absolute here. This is a recombinant fusion protein, not a short peptide. Swallowed, it meets gastric acid and pancreatic proteases and is digested to amino acids; there is no transporter for an intact protein of this size across the gut wall, and hepatic first-pass extraction would remove anything that somehow crossed. Oral bioavailability is not low for this class, it is effectively zero, and no oral preparation of it has ever existed.
The route, and the thing the route buys. Every human dose ever given was an intramuscular injection into a named muscle, bilaterally in phase 2 and unilaterally in phase 1. Subcutaneous administration is the wrong route for this molecule by design: the point is a matrix-bound depot inside the target muscle. And the difference matters clinically, because the systemic version of this idea, given subcutaneously every 2 to 4 weeks, is the one that was stopped for vascular adverse events Campbell 2017.
What would have to be true, and how you would know it was not
Three predictions. The first is the one that cuts against the compound and it is already supported by three human studies.
1. Size will move and strength will not, and you should measure both. This is the prediction the trials made for you: volume up 14.5% in healthy women with no significant strength change Glasser 2018, up 16.4% in FSHD biceps with no consistent functional improvement Statland 2022, up 13.5% in CMT tibialis anterior with no improvement in any functional outcome except ankle dorsiflexion strength Thomas 2022. The measurement that falsifies or confirms it in one person is a paired one: circumference or an ultrasound thickness at a marked point, alongside a limb-specific one-repetition maximum and grip strength, retested at 6 and 12 weeks. If size rises and the strength numbers sit flat, the compound is behaving exactly as the registered trials say it does, and the honest reading is that you bought volume.
2. Nothing systemic should move, and if it does the localization has failed. ACE-083 produced no systemic muscle effect and no endocrine perturbation in mice Pearsall 2019, whereas the systemic trap ACE-031 produced trends toward increased lean body mass, increased bone mineral density and reduced fat mass across the whole body Campbell 2017. So: IGF-1 (Insulin-like Growth Factor 1) should not change, a whole-body DEXA lean mass reading should not change beyond the injected limb, and a CBC should be unremarkable. Any of those moving means material is leaving the injected muscle, which converts this from a local compound into a systemic one and imports the safety profile of the drug that was stopped.
3. The uninjected side is the control, and using it is free. Phase 1 injected unilaterally on purpose Glasser 2018. Anyone running this without a contralateral control is throwing away the only design feature that makes a single-person result mean anything, because diet, training, sleep and expectation act on both limbs equally and the compound does not. A 6-week unilateral course with paired measurements produces a defensible personal result. A bilateral course produces an anecdote.
What nobody has tested yet
Four experiments, and the first is the one every buyer of this compound actually wants the answer to.
1. Nobody has given it to a trained, healthy adult who lifts. Phase 1 was 58 healthy postmenopausal women, given 1 or 2 doses, with no training program attached Glasser 2018; the phase 2 trials were in FSHD and CMT, where the limiting factor is disease Statland 2022 Thomas 2022. The obvious study — a resistance-trained adult, one vastus lateralis injected, the other as within-subject control, identical training, MRI volume plus isokinetic torque at 12 weeks — has never been run in any registered trial. It is also the only version of the experiment in which the added tissue would be given a reason to be recruited.
2. Nobody has published specific tension. Both phase 2 trials measured total muscle volume, contractile muscle volume, fat fraction and strength in the same participants. Force divided by contractile cross-sectional area is therefore computable from data that already exists, and it is the single number that would explain why 16.4% more contractile tissue produced no function. Nobody has reported it. This is the cheapest unrun experiment in this cohort: it requires no new participants and no new drug.
3. Nobody has said what happens after the last injection. The trials dosed for 6 months and extended for 6 more Statland 2022. There is no published follow-up describing whether the extra volume persists, decays over weeks, or decays over months once the ligand trap is gone. For a compound whose only demonstrated effect is size, the durability of that size is the entire value proposition, and the number does not exist.
4. Nobody has imaged the tendon. Adding 16% to a muscle in 6 months without a matched adaptation in tendon and enthesis is a mechanically plausible route to injury, and it is the specific concern that a local hypertrophy agent raises and a systemic one does not. No trial reported tendon imaging, tendon thickness, or a tendon adverse event category, in mice or in people.
ACE-083 — its own safety story, not its class's
The class safety block on this page warns about systemic myostatin and activin blockade. ACE-083 was specifically engineered not to do that, so the class block describes its cousin rather than it, and the real risk story here has three parts that the shared paragraph cannot reach.
1. What the human trials actually reported, which is reassuring. In phase 1 there were no serious adverse events, no dose-limiting toxicities and no discontinuations due to adverse events across 42 treated women Glasser 2018. In both phase 2 trials the most common treatment-emergent adverse events were mild to moderate injection-site reactions Statland 2022 Thomas 2022, and the CMT trial reported no serious adverse events, no grade 3 or above events and no deaths in its open-label part. Very few compounds in this catalog have a safety statement that comes from a placebo-controlled trial at all. This one does.
2. The risk it inherits if the localization fails, and the precedent is exact. ACE-031, an activin receptor type IIB and IgG1-Fc fusion given subcutaneously every 2 to 4 weeks to boys with Duchenne muscular dystrophy, was stopped after the second dosing regimen because of epistaxis and telangiectasias Campbell 2017. Nosebleeds and small dilated vessels are not muscle events; they are vascular ones, and they are what a systemic ligand trap in this family did to children. ACE-083 avoids that by staying in the muscle it is injected into. A research-market vial that is not the matrix-binding fusion protein, or a dose given subcutaneously because that is the route somebody is used to, gives up the localization and keeps the class liability.
3. The risk that is specific to this compound and has never been measured: hypertrophy that does not contribute. Three human studies produced more muscle and no more function Glasser 2018 Statland 2022 Thomas 2022. Tissue that adds mass and does not add force still adds load to the tendon, the enthesis and the joint, and it still has to be perfused. No trial in this program reported tendon imaging or a tendon adverse event category, so the honest statement is not that the risk is low — it is that nobody looked.
And the practical hazard. Every safety number above comes from a large-volume intramuscular injection placed into a named muscle by trial staff, bilaterally, every 3 weeks, at 240 mg per muscle. Self-administration of a large intramuscular volume into a specific muscle belly carries needle-track infection, sterile abscess and nerve-contact risk that the trials engineered away with technique, and there is no published guidance on doing it any other way.
Sources read for this page
- Pearsall RS, Davies MV, Cannell M, Li J, Widrick J, Mulivor AW, Wallner S, Troy ME, Spaits M, Liharska K, et al. Follistatin-based ligand trap ACE-083 induces localized hypertrophy of skeletal muscle with functional improvement in models of neuromuscular disease. Scientific Reports 2019 · PMID 31388039
- Glasser CE, Gartner MR, Wilson D, Miller B, Sherman ML, Attie KM. Locally acting ACE-083 increases muscle volume in healthy volunteers. Muscle & Nerve 2018 · PMID 29486514
- Statland JM, Campbell C, Desai U, Karam C, Diaz-Manera J, Guptill JT, Korngut L, Genge A, Tawil RN, et al. Randomized phase 2 study of ACE-083, a muscle-promoting agent, in facioscapulohumeral muscular dystrophy. Muscle & Nerve 2022 · PMID 35428982
- Thomas FP, et al. Randomized Phase 2 Study of ACE-083 in Patients With Charcot-Marie-Tooth Disease. Neurology 2022 · PMID 35545446
- Campbell C, et al. Myostatin inhibitor ACE-031 treatment of ambulatory boys with Duchenne muscular dystrophy: Results of a randomized, placebo-controlled clinical trial. Muscle & Nerve 2017 · PMID 27462804
- Nielsen TL, et al. Antimyostatin Treatment in Health and Disease: The Story of Great Expectations and Limited Success. Cells 2021 · PMID 33802348
- Rodgers BD, Ward CW. Myostatin/Activin Receptor Ligands in Muscle and the Development Status of Attenuating Drugs. Endocrine Reviews 2022 · PMID 34520530
- Schneyer AL, et al. Differential distribution of follistatin isoforms: application of a new FS315-specific immunoassay. Journal of Clinical Endocrinology and Metabolism 2004 · PMID 15472207
- Lee SJ, McPherron AC. Regulation of myostatin activity and muscle growth. Proceedings of the National Academy of Sciences 2001 · PMID 11459935
ACE-083 — safety, predicted from mechanism
Predicted from mechanism, not from a human safety trial. How that reasoning works →
What the mechanism predicts
Derived from the molecule, not a trial.
- These inhibit myostatin or activin signaling — the brake on muscle growth. Removing a brake the body installed deliberately is the whole premise, and the predicted problems follow from that.
- Myostatin and activin are not muscle-only signals. The same TGF-β family regulates tendon and connective tissue, and the concern that follows is muscle gaining force capacity faster than tendon adapts — predicting tendon and joint injury rather than muscle injury.
- Activin signaling also has roles in reproduction and inflammation, so systemic inhibition has predicted consequences well beyond the muscle the user is aiming at.
What has actually been reported
- Trials of myostatin-pathway drugs have repeatedly shown the dissociation that matters: muscle mass increases without a proportional increase in strength or function. That result recurs across programs and is the main reason several were discontinued.
- Bimagrumab produced muscle gain and fat loss in trials alongside diarrhea and muscle spasms.
- YK-11 has no human trial data at all. It is frequently described as a myostatin inhibitor on the strength of a single cell-culture study.
How to reduce the risk
Same mechanism as the prediction.
- If tendon lags muscle, the answer is loading tendon deliberately — slow heavy resistance work — and not adding load as fast as the new muscle allows.
- Treat rapid strength gain as a reason to be more conservative with progression, not less.
What it does to your bloodwork
A fact about the assay.
- Liver function, especially for the oral compounds in this group. Creatine kinase if you are getting unusual soreness or spasm.
Don't run this if
- You have a history of tendon injury, or you are progressing loading aggressively already.
The honest unknown
- Almost everything. No compound in this group has established long-term human safety, and the consistent trial finding is that mass gained this way has not translated into function.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
ACE-083 — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What ACE-083 moves on your bloodwork
Expected direction, not a measured one.
- IGF-1 (Insulin-like Growth Factor 1) — ↑ expected to rise
This is the point. IGF-1 rising is the compound doing its job — it is the stable downstream readout of a GH pulse.
What to do: Test it before you start and again at 6–8 weeks. It is the only number that tells you whether the product was real and the dose was enough. - Growth Hormone, Serum — ✕ unreliable here
A random GH level is close to meaningless here. GH is secreted in pulses during deep sleep and sits undetectable between them, so a daytime draw catches a trough almost every time — including when the compound is working perfectly.
What to do: Do not use GH to judge a secretagogue. Read IGF-1 instead. - Fasting Insulin — ↑ expected to rise
GH is a counter-regulatory hormone: it opposes insulin. Fasting insulin and glucose drifting up is the predicted trade-off, not a surprise.
What to do: Check fasting insulin and HbA1c at baseline and again at 8–12 weeks. This is the marker that decides whether you keep running it. - HbA1c (Hemoglobin A1c) — ↑ expected to rise
Same mechanism, longer window — a slow drift rather than a jump.
What to do: Pair it with fasting insulin; either alone can mislead. - Free T4 (Thyroxine) — ↓ expected to fall
GH accelerates the peripheral conversion of T4 to T3, so free T4 can fall while free T3 holds or rises. Read alone it looks like new hypothyroidism, and it usually isn't.
What to do: Run a full thyroid panel rather than TSH alone before concluding anything.
Everything above follows from one fact: these raise GH and therefore IGF-1. Nothing here needs a trial of the specific molecule.
- How to work up to it, and when not to
- When to take it, and why that window
- Cycle length
- Time off between cycles
- Fasted or fed, and when in the day
- Coach Cam's personal notes
- Which compounds push the same lever, and why the dose adds up faster than people count
- What blunts it — the stacks that waste your money
- What compounds the risk, so a side effect arrives sooner than any one of them suggests
- Coach Cam's read on running it alongside the rest of your protocol
Everything above is free and stays free. Skool is where it becomes a plan — ACE-083 in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside ACE-083
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| IGF-1 (Insulin-like Growth Factor 1) | The number that actually tracks your GH exposure — dose by this, not by feel |
| Fasting Insulin | GH raises insulin resistance; this moves before glucose does |
| HbA1c (Hemoglobin A1c) | The slower confirmation that the insulin change is real |
| Comprehensive Metabolic Panel (CMP) | Fasting glucose, and liver and kidney at baseline |
The “Running GH Peptides or MK-677” panel covers these in one order — 9 markers, $132.30 with the discount applied.
Check results you already have → · All 103 markers A–Z
ACE-083 — frequently asked questions
What is ACE-083?
ACE-083 (Localized myostatin inhibitor) is a gh & growth research compound. A follistatin-based ligand trap injected directly into a specific muscle. It sequesters myostatin and related TGF-beta ligands locally, so hypertrophy is confined to the injected muscle rather than being systemic.
Is the full ACE-083 protocol on this page?
The reported research dose is on this page, along with how ACE-083 works and the evidence behind it. The protocol — how to work up to it, frequency, cycle length, time off, what not to stack it with and Coach Cam's notes — is inside Skool.
What is the half-life of ACE-083?
ACE-083 has an approximate half-life of Local depot effect; dosed every 3 weeks in trials, which is part of what determines how often it's dosed.
What's the evidence behind ACE-083?
Current evidence level: Phase 2 trials — muscle volume increased, but strength and function did not follow. ACE-083 is offered for research purposes only and is not an approved medicine.
What ACE-083 is used for
ACE-083 appears under 2 goals in the goal router.
Related GH & Growth compounds
Where this goes next
The pages here are the frameworks. The protocols — the dosing, the order to correct things in, the week-by-week schedule and what to retest — are inside Skool.