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ACE-031 peptide vial
📈 Growth Hormone

ACE-031

ACE-031 (Ramatercept)

Also called ACE-031, ramatercept, ActRIIB-Fc

A myostatin trap built from its own receptor

ACE-031 was a serious pharmaceutical attempt at removing the brake on muscle growth, developed for muscular dystrophy. It worked: people gained muscle. It was also stopped, because the same receptor it blocks is involved in blood vessels, and trial participants developed nosebleeds and visible spidery vessels on the skin.

A soluble decoy version of the activin receptor type IIB (ActRIIB). ACE-031 acts as a trap — it circulates and binds myostatin and related growth-limiting ligands before they can reach muscle, removing the brake on growth. It reached human trials for muscular dystrophy but was discontinued over vascular safety signals, so it remains research-only.

Route
Subcutaneous injection
Typical dose
Research-only (no established dose)
Availability
Research-only
Emerging Evidence

Human trials published, with more underway

What people use ACE-031 for

Reported uses, roughly in order of how often they are the reason someone goes looking. Whether it works for any of them is a separate question, answered under each one.

Muscle growth
What it does, and it does it through a different route from anabolic steroids: it soaks up the signals that tell muscle to stop growing rather than telling it to grow.
Muscular dystrophy
Its actual development programme, in boys with Duchenne. It reached Phase 2 before being halted.

Mechanism of Action

How ACE-031 works

ACE-031 is a soluble decoy receptor that sequesters growth inhibitors:

  • ActRIIB decoy — a soluble form of the activin receptor IIB that binds myostatin and activin in circulation before they reach the real receptor on muscle.
  • Broad ligand trapping — by mopping up multiple TGF-beta-family inhibitors at once, it can produce a larger effect than blocking myostatin alone.
  • De-repressed muscle growth — with these inhibitors neutralized, muscle protein synthesis and fiber growth face less restraint.
  • Safety ceiling — human trials were stopped after vascular/bleeding signals (nosebleeds, gum bleeding, telangiectasias), reflecting ActRIIB's role beyond muscle. This is why it stayed research-only.

ACE-031 dosage calculator

Enter what is in your vial, how much water you added, and the dose you are using. It works out where to pull the plunger to.

How much is in the vial?

Printed on the label, in milligrams

How much water did you add?

Bacteriostatic water, in millilitres

What dose are you taking?

The dose you already intend to use

Which syringe?

Barrel size, printed on the wrapper

Draw to

10 units

on a 0.5 mL insulin syringe (0.1 mL)

102030405010 units
Strength once mixed
5 mg/mL
Doses in the vial
20

10 mg in 2 mL makes 5 mg/mL. A 500 mcg dose is 0.1 mL of that, which is 10 units.

This is arithmetic, not advice. It converts a dose you already have into a mark on a syringe. It does not tell you what dose to take, and ACE-031 is not prescribed by us. Dosing belongs with a qualified clinician.

Full reconstitution chart and worked examples.

ACE-031 side effects: what people reported

This one has a documented reason it was discontinued, which puts it in a different category from compounds that simply lack data. The trial was stopped over the side effects, not over the results.

What was seen in trials

  • Nosebleeds
  • Small spidery blood vessels visible on the skin
  • Gum bleeding
  • Injection-site reactions
  • Headache

Why it stopped

  • The receptor it blocks is also involved in how blood vessels form and behave. The bleeding was consistent enough across participants that the programme was halted rather than adjusted

Source: Phase 2 trials in Duchenne muscular dystrophy, halted 2013. This is a summary of published findings, not a complete safety profile and not medical advice. ACE-031 should only be considered with a qualified clinician who knows your history.

Your Genetics & ACE-031

The genes involved in how ACE-031 works

ACE-031 works through the receptors these genes build, and the genes vary from person to person. Researchers have linked some of that variation to differences in how people respond. A DNA report tells you which versions you carry.

MSTNMyostatin (growth limiter)

The K153R variant alters myostatin activity. Baseline myostatin tone sets how much brake ACE-031 has to release — higher-myostatin individuals have more to gain from trapping it.

Chromosome 11Fast-twitch muscle fiber (R577X)

ACTN3 · ••

The R577X variant sets fast-twitch fiber makeup and the hypertrophy ceiling, shaping how much a myostatin-trapping agent translates into visible muscle.

IGF1IGF-1 anabolic drive

IGF-1 promoter variants set the anabolic signal that builds muscle once growth inhibitors are removed, amplifying or limiting the net effect.

Chromosome 12Vitamin D receptor (muscle FokI)

VDR · ••

The FokI variant influences muscle strength and mass, part of the muscular background on which a myostatin-trap acts.

The dots after each gene are where your own result goes. Your report fills them in with the two letters you carry at that position.

Which variants do you carry?

Upload your DNA data, or get tested through our partner, to find out.

Get Your Report — $99

Commonly combined with

What ACE-031 is most often paired with, and why:

Follistatin-344

Myostatin StackEmerging Evidence

Follistatin-344 (FST-344)

A naturally occurring protein that binds and neutralizes myostatin and activin — the body's built-in limiters on muscle growth. By sequestering myostatin, Follistatin-344 removes a key brake on hypertrophy, which is why it's one of the most discussed (and still early-stage) research peptides for muscle and recovery.

4

Gene variants

20+

Studies

IGF-1

Muscle StackModerate Evidence

Insulin-like Growth Factor-1

The primary anabolic mediator of growth hormone. Most of GH's effects on muscle, tissue repair and growth are actually carried out by IGF-1, produced mainly in the liver. Native IGF-1 is short-acting and tightly regulated by binding proteins — making the IGF axis one of the most genetically variable in the body.

4

Gene variants

45+

Studies

Sourcing & access

Where to buy ACE-031

ACE-031 is sold as a research compound, not a licensed medicine, so quality and legal status vary widely by country and vendor. If you're sourcing it, treat independent purity testing as non-negotiable.

  • Insist on a recent third-party Certificate of Analysis (COA) for the exact batch — labs like Janoshik verify purity and identity.
  • Check the legal status where you live before ordering — it differs from country to country.
  • Reconstitute correctly with bacteriostatic water and start at a conservative dose.
ACE-031 vial

ACE-031

A myostatin trap built from its own receptor

$138.95at Swiss Chems

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Before you buy: see whether your DNA actually responds to ACE-031, and at what dose. Analyze my DNA — $99 →

Educational information only, not medical advice. Some outbound links are affiliate links (disclosed, at no extra cost to you). Most peptides are not FDA-approved — consult a qualified professional and check your local laws before purchasing.

Worth knowing before you consider ACE-031

Interactions and situations where there is a specific reason to be careful. Where the honest answer is that nobody has studied something, it says so and says what that leaves open.

It was withdrawn for safety, not for failing to work
Worth being precise about. It produced muscle gain, and it was stopped anyway. That combination is a reason for more caution rather than less.
The bleeding effects are the known outcome, not a theory
These were observed in a monitored clinical trial, which is more than can be said for most safety claims about compounds in this space.

Last updated

Frequently Asked Questions

How is ACE-031 different from Follistatin-344?

Both reduce myostatin signaling but in different ways. Follistatin-344 binds the myostatin ligand directly. ACE-031 is a decoy version of the myostatin receptor (ActRIIB) that traps myostatin and related ligands before they reach muscle. ACE-031 traps a broader set of inhibitors, which is also why its safety profile is more complex.

Why was ACE-031 discontinued?

Human trials for muscular dystrophy were halted after vascular safety signals — nosebleeds, gum bleeding and small dilated blood vessels — likely reflecting ActRIIB's roles outside muscle. It never reached approval and remains a research compound, which is essential context.

Does genetics affect ACE-031 response?

Yes. MSTN tone sets how much myostatin brake there is to release, ACTN3 fiber type shapes the hypertrophy ceiling, IGF1 sets the anabolic background, and VDR influences muscle response. A genetic peptide report profiles these — alongside the unresolved safety considerations.

Your next move

Two ways forward with ACE-031.

Not sure it's for you?

How does ACE-031 relate to your genes?

Your report scores ACE-031 against your receptor, pharmacogene and pathway variants and shows the genetic markers relevant to it, with commonly cited dosing information to review with a clinician.

Analyze my DNA — $99

Already decided?

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