Educational guide
ACE-031 Dosage Protocol - Peptide Dosages
ACE-031 (1 mg) Dosage Protocol A soluble activin receptor type IIB (ActRIIB) Fc-fusion protein that traps myostatin and related muscle-limiting factors. Its clinical development was halted for safety. Research-use-only — this page is an educational reference a
This guide cannot diagnose a condition or recommend a personal treatment plan. Discuss medical questions with a qualified professional.
ACE-031 (1 mg) Dosage Protocol
A soluble activin receptor type IIB (ActRIIB) Fc-fusion protein that traps myostatin and related muscle-limiting factors. Its clinical development was halted for safety. Research-use-only — this page is an educational reference and a caution, not a dosing recommendation.
Why ACE-031 draws research interest
These are the directions researchers and the peptide community most often explore ACE-031 for — so you know you’re in the right place. They describe what is being studied, not proven benefits, approved uses, or promised results.
It blocks the body’s brake on muscle — the myostatin pathway
Myostatin (also called GDF-8) is a member of the TGF-β family that acts as a negative regulator of muscle growth: animals engineered to lack it develop dramatically enlarged, "double-muscled" physiques. ACE-031 exploits this by presenting a soluble copy of the receptor those factors bind to, soaking them up before they reach muscle. The underlying biology is real and well established, which is exactly why several different companies have chased myostatin-pathway drugs.
Trapping more than myostatin is a double-edged design
ACE-031 is built from ActRIIB, a receptor that binds not just myostatin but a family of related ligands (activins and other TGF-β proteins). That broad reach is part of why it produced larger muscle effects than selectively blocking myostatin alone — but it is also the most likely reason it caused problems outside muscle. Those same activin-family signals are important in blood vessels, and the bleeding-type side effects (nosebleeds, dilated small vessels) that stopped its trials are generally attributed to this off-target ligand blockade. Broad is powerful and risky at the same time.
The honest headline is the safety halt, not the muscle gain
It is easy to find the encouraging numbers — a few percent more lean mass after a single dose in an early study. The responsible reading foregrounds what happened next: in the trial that mattered most, in boys with Duchenne muscular dystrophy who genuinely needed a muscle therapy, the study was stopped before it could show benefit because of bleeding-related side effects. A compound abandoned by its developer for safety is not a "muscle builder" waiting to be rediscovered; it is a cautionary chapter in myostatin-drug development.
Evidence ranges from early laboratory work to clinical trials depending on the use — the sections below cover the actual data and sources.
Mix & measure ACE-031 · 1 mg
Pre-filled with this protocol’s recommended BAC water and documented starting dose — edit any field to run your own numbers.
Reconstitution math only — not dosing advice. U-100 syringe: 100 units = 1 mL. Full reconstitution guide → · Advanced calculator →
A soluble ActRIIB-Fc decoy that traps myostatin (GDF-8) and related activin-family ligands, blocking the normal negative regulation of muscle mass. Because it captures multiple ligands — not myostatin alone — its effects are broader than selective myostatin inhibition, which is thought to underlie its off-target actions.
A discontinued investigational biologic, not a drug. It is not approved for human use and has no established dose. Its Duchenne muscular dystrophy trial was stopped early because participants developed nosebleeds and telangiectasias. Grey-market "ACE-031" vials are unverified and disconnected from any approved product.
A single subcutaneous dose increased lean and thigh-muscle mass in healthy postmenopausal women in a phase 1 study. In boys with Duchenne muscular dystrophy, only non-significant trends were seen before the study was halted for safety. Muscle biology is promising; this particular molecule was abandoned.
Quickstart Highlights
ACE-031 (research name ramatercept) is not a small peptide at all — it is a large fusion protein built from the extracellular, ligand-binding domain of the activin receptor type IIB (ActRIIB) fused to an antibody IgG1-Fc region[3]. It works as a soluble decoy receptor: released into the circulation, it mops up myostatin (GDF-8) and several related TGF-β-family proteins before they can reach the real receptors on muscle, releasing the brake those factors normally keep on muscle growth[2].
This page is an educational reference on what ACE-031 is, what its trials actually showed, and how a lyophilized research vial is reconstituted. It is not medical advice and not a protocol to administer the compound. The most important fact belongs at the top: ACE-031’s clinical program in Duchenne muscular dystrophy was stopped early for safety — participants developed nosebleeds (epistaxis) and dilated small blood vessels (telangiectasias), off-target effects that led the sponsor to discontinue the study[4]. ACE-031 is not FDA-approved, was never brought to market, and is documented here with that safety history front and center.
A soluble ActRIIB–IgG1-Fc fusion protein (ramatercept) that binds myostatin and related ligands, acting as a decoy receptor to promote muscle growth[2][3]. A large biologic, not a short peptide.
1 mL bacteriostatic water per 1 mg vial → 1 mg/mL. This is a lab-handling reference only; the site provides no dose for administration.
Not FDA-approved. Its Duchenne muscular dystrophy trial was stopped early for safety (epistaxis, telangiectasias) and the program was discontinued[4].
Early-phase human trials, then halted. A single-dose study in healthy women showed measurable muscle gains[1]; the DMD study was stopped for non-muscle safety concerns before efficacy could be established[4].