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ACE-031 (soluble activin receptor type IIB-Fc / ACVR2B-Fc)
An investigational myostatin/activin 'trap' whose only human trial in patients was STOPPED for safety. ACE-031 is a fusion protein of the activin receptor type IIB (ActRIIB) extracellular domain and an IgG1-Fc, engineered by Acceleron Pharma to soak up myostatin and related ligands and thereby release the brake on muscle growth. It has real human data — a single-dose study in healthy postmenopausal women showed a genuine ~3% gain in lean mass — but its phase 2 trial in boys with Duchenne muscular dystrophy was HALTED after the second dosing regimen because of bleeding-related safety signals (nosebleeds/epistaxis and telangiectasias, dilated surface blood vessels). It is NOT an approved drug, development was discontinued, and anything sold grey-market under this name is unregulated. This entry exists to inform, not to recommend.
Prescription medication — not a dietary supplement
ACE-031 is a prescription (or investigational) drug, not a supplement. It is included here for reference because people research and discuss it (often used off-label) — not as a recommendation. Take it only under a qualified clinician's supervision and only as prescribed; do not source it from grey-market vendors, where identity, purity, and dosing are unverified. The evidence below reflects its clinical trials.
What the evidence says
Most ACE-031 studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.
Most evidence is from medium-quality randomised trials published 2001–2026.
Based on 5 studies · 2 RCTs
Confidence
Low confidenceBy outcome
One single-dose human study showed a real ~3% lean-mass gain, but the only patient trial was halted for bleeding/vascular safety and development was discontinued.
No trials currently enrolling · 2 completed on ClinicalTrials.gov
Registered trials show research momentum for ACE-031, not proof of effect — a registration is a plan, and posted results are sponsor-reported, not peer-reviewed. They are never counted toward the evidence rating above.
Browse these trials on ClinicalTrials.govClinicalTrials.gov · as of Aug 2026
ACE-031 (soluble activin receptor type IIB-Fc; also written ActRIIB-Fc or ACVR2B-Fc, and given the proposed INN ramatercept) is a recombinant fusion protein, not a true peptide — it is the extracellular ligand-binding region of the activin type IIB receptor fused to a human IgG1-Fc, designed by Acceleron Pharma as a circulating decoy receptor.
ActRIIB is the receptor through which myostatin (GDF-8), activin A, and related TGF-β-family ligands signal to restrain skeletal-muscle mass.
By binding these ligands in the bloodstream before they can reach the muscle-cell receptor, ACE-031 disrupts that inhibitory signal and is intended to drive muscle growth — a mechanistically broader approach than antibodies that block myostatin alone, because it traps multiple negative regulators at once.
The preclinical rationale is strong and reproducible: in mice, a single course of ACE-031 increased body weight ~16% and individual muscle weights 26-46% within 28 days, independent of fibre type (Cadena 2010); in marmosets (non-human primates) 14 weeks of treatment increased lean body mass, fibre cross-sectional area, and ex-vivo force production (Cadena 2026); and the foundational genetics (Lee & McPherron 2001) showed that follistatin or a soluble dominant-negative ActRIIB produces dramatic, myostatin-knockout-like muscle hypertrophy.
The human story is where honesty matters.
In a single-ascending-dose study in 48 healthy postmenopausal women, ACE-031 was generally well tolerated and produced statistically significant increases in total-body lean mass (3.3%) and thigh-muscle volume (5.1%) at day 29 (Attie 2013) — a real, positive pharmacodynamic signal.
But the phase 2 trial that mattered — a randomized, placebo-controlled, ascending-dose study in ambulatory boys with Duchenne muscular dystrophy — was STOPPED after the second dosing regimen because of non-muscle safety concerns: epistaxis (nosebleeds), telangiectasias (clusters of dilated small blood vessels), and gum bleeding.
While the DMD trial showed encouraging trends (maintained 6-minute-walk distance, increased lean mass and bone density, reduced fat mass), those trends were not statistically significant and, crucially, did not outweigh the vascular/bleeding safety signal; Acceleron discontinued ACE-031 development.
This bleeding signature is now understood as an on-target consequence of broadly trapping ActRIIB ligands (activin/BMP-pathway effects on vasculature), and it has shaped the entire field toward more selective myostatin-only agents.
Bottom line: ACE-031 is an investigational biologic with real but discontinued clinical evidence, NOT an approved medicine. It is grouped here with research peptides by category convention.
Any material sold under this name outside a clinical trial is an unregulated grey-market product with no guarantee of identity, purity, sterility, or correct dosing, and self-administration carries the documented bleeding/vascular risk that ended its development.
The evidence here is scored low and sandboxed out of all goal- and stack-based recommendations.
ACE-031 is the extracellular ligand-binding domain of the activin type IIB receptor (ActRIIB) fused to IgG1-Fc. Circulating in the blood, it binds myostatin (GDF-8), activin A and related TGF-β-family ligands before they can reach muscle-cell receptors — a 'ligand trap' that removes their inhibitory signal. Demonstrated in cells, mice, marmosets and humans.
Myostatin and activin normally restrain skeletal-muscle mass. By neutralizing them, ACE-031 releases that brake, increasing muscle-fibre cross-sectional area and muscle mass independent of fibre type. Shown in mice (16% body-weight gain, 26-46% muscle-weight gains in 28 days), marmosets (increased lean mass and force), and a single human study (lean mass +3.3%).
Because ActRIIB also binds activin/BMP-family ligands with vascular and bone roles, trapping all of them — rather than myostatin alone — is thought to underlie ACE-031's off-target bleeding/vascular effects (epistaxis, telangiectasia). The same broad mechanism that drives the muscle effect also drove the safety signal that halted its DMD trial.
How ACE-031 works — from molecular targets to health outcomes. Click an edge to see supporting research.This visualization is in beta — pathways are being refined and expanded.
Avoid — development was discontinued after a trial halted for bleeding/vascular safety, there is no approved product, and grey-market material is unregulated.
Avoid entirely — the drug's defining safety signal is bleeding-related; combining it with bleeding risk is dangerous and unstudied.
Avoid entirely — completely unstudied, and the compound has known vascular effects.
ACE-031's development was halted specifically for bleeding-related adverse events (epistaxis, telangiectasia, gum bleeding). Combining it with any drug that increases bleeding risk is theoretically dangerous and has never been studied; this is the single most important interaction concern.
There are no controlled human drug-interaction data for self-administered ACE-031. As a broad ActRIIB-ligand trap with vascular effects, interactions cannot be reliably predicted.
Tip: Part of the bleeding/telangiectasia signal that halted the DMD trial; there is no validated mitigation outside stopping the drug under medical supervision.
Tip: Reported in the DMD trial and contributed to its discontinuation; thought to reflect on-target activin/BMP-pathway vascular effects.
Tip: Part of the bleeding cluster that drove the safety stop; signals broad vascular involvement.
Tip: Reported in the healthy-volunteer single-dose study; the most common non-bleeding adverse event.
The current evidence for ACE-031 is insufficient to assign an evidence score, based on 5 indexed studies. An investigational myostatin/activin 'trap' whose only human trial in patients was STOPPED for safety. ACE-031 is a fusion protein of the activin receptor type IIB (ActRIIB) extracellular domain and an IgG1-Fc, engineered by Acceleron Pharma to soak up myostatin and related ligands and thereby release the brake on muscle growth. It has real human data — a single-dose study in healthy postmenopausal women showed a genuine ~3% gain in lean mass — but its phase 2 trial in boys with Duchenne muscular dystrophy was HALTED after the second dosing regimen because of bleeding-related safety signals (nosebleeds/epistaxis and telangiectasias, dilated surface blood vessels). It is NOT an approved drug, development was discontinued, and anything sold grey-market under this name is unregulated. This entry exists to inform, not to recommend. Representative study: PMID 23169607.
The commonly studied dose of ACE-031 is No legitimate or recommended dose for general use — ACE-031 is an investigational biologic whose development was discontinued after a trial was halted for safety, and it is not an approved medicine. We do NOT provide a dosing protocol. In trials it was given subcutaneously (single doses of 0.02-3 mg/kg in healthy volunteers; repeated subcutaneous dosing every 2-4 weeks in the DMD study), but those were monitored clinical-trial regimens, not a recommendation for self-use.. Individual needs vary — start at the lower end of the range and adjust based on how you respond.
Timing is flexible for ACE-031 — consistent daily use matters more than the time of day. There is no validated self-administration schedule.
ACE-031 should be used with caution — talk to a healthcare provider before taking it. The most commonly reported side effects are epistaxis (nosebleeds), telangiectasias (clusters of dilated surface blood vessels), gum bleeding / mucosal bleeding. Use caution if any of these apply to you: Documented bleeding/vascular safety signal — the pivotal DMD trial was halted for epistaxis, telangiectasias and gum bleeding; Not an approved medicine — investigational biologic whose development was discontinued; do not self-source; Bleeding disorders or use of anticoagulant/antiplatelet medication (the bleeding signal is the reason the trial stopped).
Mecasermin (IGF-1)
Mostly mechanism / observationalThe pharmaceutical-grade version of IGF-1 — an FDA/EMA-approved prescription injectable, but approved ONLY for a rare childhood growth disorder (severe primary IGF-1 deficiency / Laron syndrome), where it genuinely raises height velocity in clinical trials. It is the regulated counterpart to the grey-market igf-1-lr3 peptide bodybuilders inject, and shares the same core risks. Crucially, there is NO trial supporting its off-label use for muscle, performance, or anti-aging in healthy adults — and IGF-1's documented harms (hypoglycemia, intracranial hypertension, lymphoid/tonsillar hypertrophy, and a theoretical cancer concern because IGF-1 is mitogenic) are real. Not a dietary supplement, not a longevity drug.
Insulin (bodybuilding use)
Mostly mechanism / observationalInsulin is a life-saving prescription hormone for diabetes — and, used illicitly by bodybuilders as an off-label 'anabolic,' one of the most dangerous performance drugs in existence. The theory is nutrient partitioning: insulin drives glucose and amino acids into muscle and suppresses muscle-protein breakdown. But there is NO controlled evidence that insulin builds muscle or improves performance in healthy, non-diabetic athletes — and a non-diabetic who injects it risks profound, sometimes FATAL hypoglycemia (coma, seizures, brain injury, death), plus fat gain. This is a harm-reduction reference documenting a popular, deadly misuse, NOT a recommendation and NOT a dietary supplement.
CJC-1295
Mostly mechanism / observationalA synthetic long-acting analog of growth-hormone-releasing hormone (GHRH), promoted online to raise GH and IGF-1 for muscle, fat loss and 'anti-aging'. Honest appraisal: the only real human data are two small early-phase pharmacokinetic / safety studies from ~2006 that showed it raises GH and IGF-1 for days — they were never followed by efficacy trials in muscle, body composition or aging. There are NO human outcome RCTs. It is not a dietary supplement: it is sold 'for research use only', is injectable, and is banned by WADA. The original DAC version's clinical development was abandoned.
Follistatin
Mostly mechanism / observationalA myostatin/activin-binding protein with essentially NO human evidence as an injectable supplement — the real human data are from gene-therapy trials that deliver the follistatin GENE, not the grey-market peptide sold online. Follistatin is a naturally occurring protein that binds and neutralizes myostatin and activin, the molecules that restrain muscle growth. In animals, follistatin (or the follistatin gene) produces dramatic, myostatin-knockout-like muscle hypertrophy, and small open-label gene-therapy trials in Becker muscular dystrophy and inclusion-body myositis reported walking-distance gains. But none of that is the same as injecting recombinant follistatin peptide, which has never been tested in a controlled human supplement trial. It is not an approved drug or a regulated supplement, and the grey-market injectable is unregulated. This entry exists to inform, not to recommend.
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Reviewed by Dr. Baher Al Hakim · Last reviewed June 2026 · evidence from 5 studies · how we score · editorial policy
This information is for educational purposes only. It is not a substitute for professional medical advice. Always consult a qualified healthcare provider before starting, stopping, or changing any supplement or medication.
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