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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. It is described here 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 8 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research momentum for ACE-031, not proof of effect — a registration is a plan, and posted results are sponsor-reported, not peer-reviewed.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 Nov 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.
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, 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 8 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. It is described here to inform, not to recommend. Representative study: PMID 23169607.
Dosing for ACE-031: No self-directed dose is recommended by SupStack. 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.
Timing is flexible for ACE-031 — consistent daily use matters more than the time of day. There is no validated self-administration schedule.
No consumer dose of ACE-031 is endorsed, so there is no dose at which it can be called safe. Talk to a healthcare provider before taking it. Reported side effects include epistaxis (nosebleeds), telangiectasias (clusters of dilated surface blood vessels), gum bleeding / mucosal bleeding. How often they occur is not established for all of them. 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)
Too few graded studiesThe 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 cancer concern because IGF-1 is mitogenic) are real. Not a dietary supplement, not a longevity drug.
Insulin (bodybuilding use)
Too few graded studiesInsulin 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. It is described here to inform, not to recommend.
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Reviewed by Dr. Baher Al Hakim · Last reviewed June 2026 · evidence from 8 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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