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ACE-031Small moleculeNo amino acid sequence. Icon reflects category theme only.Also known as: ACVR2B-Fc, soluble ActRIIB-Fc, ACE-031
A single injection produced 3.3% lean mass gain in 29 days. ACE-031 is a soluble ActRIIB decoy receptor, a fusion protein that traps myostatin before it can signal muscle breakdown. Phase 2 confirmed the effect in boys with Duchenne muscular dystrophy, but epistaxis and telangiectasias from off-target BMP-9/10 inhibition ended the clinical program in 2011. Acceleron never restarted it. Community users now work with fixed doses 50 to 400 times below clinical levels, chasing that same lean mass signal while watching their skin for spider veins. (Word count: 91)
One injection. 3.3% more lean mass by day 29. That Phase 1 result in 48 postmenopausal women (Attie et al.)[1] remains the single strongest muscle-building response ever recorded from a peptide dose. ACE-031 (also called soluble ActRIIB-Fc or ACVR2B-Fc) is a recombinant fusion protein. It combines the extracellular domain of activin receptor type IIB with a human IgG1 Fc fragment. The molecule floats through the bloodstream and intercepts myostatin, the primary brake on skeletal muscle growth. Without myostatin signaling, muscle protein synthesis accelerates while protein degradation slows. The problem is selectivity. ACE-031 also captures activin A, activin B, GDF-11, BMP-9, and BMP-10. Trapping activins likely contributes to its muscle and bone effects. Trapping BMP-9 and BMP-10 destabilizes endothelial cells. The Phase 2 trial in ambulatory boys with Duchenne muscular dystrophy (Campbell et al.)[2] confirmed the muscle gains, showing 5.2% lean mass increase versus 2.6% on placebo. It also confirmed the vascular cost. Epistaxis and telangiectasias appeared at doses of 1.0 to 2.5 mg/kg given biweekly. Acceleron terminated the program in April 2011. All adverse events resolved after stopping. Community users now dose at 500 to 1500 mcg every two weeks, roughly 50 to 400 times below clinical levels. Whether vascular risk scales linearly with dose is unknown. Forum discussion far outweighs actual use reports; maybe 15 to 30 people have documented personal experience. (Word count: 232)
ACE-031 works as a ligand trap. The molecule is a soluble version of the membrane-bound activin receptor type IIB (ActRIIB), fused to a human IgG1 Fc fragment for stability and extended half-life. Under normal conditions, myostatin (GDF-8) binds to ActRIIB on muscle cell surfaces. That binding recruits the type I receptor ALK4 or ALK5 and triggers phosphorylation of Smad2 and Smad3. These phosphorylated Smads pair with Smad4 and move into the nucleus. There they suppress muscle protein synthesis genes and activate degradation pathways, including MuRF1 and MAFbx/atrogin-1 in the ubiquitin-proteasome system. ACE-031 intercepts myostatin before it reaches those membrane receptors. No binding means no Smad2/3 phosphorylation, no nuclear translocation, and no brake on muscle growth. The selectivity problem is straightforward. ActRIIB binds multiple ligands. ACE-031 captures activin A, activin B, and GDF-11 alongside myostatin. Those extra captures probably help with muscle and bone density effects. But ACE-031 also traps BMP-9 and BMP-10. These two ligands signal through ALK1 on endothelial cells and keep blood vessels stable. Removing them causes telangiectasias and epistaxis. The 43% FSH reduction observed in healthy women at 3 mg/kg reflects activin A sequestration; activin A drives pituitary FSH secretion. (Word count: 195)
ACE-031 is the strongest proof-of-concept for myostatin inhibition as a muscle-building strategy. Phase 1 data in healthy women showed statistically significant lean mass gains from a single injection. Phase 2 data in DMD boys confirmed efficacy. But the program was terminated due to vascular adverse events caused by off-target BMP-9/10 inhibition. A 2025 review (PMC11842502) places ACE-031 as a key but failed molecule that informed all subsequent myostatin inhibitor design. A 2025 bioRxiv preprint confirmed efficacy in marmosets, adding primate data to the evidence base.
Attie et al. 2013, "A single ascending-dose study of muscle regulator ACE-031 in healthy volunteers" (PMID 23169607): 48 healthy postmenopausal women, single SC dose 0.02-3 mg/kg, 3.3% lean mass gain at 3 mg/kg by day 29
Only 2 human studies ever completed (Phase 1 + Phase 2 DMD). Phase 2 was terminated early: no full efficacy dataset. No long-term safety data. No dose-finding study in healthy adults for body composition. All community dosing is extrapolated, not validated. The molecule captures BMP-9/10 at every tested dose: it's unclear if there is a dose where muscle effects occur without vascular risk.
ACE-031 generates intense curiosity but very few people have actually used it. It's expensive, hard to authenticate, and the vascular side effects are genuinely scary. Community protocols exist but are based on small numbers of self-experimenters working with doses far below clinical trial levels. Most discussion is theoretical: people analyzing the clinical data rather than reporting personal experience.
Science and community agree on mechanism, efficacy direction, and vascular risks. They diverge massively on dose: clinical trials used 35-210 mg per injection; community uses 0.5-1.5 mg. No data bridges this gap: community doses are extrapolated, not validated. The safety profile at community doses is unknown.
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 500mcg | Every 2 weeks |
| Moderate | 1mg | Every 2 weeks |
| Aggressive | 1,500mcg | Every 2 weeks |
ACE-031 is a large fusion protein, not a standard peptide. Reconstitution matters more here than with most compounds. For a 1 mg vial with 1 mL bacteriostatic water: concentration is 1000 mcg/mL. A 500 mcg dose is 50 units on an insulin syringe. A 1000 mcg dose uses the full vial. For a 5 mg vial with 2 mL bacteriostatic water: concentration is 2500 mcg/mL. A 500 mcg dose is 20 units. A 1000 mcg dose is 40 units. A 1500 mcg dose is 60 units. Add water slowly along the vial wall. Do not shake. ACE-031 is an 82 kDa protein that can denature with aggressive mixing; swirl gently until clear. If the solution looks cloudy or has particles after reconstitution, do not inject it. Protein aggregation means the compound may be damaged or degraded. The single biggest concern with ACE-031 is product authenticity. Standard HPLC purity testing tells you the mass is correct, not that the protein is properly folded and glycosylated. Request SDS-PAGE gel data from your supplier. If they can't provide it, you're guessing. (Word count: 186)
The Phase 2 DMD trial used a 12-week treatment period. No established cycling protocol exists for research use outside clinical trials. Extended use is not recommended given the known vascular safety signals. Periodic monitoring for telangiectasias, epistaxis, and gum bleeding should be performed throughout any research protocol.
ACE-031 is a recombinant fusion protein: the immune system can develop anti-drug antibodies (ADAs) with repeated exposure. The related compound ACE-2494 was discontinued specifically because of high ADA rates in Phase 1. Clinical trials used 12-week treatment periods. Cycling off allows ADA titers to decline before re-exposure. Continuous BMP-9/10 suppression raises cumulative vascular risk: breaks allow endothelial recovery.
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Expected: Unknown at community doses. Clinical doses produced 3.3-5.2% lean mass gains, but community doses are 50-400x lower. Modest body composition changes if the compound is authentic and bioactive.
Monitor: Baseline CBC + coagulation panel. Weekly skin checks for telangiectasias. FSH/LH if female. Immediate stop protocol for any bleeding event.
Reconstitute by adding bacteriostatic water slowly along the vial wall. For a 1 mg vial, use 1 mL. For a 5 mg vial, use 2 mL. Swirl gently until the powder dissolves completely. Never shake or vortex.
Draw the calculated dose using an insulin syringe (29 to 31 gauge). For 500 mcg from a 1 mg/1 mL vial, draw to the 50 unit mark. For 500 mcg from a 5 mg/2 mL vial, draw to the 20 unit mark. For 1000 mcg from a 5 mg/2 mL vial, draw to the 40 unit mark. For 1500 mcg from a 5 mg/2 mL vial, draw to the 60 unit mark.
Inject subcutaneously into the abdomen, upper thigh, or upper arm. Rotate injection sites between doses. With biweekly dosing, you have plenty of time for site recovery.
ACE-031 is a large protein, and injecting too fast or too shallow can cause local lumps or hardness.
Use within 14 to 21 days. Do not freeze after reconstitution.
No specific timing requirements around meals or sleep were established in clinical trials.
Mark your calendar. The 10 to 15 day half-life supports this interval.
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Theoretical anabolic synergy: myostatin removal + IGF-1 stimulation targets two different growth pathways. Discussed on forums but no human data on the combination.
Growth hormone + myostatin inhibition for maximum muscle growth signaling. Commonly discussed but never studied together in humans.
MGF is a splice variant of IGF-1 released during muscle damage. Combining with ACE-031 theoretically amplifies the growth response. Speculative.
Both inhibit myostatin/activin pathways. Stacking two ligand traps risks excessive TGF-beta superfamily suppression with unpredictable vascular and hormonal consequences.
Do not combineACE-031 caused epistaxis and gum bleeding through BMP-9/10 inhibition. Adding blood thinners amplifies bleeding risk substantially.
Do not combineOverlapping TGF-beta/BMP pathway modulation. Co-administration could produce dangerous levels of BMP signaling disruption.
Do not combinePricing updated 2026-04-09
Epistaxis and telangiectasias ended this clinical program. That deserves to lead any safety discussion. In the Phase 2 DMD trial (Campbell et al.)[2], boys receiving 1.0 to 2.5 mg/kg every two weeks developed nosebleeds and small dilated blood vessels visible on the skin. The mechanism is specific and well understood: ACE-031 sequesters BMP-9 and BMP-10, two ligands that endothelial cells need to maintain vascular integrity. Remove them, and blood vessel walls become fragile. Acceleron Pharma terminated the program in April 2011 because of these signals. All vascular events resolved completely after stopping the drug. No serious or severe adverse events were reported in either trial. That's the good news. The bad news is that no one knows if there's a dose where muscle effects happen without vascular risk. The molecule captures BMP-9 and BMP-10 at every tested dose. Published side effects from the two clinical trials include: Epistaxis (nosebleeds), observed at clinical doses of 1.0 mg/kg and above. This was the primary safety signal. Telangiectasias (spider veins on skin), same dose range and same mechanism. Minor gum bleeding, reported in both trials at higher doses. Erythema at injection sites, mild and transient across all dose levels. FSH suppression of 43% in healthy postmenopausal women at 3 mg/kg (Phase 1). This reflects activin A sequestration, not a direct hormonal effect. For premenopausal women, this level of FSH disruption could affect ovulation and fertility. Community reports are limited. Roughly 15 to 30 self-experimenters have shared experiences online. Their doses (500 to 1500 mcg) are 50 to 400 times below clinical levels. Some report nosebleeds even at these low doses. Whether that reflects true pharmacological effect or contaminated product is impossible to determine without product verification. Long-term safety has never been studied. The clinical program lasted months, not years. Anti-drug antibody formation is a theoretical concern based on the related compound ACE-2494, which was discontinued specifically because of high ADA rates. Anyone with hereditary hemorrhagic telangiectasia, bleeding disorders, or on anticoagulants should not use this compound. Pregnancy is contraindicated given the FSH effects and absence of reproductive safety data. Stop immediately if you experience any nosebleed, new spider veins, gum bleeding, or unusual bruising. These are the exact signals that terminated a clinical program. (Word count: 365)
Verify ACE-031 dosing and safety with a second opinion
ACE-031 is an ~82 kDa recombinant fusion protein that requires mammalian cell expression, proper folding, and glycosylation to be biologically active. It can't be made by standard solid-phase peptide synthesis. A 2025 study (Reichel, Drug Testing and Analysis) analyzed black-market ACE-031 and found major inconsistencies: some samples contained the right protein, others were degraded or mislabeled. Standard peptide purity testing cannot validate this compound.
| Test | When | Target |
|---|---|---|
| CBC with differential | Baseline, then every 4 weeks during use | — |
| Coagulation panel (PT/INR, aPTT) | Baseline and week 4 | — |
| Skin inspection for telangiectasias | Weekly throughout use | — |
| FSH / LH | Baseline and week 8 (especially for women) | — |
| DEXA body composition scan | Baseline and week 12 | — |
Detect any changes in platelet count or coagulation parameters that could indicate vascular effects
ACE-031 caused bleeding events through BMP-9/10 disruption: monitor clotting function
New spider veins are the most visible early warning sign of vascular endothelial destabilization. Check face, chest, arms, and legs in good lighting.
Phase 1 data showed 43% FSH reduction at 3 mg/kg via activin A sequestration. Reproductive hormone monitoring is warranted.
The only objective way to know if the compound is doing anything at community doses. Without pre/post measurement, you're guessing.
Based on Phase 1 data, initial increases in lean body mass may begin within the first two weeks following administration. Pharmacokinetic steady state has not yet been reached.
Lean mass gains become measurable by DXA. In the Phase 1 study, peak lean mass increase (3.3%) was observed by day 29 after a single 3 mg/kg dose. Bone mineral density markers may begin to shift.
With repeated dosing (as in the Phase 2 trial), lean mass gains of approximately 5% are possible. Vascular adverse events (telangiectasias, epistaxis) may emerge during this window, particularly at doses of 1 mg/kg or above given biweekly.
Weeks 1-2 (First injection): Phase 1 pharmacokinetic data shows ACE-031 reaches steady circulating levels after the first dose. Myostatin and activin sequestration begins immediately. At community doses (500 to 1500 mcg), expect nothing visible. Most users report no changes, and any "muscle fullness" at this point is likely placebo. No vascular events are expected from a single low dose. Weeks 3-6 (Building exposure): With biweekly dosing, trough drug levels establish. In clinical trials at much higher doses, lean mass was measurable by DXA at day 29. At community doses, detectable changes are uncertain. Some users claim better workout recovery and slight visual fullness, but separating real effect from training variables and expectation is difficult. This is the window where nosebleeds and telangiectasias could first appear, especially at higher dose ranges. Weeks 8-12 (Assessment window): The Phase 2 trial showed approximately 5% lean mass gain in DMD boys at clinical doses over this timeframe. At community doses, any effect would be much smaller. Users who report positive results typically describe modest improvements by this point. Those with no results often suspect the product is inactive or mislabeled. If telangiectasias or epistaxis haven't appeared by week 12, vascular tolerance at the current dose is probably acceptable.
Based on Phase 1 PK data, ACE-031 reaches steady circulating levels. Initial myostatin/activin sequestration begins. No measurable body composition change yet.
Most users report nothing noticeable after one injection at community doses. Some report a vague "fullness" feeling in muscles, likely placebo.
With biweekly dosing, trough levels establish. At clinical doses, lean mass was measurable by DXA at day 29. Community doses are far lower: detectable changes are uncertain.
Some users claim improved workout recovery and slight visible muscle fullness. Hard to separate from placebo and training variables at these doses.
Phase 2 showed ~5% lean mass gain in DMD boys at clinical doses over this timeframe. At community doses, any effect would be much smaller.
Users who report positive results typically describe modest lean mass improvements by this point: nothing dramatic at community doses. Those with no results often suspect product authenticity.
Source: Half-life of 10-15 days (~240-360 hours) based on Phase 1 single ascending-dose study in healthy postmenopausal women at 3 mg/kg (Attie et al. 2013, PMID 23169607). Linear pharmacokinetics across all tested doses.
Loading the interactive decay curve.
ACE-031 is not approved by the FDA or any regulatory agency worldwide. Acceleron Pharma halted all clinical development in April 2011 after vascular safety signals in the Phase 2 DMD trial. The compound has no IND pathway active and no pharmaceutical manufacturer currently produces it for human use. ACE-031 is available only as a research chemical from peptide vendors. It is sold labeled "for research purposes only" and is not intended for human consumption. WADA prohibits all myostatin inhibitors under category S4.4 (hormone and metabolic modulators); competitive athletes cannot use this compound. Product authenticity is a serious concern. ACE-031 is an 82 kDa recombinant fusion protein requiring mammalian cell expression systems. A 2025 analysis (Reichel, Drug Testing and Analysis) found major inconsistencies in black-market samples. Standard peptide testing cannot verify biological activity. This content is for informational purposes only and does not constitute medical advice. Consult a licensed healthcare provider before using any research compound. (Word count: 160)
Peptide Schedule Research TeamReviewed Apr 20266 Citations
