Peptide Schedule
ACE-031Small moleculeNo amino acid sequence. Icon reflects category theme only.ACE-031 Dosage Calculator
ACE-031 is a recombinant fusion protein designed to act as a decoy receptor for myostatin and related ligands in the TGF-beta superfamily.
3mg · 2x/week
Summary: Add 1mL BAC water to your 1mg vial. Draw to 300.0 units on a U-100 syringe for a 3mg dose. This vial will last 0 doses.
Cycle Planner
ACE-031 Pharmacokinetics
Pharmacokinetics — Active Dose Over Time
t½ = 10-15 daysDisclaimer: This curve is a simplified first-order exponential decay model. Actual pharmacokinetics vary based on injection site, individual metabolism, body composition, and other factors. Half-life values are approximate and based on available preclinical and clinical literature. Many research peptides lack formal human pharmacokinetic studies. This is for educational purposes only — not medical advice.
ACE-031 Dosing Protocol
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 3mg | 2x/week |
| Moderate | 5mg | 2x/week |
| Aggressive | 10mg | 2x/week |
Note: ACE-031 is a soluble activin receptor type IIB (ActRIIB) decoy receptor — a fusion protein combining the extracellular domain of ActRIIB with a human IgG1 Fc fragment. Developed by Acceleron Pharma for Duchenne muscular dystrophy. Clinical development halted in April 2011 after vascular safety signals (epistaxis and telangiectasias) emerged during the Phase 2 DMD trial. These events were attributed to off-target inhibition of BMP-9 and BMP-10. All adverse events resolved upon discontinuation.
About ACE-031
ACE-031 is a recombinant fusion protein designed to act as a decoy receptor for myostatin and related ligands in the TGF-beta superfamily. It consists of the extracellular domain of the activin type IIB receptor (ActRIIB) fused to the Fc portion of human IgG1, which extends its circulating half-life and allows for subcutaneous dosing every 2-4 weeks. The biological rationale behind ACE-031 is straightforward. Myostatin is the primary negative regulator of skeletal muscle growth. Animals and humans with naturally occurring myostatin mutations develop pronounced muscular hypertrophy. By flooding the extracellular space with a soluble version of myostatin's receptor, ACE-031 intercepts the ligand before it can bind the membrane-bound receptor and activate its downstream signaling cascade (Smad2/3 phosphorylation), effectively removing the brake on muscle protein synthesis. The problem is that ActRIIB doesn't bind only myostatin. It also captures activin A, activin B, GDF-11, and critically, BMP-9 and BMP-10. Those last two ligands are essential for maintaining vascular endothelial integrity. When ACE-031 sequesters BMP-9 and BMP-10, it destabilizes endothelial cells, leading to the formation of telangiectasias (small dilated blood vessels in the skin) and epistaxis (nosebleeds). This is the mechanism that ended the clinical program. In the Phase 1 single ascending-dose study, 48 healthy postmenopausal women received a single injection of ACE-031 at doses ranging from 0.02 to 3 mg/kg. At the highest dose, participants gained a mean 3.3% total body lean mass and 5.1% thigh muscle volume by day 29 — from a single injection. Pharmacokinetics were linear across all doses, with a half-life of 10-15 days. The Phase 2 trial enrolled ambulatory boys with DMD ages 4-16. Cohort 2 showed a statistically significant 5.2% increase in total body lean mass versus 2.6% in the placebo group. Bone mineral density markers also improved. However, the trial was terminated before enrolling additional cohorts due to epistaxis and telangiectasias at doses in the 1.0-2.5 mg/kg range. ACE-031 remains an important proof of concept for myostatin inhibition as a therapeutic strategy. Subsequent programs (like ACE-2494 and bimagrumab) attempted to refine the ligand selectivity to avoid the BMP-9/10 trap.