Side-by-side · Research reference
ACE-031vsGLP-1 (7-37)
Side-by-side comparison across mechanism, dosage, evidence, side effects, administration, and stack synergies. Citations on every claim where available.
APhase 2HUMAN-REVIEWED10/44 cited
BHuman-MechanisticHUMAN-REVIEWED16/43 cited
ACE-031
ActRIIB-Fc Fusion · Phase 2 Halted
SQ · Weekly dosing investigated
GLP-1 (7-37)
Incretin Hormone · Native Peptide
Research use only · IV/SC in experimental settings
01Mechanism of Action
Parameter
ACE-031
GLP-1 (7-37)
Primary target
Myostatin, GDF11, activin A — TGF-β superfamily ligands
GLP-1 receptor (class B GPCR)Koole 2015
Pathway
Soluble decoy receptor binds circulating myostatin/TGF-β ligands → prevents ActRIIB activation → SMAD2/3 pathway inhibition
GLP-1R activation → cAMP production → PKA signaling → insulin secretion (pancreatic β-cells)Lu 2025Koole 2015
Downstream effect
Disinhibition of myogenic signaling, increased skeletal muscle mass and strength
Feedback intact?
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Yes — physiological secretion and degradation preserved
Origin
Recombinant fusion protein: human ActRIIB extracellular domain + IgG1-Fc fragmentReichel 2025
Endogenous peptide cleaved from proglucagon in intestinal L cells; secreted postprandially
Antibody development
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02Dosage Protocols
Parameter
ACE-031
GLP-1 (7-37)
Clinical dosing
Weekly or biweekly SQ injections (exact doses undisclosed pre-halt)
Phase 2 DMD trial protocol not fully published.
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Black market products
Variable purity; 12/14 tested products contained target protein plus contaminantsReichel 2025
SDS-PAGE revealed multiple protein bands; quality control absent.Reichel 2025
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Evidence basis
Phase 2 trial discontinued — incomplete dataset
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Half-life
Days to weeks (Fc-fusion typical kinetics)
IgG1-Fc domain confers extended circulation time.
~2 minutes (plasma)Alavi 2021Ding 2017
Requires continuous infusion for sustained effect.
Duration investigated
12–24 weeks (trial cut short)
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Clinical use
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None — native GLP-1 not used therapeutically
Engineered analogues (semaglutide, liraglutide) used clinically.Friedman 2024
Research dosing
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Variable — 0.1–10 nmol/kg in animal models
Used as reference standard for analogue comparison.
Modified analogues
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t½ extended to 13 h (liraglutide), 165 h (semaglutide)
Via DPP-4 resistance + fatty acid acylation.
03Metabolic / Fat Loss Evidence
Parameter
ACE-031
GLP-1 (7-37)
Mechanism
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Native GLP-1 efficacy
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Minimal — rapid degradation prevents sustained appetite suppression
Gastric emptying
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Delayed in animal models, contributing to satiety
Body weight impact
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Not observed with native GLP-1 — requires analogue formulations
04Side Effects & Safety
Parameter
ACE-031
GLP-1 (7-37)
Epistaxis (nosebleeds)
Significant incidence in Phase 2 DMD trial — primary safety signal
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Telangiectasia
Dilated capillaries / spider veins observed
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Vascular abnormalities
Mechanism: ActRIIB/ALK1 pathway disruption affects vascular homeostasis
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Injection site reactions
Local erythema, induration (biologics class effect)
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Antibody development
Potential for anti-drug antibodies (Fc-fusion proteins); incidence not reported
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Black market contaminants
12/14 tested products contained multiple unidentified proteins alongside ACE-031Reichel 2025
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Native GLP-1
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Well-tolerated in research settings; no prolonged exposure data
Hypoglycemia risk
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Low — insulin secretion is glucose-dependent
Analogue side effects
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Nausea, vomiting, diarrhea (GLP-1R agonists)
Not applicable to native GLP-1 due to non-therapeutic use.
GLP-1 resistance
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High glucose-induced PKCβ overexpression may reduce GLP-1 responsiveness in endothelial cellsPujadas 2016
Absolute Contraindications
ACE-031
- ·History of vascular disorders (epistaxis, telangiectasia, HHT)
- ·Pregnancy (TGF-β pathway critical for fetal development)
- ·Active malignancy (myostatin inhibition may affect tumour growth)
- ·Use of non-pharmaceutical grade ACE-031 (contamination risk)Reichel 2025
GLP-1 (7-37)
—Relative Contraindications
ACE-031
- ·Coagulation disorders or anticoagulant use (epistaxis risk)
- ·Hereditary hemorrhagic telangiectasia (HHT) family history
- ·Cardiovascular disease (vascular remodeling effects unknown)
GLP-1 (7-37)
—05Administration Protocol
Parameter
ACE-031
GLP-1 (7-37)
1. Pharmaceutical status
ACE-031 is not FDA-approved or commercially available. Phase 2 development was discontinued in 2011 due to safety concerns. Any ACE-031 on the black market is unregulated research chemical.
Native GLP-1(7-37) is not formulated for therapeutic use. Administered IV or SC in experimental protocols to study GLP-1R pharmacology and as reference standard for analogue development.
2. Black market quality
12 of 14 tested black market ACE-031 products contained the target protein but also carried multiple unidentified protein contaminants detectable by SDS-PAGE. Two products contained no ACVR2B-immunoreactive material.Reichel 2025
Lyophilised peptide stored at -20°C or below. Reconstituted solutions should be prepared fresh and used immediately due to rapid degradation.
3. Detection in sport
ACE-031 is prohibited under WADA S4.3 (Myostatin Inhibitors). Gel electrophoresis and Western blotting using ACVR2B-specific antibodies can detect the ~58.4 kDa protein in biological samples.Reichel 2025
For therapeutic GLP-1R activation, use FDA-approved long-acting analogues: semaglutide (once weekly), liraglutide (once daily), dulaglutide (once weekly), or exenatide (twice daily or once weekly).
4. Clinical trial route
Phase 2 protocol used subcutaneous injections at weekly or biweekly intervals. Exact dosing protocols remain unpublished.
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