ACE-031
← Back to LibraryCompound Profile
ACE-031 is reviewed here for growth-hormone signaling and recovery context.
Research Summary
Human studies, published literature, supporting research
Growth-hormone signaling, Recovery, Body composition
Target context: Activin Type IIB
Human data exists, but longer-term context is still developing.
Human research exists, but confidence depends on product, dose, and population.
Route(s)
Subcutaneous
Typical dose
1.0mg to 2.0mg
Dosing window
Anytime
Receptor / target
Activin Type IIB
Properties
Not listed
Pre-mixed
No
How ACE-031 works in the body
ACE-031 is an activin receptor decoy that blocks myostatin-family signaling.
Muscle (Human trial (halted))
Studied in clinical trials to increase muscle mass by blocking myostatin/activin. Trials were stopped over safety signals.
Educational only, not medical advice. Labels describe the type of research behind each area, not a recommendation.
Protocols
Standard Protocol
| Timeframe | Dose | Notes |
|---|---|---|
| Weeks 1-4 | 1.0mg to 2.0mg twice weekly | Due to vascular side effects, research doses are kept conservative. |
Protocol example for research-context comparison; verify against the evidence status and listed medical sources.
Alternative: Micro-Assessment
| Timeframe | Dose | Notes |
|---|---|---|
| Weeks 1-2 | 500mcg twice weekly | Used to assess tolerance to epistaxis (nosebleeds) before escalating to full dose. |
Alternative research-context example; not an approved-label regimen unless marked above.
Protocol logic check
Medical literature and study context
Medical-source summary: This section ties the page to medical literature, drug labels, trial registries, and regulatory sources. It is educational context only and should not be read as medical advice or a use recommendation.
| Evidence position | No approved FDA label was identified for this entry; evidence should be treated as literature context rather than validated dosing guidance. |
|---|---|
| Where studied | Studied around pituitary GH signaling, IGF-1 response, body-composition endpoints, growth-hormone deficiency models, or discontinued anabolic programs depending on the compound. |
| Source systems checked | FDA regulatory pages; PubMed/PMC literature; ClinicalTrials.gov records |
| Target and route context | Target/receptor: Activin Type IIB. Route(s): Subcutaneous. Dosing window on page: Anytime. |
| Protocol anchor | No source-backed label or clinical-trial regimen was identified for this page; protocol examples are research-context comparisons only. |
| Main evidence limit | Key limitation: literature may be preclinical, indirect, old, region-specific, or sparse; absence of a label means no validated dosing standard. |
Source-linked findings
- GH-axis compounds are best interpreted through pituitary physiology, IGF-1 response, pulse timing, and metabolic adverse effects rather than dose escalation alone.
- Evidence strength ranges from approved labels for specific agents to sparse or discontinued development programs for research peptides.
- No approved-label regimen was identified for this entry. Dosing examples should be treated as unverified protocol examples.
Protocol and study notes
- No source-backed label or clinical-trial regimen was identified for this page; protocol examples are research-context comparisons only.
- On-page protocol examples summarized for comparison: Standard Protocol: Weeks 1-4, 1.0mg to 2.0mg twice weekly; Alternative: Micro-Assessment: Weeks 1-2, 500mcg twice weekly.
- Key limitation: literature may be preclinical, indirect, old, region-specific, or sparse; absence of a label means no validated dosing standard.
- Monitor IGF-1 response, fasting glucose/A1c, edema, carpal-tunnel symptoms, blood pressure, sleep apnea, and malignancy history.
Selected medical sources
Independent evidence
Regulatory status: no approved label identified
Storage
No approved-label storage guidance was identified for this entry. Use conservative sterile handling and see the general storage guidance in the FAQ.
Contraindications & cautions
Evidence varies by item. Some points come from labels, published literature, or regulatory context; others are mechanism-based cautions that still need confirmation against medical literature. Use the medical sources below to verify details.
- Bleeding disorders of any type: epistaxis and vascular fragility are direct pharmacological consequences of ACE-031's mechanism; any pre-existing coagulation disorder dramatically amplifies hemorrhagic risk.
- Anticoagulant or antiplatelet therapy: warfarin, heparin, aspirin, clopidogrel, NOACs; additive bleeding risk with BMP9/BMP10 pathway disruption.
- Uncontrolled hypertension: elevated blood pressure combined with compromised vascular wall integrity from BMP9/BMP10 blockade increases risk of spontaneous vessel rupture.
- Known hereditary hemorrhagic telangiectasia (HHT) or family history of vascular malformations: BMP9 is the primary genetic driver of HHT; ACE-031 mechanistically recapitulates HHT pathology.
- Active malignancy: ActRIIB ligand trapping removes activin A suppression, which may release growth restraints on tumor cells.
- History of cancer: exercise caution; myostatin/activin pathway manipulation has theoretical tumor growth implications.
- Pregnancy: fusion protein safety not established; avoid.
- Breastfeeding: safety not established.
- Known hypersensitivity to ACE-031, IgG1 Fc fusion proteins, or any formulation components.
- Cardiovascular disease or history of stroke: vascular integrity compromise from BMP9/BMP10 blockade in subjects with pre-existing vascular disease is high risk.
- Severe anemia: epistaxis-related blood loss may worsen anemia.
- Pulmonary arterial hypertension: BMP9 and BMP10 are critical regulators of pulmonary vascular tone; blocking them may worsen PAH.
- Pediatric use: the DMD trial that drove program discontinuation was in pediatric subjects; the vascular risk is not offset by muscle benefit in children.
- History of hereditary angioedema or vascular fragility syndromes.
Possible side effects
Evidence varies by item. Some points come from labels, published literature, or regulatory context; others are mechanism-based cautions that still need confirmation against medical literature. Use the medical sources below to verify details.
- Epistaxis (spontaneous nosebleeds): the primary and program-terminating adverse effect from clinical trials; directly caused by BMP9/BMP10 trapping disrupting nasal mucosal vascular integrity; onset typically within the first 2-4 weeks; severity ranges from minor to persistent bleeding requiring intervention.
- Telangiectasias (dilated superficial blood vessels): small, visible dilated capillaries on the skin and mucosal surfaces; a direct consequence of BMP9/BMP10 pathway disruption; may persist after cessation of ACE-031.
- Injection site erythema and local reactions: redness, swelling, induration at subcutaneous injection site; reported in Phase 1 trials as the most common injection-related adverse event.
- Headache: common; likely related to vasodilation from BMP9/BMP10 disruption and changes in cerebral vascular tone.
- Elevated blood pressure or blood pressure variability: secondary to disrupted vascular endothelial signaling.
- Nausea: mild; reported in Phase 1 data.
- Fatigue: mild; self-resolving.
- Dizziness: vasodilation-mediated; transient.
- Theoretical long-term vascular remodeling: chronic BMP9/BMP10 blockade in animal models produces arteriovenous malformation-like lesions; human clinical exposure was too short to assess this risk fully.
- Immunogenicity: ACE-031 is a fusion protein; anti-drug antibodies are possible with repeated administration, potentially reducing efficacy and causing hypersensitivity reactions.
- Gum bleeding: oral mucosal vascular fragility from BMP9/BMP10 disruption.
- Risk of pathological vascular shunting: theoretical; loss of arteriovenous boundary signaling.
Compatibility
The relationships below are heuristic compatibility notes and were not independently verified. Treat them as a starting point for a conversation with a clinician. They carry no safety guarantee.
Reported synergistic:
Reported contraindicated combinations:
None listed.