GH Secretagogues
ACE-031
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Limited / unverified Limited / unverified Limited / unverified GH Axis Muscle Hypertrophy
Educational reference only. Read the full disclaimer.
The protocols below are not automatically an FDA-approved or clinically verified regimen unless
explicitly marked as label-verified or clinical-trial above.
Overview
Route(s): Subcutaneous
Typical vial sizes: 1 mg
Dosing window: Anytime
Receptor / target: Activin Type IIB
Properties: Not stated
Pre-mixed: No
Unverified protocol notes
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. |
Unverified protocol note; not label dosing unless graded otherwise on this page.
Alternative: Micro-Assessment
| Timeframe | Dose | Notes |
|---|---|---|
| Weeks 1-2 | 500mcg twice weekly | Used to assess tolerance to epistaxis (nosebleeds) before escalating to full dose. |
Unverified alternative protocol; not an approved-label regimen unless graded otherwise on this page.
Protocol logic check
Protocol context: GH-axis protocols are not 'more is better.' The logic is pulse quality, recovery time, IGF-1/glucose monitoring, and avoiding receptor desensitization, edema, appetite spikes, numbness, or blood-pressure strain. Entry context: target (Activin Type IIB); route Subcutaneous; timing Anytime. Limited-evidence dosing tables are hypotheses, not recommendations.
Independent evidence
Independent safety notes: No independent approved-label regimen is listed for this entry. Dosing notes remain unverified.
Regulatory status: no approved label identified
Storage
No independently verified storage guidance found. Treat any unverified storage claim as unverified, and see the general storage guidance in the FAQ.
Contraindications (limited evidence)
- 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. Limited / unverified
- Anticoagulant or antiplatelet therapy: warfarin, heparin, aspirin, clopidogrel, NOACs; additive bleeding risk with BMP9/BMP10 pathway disruption. Limited / unverified
- Uncontrolled hypertension: elevated blood pressure combined with compromised vascular wall integrity from BMP9/BMP10 blockade increases risk of spontaneous vessel rupture. Limited / unverified
- 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. Limited / unverified
- Active malignancy: ActRIIB ligand trapping removes activin A suppression, which may release growth restraints on tumor cells. Limited / unverified
- History of cancer: exercise caution; myostatin/activin pathway manipulation has theoretical tumor growth implications. Limited / unverified
- Pregnancy: fusion protein safety not established; avoid. Limited / unverified
- Breastfeeding: safety not established. Limited / unverified
- Known hypersensitivity to ACE-031, IgG1 Fc fusion proteins, or any formulation components. Limited / unverified
- Cardiovascular disease or history of stroke: vascular integrity compromise from BMP9/BMP10 blockade in subjects with pre-existing vascular disease is high risk. Limited / unverified
- Severe anemia: epistaxis-related blood loss may worsen anemia. Limited / unverified
- Pulmonary arterial hypertension: BMP9 and BMP10 are critical regulators of pulmonary vascular tone; blocking them may worsen PAH. Limited / unverified
- Pediatric use: the DMD trial that drove program discontinuation was in pediatric subjects; the vascular risk is not offset by muscle benefit in children. Limited / unverified
- History of hereditary angioedema or vascular fragility syndromes. Limited / unverified
Side effects (limited evidence)
- 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. Limited / unverified
- 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. Limited / unverified
- 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. Limited / unverified
- Headache: common; likely related to vasodilation from BMP9/BMP10 disruption and changes in cerebral vascular tone. Limited / unverified
- Elevated blood pressure or blood pressure variability: secondary to disrupted vascular endothelial signaling. Limited / unverified
- Nausea: mild; reported in Phase 1 data. Limited / unverified
- Fatigue: mild; self-resolving. Limited / unverified
- Dizziness: vasodilation-mediated; transient. Limited / unverified
- 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. Limited / unverified
- Immunogenicity: ACE-031 is a fusion protein; anti-drug antibodies are possible with repeated administration, potentially reducing efficacy and causing hypersensitivity reactions. Limited / unverified
- Gum bleeding: oral mucosal vascular fragility from BMP9/BMP10 disruption. Limited / unverified
- Risk of pathological vascular shunting: theoretical; loss of arteriovenous boundary signaling. Limited / unverified
Compatibility
The relationships below come from the source site's internal engine and were not verified independently. Treat them as a starting point for a conversation with a clinician. They carry no safety guarantee.
Reported synergistic:
Reported contraindicated combinations:
None listed.