Side-by-side · Research reference

ACE-031vsMGF

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

BAnimal-StrongHUMAN-REVIEWED14/55 cited

ACE-031

ActRIIB-Fc Fusion · Phase 2 Halted

Phase 2Highest trial stage

2011Development halted

~58.4 kDaMolecular weightReichel 2025

SQ · Weekly dosing investigated

MGF

IGF-1Ec Splice Variant · Muscle-Specific

IGF-1EcSplice variantArmakolas 2016

24-AASynthetic E-domain

Animal onlyHuman evidence

SQ · Research context only

01Mechanism of Action

Parameter

ACE-031

MGF

Primary target

Myostatin, GDF11, activin A — TGF-β superfamily ligands

Satellite cells (Pax7+) in skeletal muscleMoore 2018

Pathway

Soluble decoy receptor binds circulating myostatin/TGF-β ligands → prevents ActRIIB activation → SMAD2/3 pathway inhibition

Mechanical stress → IGF-1Ec mRNA upregulation → Local E-domain peptide release → Satellite cell activation

Downstream effect

Disinhibition of myogenic signaling, increased skeletal muscle mass and strength

Satellite cell proliferation, myoblast differentiation, muscle fiber repair

Feedback intact?

—

Origin

Recombinant fusion protein: human ActRIIB extracellular domain + IgG1-Fc fragmentReichel 2025

Alternative splicing of IGF-1 gene (exons 4-6) produces IGF-1Ec precursor; E-domain cleaved post-translationallyArmakolas 2016 Vassilakos 2017

Antibody development

—

02Dosage Protocols

Parameter

ACE-031

MGF

Clinical dosing

Weekly or biweekly SQ injections (exact doses undisclosed pre-halt)

Phase 2 DMD trial protocol not fully published.

—

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

—

Evidence basis

Phase 2 trial discontinued — incomplete dataset

Animal models + in vitro only

Half-life

Days to weeks (Fc-fusion typical kinetics)

IgG1-Fc domain confers extended circulation time.

—

Duration investigated

12–24 weeks (trial cut short)

—

Synthetic peptide

—

24-amino-acid E-domain sequence

Corresponds to human IGF-1Ec exons 4-6 region.

Rodent cardiac model

—

200 μg/kg via peptide-eluting microstructures

Post-MI injection; improved ejection fraction by 8 weeks.

Acute delivery (mouse MI)

—

Single bolus within 12 hrs post-infarctionShioura 2014

Delayed decompensation; no human protocol established.

Human evidence

—

None — no published clinical trials

All dosing extrapolated from animal models.

Detection in doping

—

Full-length MGF detected via LC-MS in illicit productsThevis 2014

WADA-prohibited since 2005; no therapeutic indication.

04Side Effects & Safety

Parameter

ACE-031

MGF

Epistaxis (nosebleeds)

Significant incidence in Phase 2 DMD trial — primary safety signal

—

Telangiectasia

Dilated capillaries / spider veins observed

—

Vascular abnormalities

Mechanism: ActRIIB/ALK1 pathway disruption affects vascular homeostasis

—

Injection site reactions

Local erythema, induration (biologics class effect)

—

Antibody development

Potential for anti-drug antibodies (Fc-fusion proteins); incidence not reported

Unknown — no longitudinal human exposure data

Black market contaminants

12/14 tested products contained multiple unidentified proteins alongside ACE-031Reichel 2025

—

Human safety data

—

None — no clinical trials published

Theoretical IGF-1 axis risk

—

Chronic IGF-1Ec overexpression linked to cancer progression (prostate, colorectal, breast)

Tumor promotion

—

IGF-1Ec overexpressed in osteosarcoma, colorectal polyps with dysplasia, endometrial cancer

Local injection reaction

—

Presumed similar to other peptides (erythema, induration) — no direct evidence

Dysregulated expression with age

—

Older adults (70+ yrs) show blunted IGF-1Ec response post-exercise vs youngMoore 2018

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

MGF

·Active malignancy or history of IGF-1-sensitive cancers (prostate, colorectal, breast, osteosarcoma)
·No established therapeutic use — investigational only

Relative Contraindications

ACE-031

·Coagulation disorders or anticoagulant use (epistaxis risk)
·Hereditary hemorrhagic telangiectasia (HHT) family history
·Cardiovascular disease (vascular remodeling effects unknown)

MGF

·Family history of IGF-1-axis malignancies
·Use outside research setting

05Administration Protocol

Parameter

ACE-031

MGF

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.

MGF (E-domain peptide) has no approved clinical protocol. All published data derive from animal models or in vitro experiments.

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

Commercially available MGF corresponds to the 24-amino-acid human E-domain (hEc). Rodent E-domain (Eb) is structurally distinct and not interchangeable.

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

Rodent studies used peptide-eluting polymeric microstructures (cardiac) or direct intramuscular injection. Routes and doses non-translatable to humans.Peña 2015 Shioura 2014

4. Clinical trial route

Phase 2 protocol used subcutaneous injections at weekly or biweekly intervals. Exact dosing protocols remain unpublished.

MGF peptides prohibited in sport since 2005. Detection via LC-MS established for full-length MGF products.Thevis 2014

5. Research context only

—

Any human use falls outside approved medical practice and regulatory frameworks. No safety or efficacy data exist.

06Stack Synergy

ACE-031

— no documented stacks

MGF

+ BPC-157

Multi-pathway

View BPC-157 →

MGF activates satellite cells for muscle fiber repair; BPC-157 promotes angiogenesis, collagen synthesis, and tendon healing via distinct pathways (VEGF, FAK, integrin signaling). Theoretical synergy in post-injury contexts combines myogenic (MGF) and stromal (BPC-157) repair mechanisms. Both lack human validation.

MGF: No established dose
BPC-157: 250–500 mcg SQ near injury site
Context: Animal models only
Primary benefit: Theoretical multi-tissue repair (muscle + tendon/ligament)

+ TB-500

Moderate

View TB-500 →

TB-500 (thymosin beta-4 fragment) enhances actin polymerization, cell migration, and angiogenesis—complementary to MGF satellite cell activation. Both upregulated post-injury; combined use presumed additive for muscle regeneration in preclinical models.

MGF: No established dose
TB-500: 2–5 mg SQ weekly
Context: Animal models only
Primary benefit: Satellite cell activation + enhanced migration/angiogenesis