Side-by-side · Research reference
ACE-031vsProstamax
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-MechanisticHUMAN-REVIEWED11/38 cited
ACE-031
ActRIIB-Fc Fusion · Phase 2 Halted
SQ · Weekly dosing investigated
Prostamax
Khavinson Bioregulator · Tissue-Specific Peptide
4 AAPeptide length
SQ · Protocol per Khavinson tradition
01Mechanism of Action
Parameter
ACE-031
Prostamax
Primary target
Myostatin, GDF11, activin A — TGF-β superfamily ligands
Chromatin in prostatic cells — pericentromeric heterochromatin regions
Pathway
Soluble decoy receptor binds circulating myostatin/TGF-β ligands → prevents ActRIIB activation → SMAD2/3 pathway inhibition
Epigenetic modulation → heterochromatin decondensation → transcriptional derepressionDzhokhadze 2012
Downstream effect
Disinhibition of myogenic signaling, increased skeletal muscle mass and strength
Increased sister chromatid exchange, Ag-NOR activation, reduced C-heterochromatin condensation; tissue-specific regenerative stimulation in prostate organotypic culturesDzhokhadze 2012Zakutskiĭ 2006
Feedback intact?
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Origin
Recombinant fusion protein: human ActRIIB extracellular domain + IgG1-Fc fragmentReichel 2025
Synthetic tetrapeptide modeled on naturally occurring protein-derived bioregulators isolated between lysine-arginine motifs in long-lived speciesKhavinson 2017
Antibody development
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02Dosage Protocols
Parameter
ACE-031
Prostamax
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
Animal / organotypic cultureZakutskiĭ 2006Dzhokhadze 2012
No randomized controlled trials in humans.
Half-life
Days to weeks (Fc-fusion typical kinetics)
IgG1-Fc domain confers extended circulation time.
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Duration investigated
12–24 weeks (trial cut short)
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Effective concentration (in vitro)
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0.05 ng/mLZakutskiĭ 2006
Organotypic culture model; demonstrated tissue-specific stimulation.
Human clinical dose
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Not established
No published human trials; dosing extrapolated from Russian clinical tradition (not peer-reviewed).
Age groups studied
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Young (3-week) and aged (18-month) rats; elderly humans (75–86 years) in vitroZakutskiĭ 2006Dzhokhadze 2012
Duration
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Not specified
Khavinson protocols typically 10–20 days per cycle; no long-term safety data.
04Side Effects & Safety
Parameter
ACE-031
Prostamax
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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Published adverse events
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None reported in available literature
Genotoxicity signals
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Increased sister chromatid exchange (SCE) — marker of DNA recombination/repair; unclear long-term implications
Metal ion interactions
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Modulates Cu(II) and Cd(II) chromatin effects; unknown clinical relevance
Human safety data
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Absent — no published Phase 1/2/3 trials
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
Prostamax
- ·Active prostate malignancy — epigenetic modulation effects unknown in cancer
Relative Contraindications
ACE-031
- ·Coagulation disorders or anticoagulant use (epistaxis risk)
- ·Hereditary hemorrhagic telangiectasia (HHT) family history
- ·Cardiovascular disease (vascular remodeling effects unknown)
Prostamax
- ·History of prostate cancer — theoretical concern re: transcriptional activation
- ·Undiagnosed prostatic nodules or elevated PSA
05Administration Protocol
Parameter
ACE-031
Prostamax
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.
Subcutaneous or intramuscular — per Khavinson bioregulator tradition. No published human pharmacokinetic data.
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
If lyophilised: reconstitute with sterile water per manufacturer protocol (not standardized in literature).
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
Typically daily or every-other-day in Russian clinical tradition; duration 10–20 days per cycle.
4. Clinical trial route
Phase 2 protocol used subcutaneous injections at weekly or biweekly intervals. Exact dosing protocols remain unpublished.
No established biomarkers. Theoretical: PSA, prostate imaging, symptom scores (IPSS for BPH).
5. Note
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All protocols derived from non-peer-reviewed Russian clinical practice; Western regulatory approval absent.