Side-by-side · Research reference

ACE-031vsCrystagen

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-REVIEWED12/40 cited

ACE-031

ActRIIB-Fc Fusion · Phase 2 Halted

Phase 2Highest trial stage

2011Development halted

~58.4 kDaMolecular weightReichel 2025

SQ · Weekly dosing investigated

Crystagen

Khavinson Bioregulator · Immune-Thymic

B-cellPrimary targetСhervyakova 2014

SpleenTissue specificityСhervyakova 2014

AnimalEvidence level

SQ · Protocol variable

01Mechanism of Action

Parameter

ACE-031

Crystagen

Primary target

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

B-lymphocytes in splenic tissueСhervyakova 2014

Pathway

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

B-cell activation → Immune modulation during agingСhervyakova 2014

Downstream effect

Disinhibition of myogenic signaling, increased skeletal muscle mass and strength

B-cell activation via apoptosis reduction; no observed increase in splenic cell renewalСhervyakova 2014

Feedback intact?

—

Unknown — bioregulator mechanism not fully characterized

Origin

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

Synthetic Lys-Glu-Asp-Gly tetrapeptide — Khavinson bioregulator series

Antibody development

—

02Dosage Protocols

Parameter

ACE-031

Crystagen

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 / mechanistic

Half-life

Days to weeks (Fc-fusion typical kinetics)

IgG1-Fc domain confers extended circulation time.

Not reported

Duration investigated

12–24 weeks (trial cut short)

—

Standard dose

—

Not standardized — variable protocols

Russian bioregulator literature does not specify unified human dosing.

Route

—

Subcutaneous (presumed from bioregulator class)

Frequency

—

Unknown — bioregulator protocols variable

Duration

—

Unknown — chronic administration presumed in animal models

04Side Effects & Safety

Parameter

ACE-031

Crystagen

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

—

Black market contaminants

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

—

Published adverse events

—

None reported in available animal literature

Human safety data

—

Absent — no controlled human trials identified

Autoimmune considerations

—

Theoretical concern with B-cell modulators in predisposed individuals

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

Crystagen

·Active autoimmune disease (theoretical)

Relative Contraindications

ACE-031

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

Crystagen

·Pregnancy / lactation (no data)
·Active B-cell malignancies

05Administration Protocol

Parameter

ACE-031

Crystagen

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 injection — presumed from bioregulator class convention. Specific anatomical sites not standardized.

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

Protocol not standardized. If lyophilized, sterile water or bacteriostatic saline typical for peptide bioregulators.

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

Not specified. Bioregulator protocols vary — some practitioners advocate evening dosing, others morning.

4. Clinical trial route

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

Lyophilized: room temperature, light-protected. Reconstituted: refrigerate, use within days to weeks depending on preservative.

06Stack Synergy

ACE-031

— no documented stacks

Crystagen

+ Vilon

Multi-pathway

View Vilon →

Vilon (Lys-Glu) activates T-helper cells via apoptosis reduction, while Crystagen activates B-cells. Dual T/B immune modulation in aging models may provide complementary thymic-immune support within the Khavinson bioregulator framework. Both target splenic immune aging through distinct lymphocyte subsets.

Crystagen: Dose unknown · SQ
Vilon: Dose unknown · SQ
Frequency: Protocol variable
Primary benefit: Broader thymic-immune coverage (T-cell + B-cell)

Сhervyakova 2014