Side-by-side · Research reference

ACE-031vsVesugen

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-REVIEWED5/43 cited

ACE-031

ActRIIB-Fc Fusion · Phase 2 Halted

Phase 2Highest trial stage

2011Development halted

~58.4 kDaMolecular weightReichel 2025

SQ · Weekly dosing investigated

Vesugen

Bioregulatory Tripeptide · Vascular Endothelium

3 AATripeptide

Endothelin-1 ↓Atherosclerotic tissue

Ki-67 ↑Aged endothelium

SQ / IM · Protocol varies

01Mechanism of Action

Parameter

ACE-031

Vesugen

Primary target

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

Vascular endothelial cell nucleus — MKI67 gene promoter

Pathway

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

KED → MKI67 promoter interaction (CATC binding motif -14 to +12 bp) → Ki-67 proliferation protein ↑

Downstream effect

Disinhibition of myogenic signaling, increased skeletal muscle mass and strength

Normalised endothelin-1 expression in atherosclerotic/restenotic endothelium, restored connexin expression for cell-cell communication, enhanced proliferative capacity in senescent endothelial culturesKozlov 2016 Khavinson 2014

Feedback intact?

—

Not applicable — does not operate via hormone axis

Origin

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

Khavinson bioregulatory peptide school — designed as tissue-specific (vascular) cytomodulator

Antibody development

—

02Dosage Protocols

Parameter

ACE-031

Vesugen

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 (atherosclerosis, restenosis, aging) · Russian case series

Half-life

Days to weeks (Fc-fusion typical kinetics)

IgG1-Fc domain confers extended circulation time.

Not reported

Tripeptides typically cleared rapidly.

Duration investigated

12–24 weeks (trial cut short)

—

Standard dose (reported)

—

Not standardised — Russian clinical case series

Protocols vary; no FDA-approved regimen.

Route

—

Subcutaneous or intramuscular

Frequency

—

Not specified in available literature

Duration

—

Case series report treatment courses in elderly arterial insufficiency

04Side Effects & Safety

Parameter

ACE-031

Vesugen

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

—

Reported adverse events

—

None documented in available abstracts

Injection site

—

Assumed minimal — typical for small peptides

Long-term safety

—

Unknown — no long-term RCT data

Epigenetic mechanism risk

—

Theoretical concern: direct gene promoter interaction — proliferative effects in non-target tissues not characterised

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

Vesugen

—

Relative Contraindications

ACE-031

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

Vesugen

·Active malignancy — proliferative mechanism (Ki-67 upregulation) untested in oncologic context

05Administration Protocol

Parameter

ACE-031

Vesugen

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.

Lyophilised powder reconstituted with sterile water or bacteriostatic water per supplier protocol. No standardised formulation.

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

Subcutaneous (abdomen, thigh) or intramuscular. Rotate sites if multi-dose protocol.

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

No reported circadian or fasting requirement. Russian protocols typically integrated into geroprotective regimens.

4. Clinical trial route

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

Lyophilised: refrigerate 2–8 °C, light-protected. Reconstituted: use immediately or refrigerate per supplier guidance (typically <7 days).

06Stack Synergy

ACE-031

— no documented stacks

Vesugen

+ Thymalin

Multi-pathway

View Thymalin →

Both from Khavinson bioregulatory school. Thymalin targets thymic/immune axis, Vesugen targets vascular endothelium. Rationale: multi-system geroprotection in elderly — immune senescence + vascular aging. Documented in Khavinson-tradition protocols combining tissue-specific peptides for poly-organ rejuvenation. No direct synergy study; combinatorial logic based on distinct target tissues.

Vesugen: Per protocol (SQ/IM)
Thymalin: Per protocol (SQ/IM)
Frequency: Sequential or concurrent per geroprotective protocol
Primary benefit: Multi-system age-related decline mitigation (vascular + immune)