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Specimen Atlas of Research Peptides81 plates · MIT
Side-by-side · Research reference

ACE-031vsTB-500

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
BPhase 2HUMAN-REVIEWED8/46 cited
ACE-031
ActRIIB-Fc Fusion · Phase 2 Halted
Phase 2Highest trial stage
2011Development halted
~58.4 kDaMolecular weightReichel 2025
SQ · Weekly dosing investigated
TB-500
Thymosin β4 fragment · Healing
2 mgPer doseGoldstein 2012
Phase 2Evidence levelGoldstein 2012
~2 hrHalf-life
SQ or IM · Multiple sites · 2–3×/week

01Mechanism of Action

Parameter
ACE-031
TB-500
Primary target
Myostatin, GDF11, activin A — TGF-β superfamily ligands
G-actin (sequestering) + cell-surface integrinsGoldstein 2012
Pathway
Soluble decoy receptor binds circulating myostatin/TGF-β ligands → prevents ActRIIB activation → SMAD2/3 pathway inhibition
Actin remodelling → cell migration; integrin-linked signaling → angiogenesis; anti-inflammatory cytokine modulationGoldstein 2012Malinda 1999
Downstream effect
Disinhibition of myogenic signaling, increased skeletal muscle mass and strength
Accelerated wound healing, endothelial migration, hair follicle regeneration, cardiac repair (preclinical)Goldstein 2012
Feedback intact?
Endogenous protein at baseline; supplementation amplifies
Origin
Recombinant fusion protein: human ActRIIB extracellular domain + IgG1-Fc fragmentReichel 2025
17-AA active fragment of endogenous 43-AA thymosin β4 (TMSB4X gene)Goldstein 2012
Antibody development

02Dosage Protocols

Parameter
ACE-031
TB-500
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-strong + Phase 2 dermal/ocular trialsGoldstein 2012
Half-life
Days to weeks (Fc-fusion typical kinetics)
IgG1-Fc domain confers extended circulation time.
~2 hours (estimated; tissue uptake longer)
Duration investigated
12–24 weeks (trial cut short)
Standard dose
2 mg per injectionGoldstein 2012
Anecdotal community range; clinical Phase 2 trials used 70–840 mcg/kg IV.
Frequency
2× per week (loading); then 1× per week (maintenance)
Lower / starter dose
1 mg per injection
Duration
4–8 weeks loading; longer maintenance for chronic injury
Reconstitution
Bacteriostatic water, 1–2 mL per 5 mg vial
Timing
Evening or pre-rest preferred (anecdotal)

04Side Effects & Safety

Parameter
ACE-031
TB-500
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
Injection site reaction
Mild erythema, transient pain
GI symptoms
Rare nausea (anecdotal)
Cancer risk
Theoretical via angiogenesis pathway
Lethargy / fatigue
Reported anecdotally during loading phase
Antibody formation
No data (no long-term human trials)
Pregnancy / OB
Avoid
Long-term safety
Unknown beyond Phase 2
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
TB-500
  • ·Active malignancy (theoretical angiogenesis concern)
  • ·Pregnancy / breastfeeding
Relative Contraindications
ACE-031
  • ·Coagulation disorders or anticoagulant use (epistaxis risk)
  • ·Hereditary hemorrhagic telangiectasia (HHT) family history
  • ·Cardiovascular disease (vascular remodeling effects unknown)
TB-500
  • ·Cancer history
  • ·Concurrent VEGF inhibitor therapy

05Administration Protocol

Parameter
ACE-031
TB-500
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.
Add 1–2 mL bacteriostatic water to 5 mg vial → 2.5–5 mg/mL. Roll gently.
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
SQ near injury site (preferred), or systemic SQ (abdomen). Rotate sites.
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
Evening or pre-sleep is most common anecdotal timing.
4. Clinical trial route
Phase 2 protocol used subcutaneous injections at weekly or biweekly intervals. Exact dosing protocols remain unpublished.
Lyophilised: room temp, light-protected. Reconstituted: refrigerate, ≤30 days.
5. Needle
27–31G, 4–8 mm insulin syringe.

06Stack Synergy

ACE-031
— no documented stacks
TB-500
+ BPC-157
Strong
View BPC-157

TB-500 and BPC-157 cover complementary halves of tissue repair: BPC-157 upregulates VEGFR2-driven angiogenesis and fibroblast outgrowth; TB-500 sequesters G-actin to enable endothelial / epithelial migration. The anecdotal canonical "healing stack" — pairs especially well for tendon and ligament injuries.

TB-500
2 mg SQ · 2× per week
BPC-157
250–500 mcg SQ · daily
Primary benefit
Combined angiogenesis + cell migration for tendon/ligament/muscle repair