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

ACE-031vsAdipotide

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-REVIEWED15/49 cited
ACE-031
ActRIIB-Fc Fusion · Phase 2 Halted
Phase 2Highest trial stage
2011Development halted
~58.4 kDaMolecular weightReichel 2025
SQ · Weekly dosing investigated
Adipotide
Pro-apoptotic Vascular-Targeting Peptide · Preclinical Only
PreclinicalStatus
PHB1TargetHossen 2013
ApoptosisMechanismHossen 2013
IV · Systemic · Preclinical Protocols OnlyHossen 2013

01Mechanism of Action

Parameter
ACE-031
Adipotide
Primary target
Myostatin, GDF11, activin A — TGF-β superfamily ligands
Prohibitin-1 (PHB1) on adipose vasculature endotheliumHossen 2013
Pathway
Soluble decoy receptor binds circulating myostatin/TGF-β ligands → prevents ActRIIB activation → SMAD2/3 pathway inhibition
CKGGRAKDC domain binds PHB1 → Peptide internalisation → D(KLAKLAK)₂ mitochondrial membrane disruption
Downstream effect
Disinhibition of myogenic signaling, increased skeletal muscle mass and strength
Endothelial apoptosis → Adipose vascular collapse → Adipocyte involution → Weight loss
Feedback intact?
N/A — Direct apoptotic mechanism, non-hormonal
Origin
Recombinant fusion protein: human ActRIIB extracellular domain + IgG1-Fc fragmentReichel 2025
Synthetic bioconjugate: PHB1-targeting homing peptide + pro-apoptotic KLA sequence
Antibody development

02Dosage Protocols

Parameter
ACE-031
Adipotide
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
Preclinical animal models 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)
Animal dose (mouse)
Low dose (not specified in abstract)Hossen 2013
Systemic injection in diet-induced obesity (DIO) models.Hossen 2013
Route
Intravenous (systemic injection)
Frequency
Not specified in available data
Human data
None — no clinical trials reported

03Metabolic / Fat Loss Evidence

Parameter
ACE-031
Adipotide
Primary fat target
White adipose tissue (all depots)
Mechanism
Vascular apoptosis → adipose blood supply collapse → adipocyte deathHossen 2013
Body weight reduction
Significant reduction in DIO miceHossen 2013
Absolute values not provided in abstract.
Leptin levels
Significant decrease
Parallel to adipose mass reduction.
Effect on adipocytes
Antiobesity effect on dysfunctional adipose cells (adipocytes + macrophages)Hossen 2013
Ectopic fat
Reduction in ectopic fat depositionHossen 2013
Marker of dysfunctional adipose tissue / metabolic syndrome.
Species tested
Obese rhesus monkeys, DIO mice
Human translation
Unknown — no clinical trials

04Side Effects & Safety

Parameter
ACE-031
Adipotide
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
Safety profile
Unknown — preclinical data only
Vascular selectivity
Targets adipose vasculature; off-target vascular effects unknown
Apoptotic mechanism risk
Pro-apoptotic payload may affect unintended tissues if selectivity incomplete
Kidney / liver toxicity
Not reported in available data
Immunogenicity
Not assessed in available data
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
Adipotide
  • ·Human use — not approved, no clinical safety data
Relative Contraindications
ACE-031
  • ·Coagulation disorders or anticoagulant use (epistaxis risk)
  • ·Hereditary hemorrhagic telangiectasia (HHT) family history
  • ·Cardiovascular disease (vascular remodeling effects unknown)
Adipotide
  • ·Any condition requiring intact adipose-tissue vascularisation

05Administration Protocol

Parameter
ACE-031
Adipotide
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.
Intravenous injection (systemic) in preclinical models. No human protocols exist.
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
Bioconjugate peptide. May also be encapsulated in nanoparticles (prohibitin-targeted nanoparticle formulation, KLA-PTNP, showed superior efficacy vs. free bioconjugate in mice).Hossen 2013
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
Low-dose systemic injection (exact dosing not specified in available abstract). Frequency and duration not detailed.Hossen 2013
4. Clinical trial route
Phase 2 protocol used subcutaneous injections at weekly or biweekly intervals. Exact dosing protocols remain unpublished.
Not specified — likely requires peptide-grade lyophilised storage and reconstitution.