Side-by-side · Research reference

ACE-031vsHGH Fragment 176-191

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-REVIEWED28/59 cited

ACE-031

ActRIIB-Fc Fusion · Phase 2 Halted

Phase 2Highest trial stage

2011Development halted

~58.4 kDaMolecular weightReichel 2025

SQ · Weekly dosing investigated

HGH Fragment 176-191

GH Fragment · Pre-Clinical

50%Weight gain reductionNg 2000

~26 minHalf-life (est.)

No IGF-1 ↑GH axis impact

SQ · IP (animal) · Oral (tested)

01Mechanism of Action

Parameter

ACE-031

HGH Fragment 176-191

Primary target

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

Beta-3 adrenergic receptors on adipocytesHeffernan 2001

Pathway

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

Fragment → β3-AR upregulation → Enhanced lipolytic sensitivityHeffernan 2001

Downstream effect

Disinhibition of myogenic signaling, increased skeletal muscle mass and strength

Increased lipolysis and beta-3 AR mRNA expression without IGF-1 axis activation

Feedback intact?

—

N/A — does not interact with GH/IGF-1 axis

Origin

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

Synthetic peptide derived from hGH residues 176-191; AOD9604 includes N-terminal tyrosine (177-191)Cox 2015

Antibody development

—

Not reported in available studies

02Dosage Protocols

Parameter

ACE-031

HGH Fragment 176-191

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 studies 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 (oral)

—

500 mcg/kg body weightNg 2000

Obese Zucker rats, 19 days.

Animal dose (IP)

—

Not specified (14-day chronic administration)Heffernan 2001

Obese mice, daily IP injection.

Human equivalent dose

—

Not established — no published human RCTs

Frequency

—

Once daily (animal models)

Duration tested

—

14–19 daysHeffernan 2001 Ng 2000

Detection window

—

50 pg/mL LOD in urine; stable metabolite extends detectionCox 2015

WADA-banned; anti-doping testing available.

Oral bioavailability

—

Demonstrated efficacy in animal oral administrationNg 2000

Potential for oral therapeutic development.

03Metabolic / Fat Loss Evidence

Parameter

ACE-031

HGH Fragment 176-191

Primary fat target

—

Adipose tissue (general) — beta-3 AR mediated lipolysisHeffernan 2001

Weight gain reduction

—

50% reduction vs control (15.8 ± 0.6 g vs 35.6 ± 0.8 g)Ng 2000

Obese Zucker rats, 19 days oral administration.

Body fat reduction

—

Significant decrease in body weight and body fat in obese mice (14 days)Heffernan 2001

Lipolytic activity

—

Increased adipose tissue lipolytic activityNg 2000

Direct measurement in treated animals.

Beta-3 AR expression

—

Upregulated β3-AR mRNA in obese mice to lean-comparable levelsHeffernan 2001

Insulin sensitivity

—

No adverse effect — euglycemic clamp confirmedNg 2000

Contrasts with intact hGH diabetogenic effects.

IGF-1 impact

—

No elevation — fragment does not activate GH/IGF-1 axis

Beta-3 AR dependency

—

Effect abolished in β3-AR knockout miceHeffernan 2001

Confirms β3-AR as primary mechanism.

Route of administration

—

Efficacy demonstrated via oral and IP routesNg 2000 Heffernan 2001

Human evidence

—

None published — pre-clinical only

04Side Effects & Safety

Parameter

ACE-031

HGH Fragment 176-191

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

—

Insulin sensitivity

—

No adverse effects observed in euglycemic clamp (animal)Ng 2000

GH/IGF-1 axis

—

No activation — avoids diabetogenic effects of full GHNg 2000

Human safety data

—

Not available — no published human trials

WADA status

—

Banned as performance-enhancing drugCox 2015

Metabolic profile

—

Six metabolites identified; CRSVEGSCG most stableCox 2015

Detection window implications for doping control.

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

HGH Fragment 176-191

·Competitive athletes (WADA-banned)Cox 2015

Relative Contraindications

ACE-031

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

HGH Fragment 176-191

·Absence of human safety data — experimental use only

05Administration Protocol

Parameter

ACE-031

HGH Fragment 176-191

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 primary route in research context. Oral administration demonstrated efficacy in animal models at 500 mcg/kg.

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

Once daily dosing used in animal studies. Timing not specified; GH-independent mechanism suggests flexibility.

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

Animal protocols: 14–19 days. Human duration not established — no published trials.

4. Clinical trial route

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

Lyophilized peptide storage per standard peptide protocols. Metabolite stability suggests refrigerated reconstituted solution viable.

5. Detection

—

Detectable in urine via SPE-LC-MS at 50 pg/mL LOD. Extended detection window via stable metabolite CRSVEGSCG.Cox 2015