Side-by-side · Research reference

ACE-031vsBPC-157

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-REVIEWED9/53 cited

ACE-031

ActRIIB-Fc Fusion · Phase 2 Halted

Phase 2Highest trial stage

2011Development halted

~58.4 kDaMolecular weightReichel 2025

SQ · Weekly dosing investigated

BPC-157

Stable Gastric Pentadecapeptide · Healing

250–500 mcgDaily doseHwang 2016

Phase 2Evidence levelHwang 2016 Sikiric 2018

~30 minHalf-life (est.)

SQ or IM · Local · Once or twice daily

01Mechanism of Action

Parameter

ACE-031

BPC-157

Primary target

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

VEGFR2 / nitric oxide / FAK-paxillin axes (proposed)Chang 2011 Sikiric 2018

Pathway

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

Upregulates VEGFR2 → angiogenesis; modulates NO synthase; promotes fibroblast outgrowth via FAK-paxillinChang 2011

Downstream effect

Disinhibition of myogenic signaling, increased skeletal muscle mass and strength

Accelerated tissue repair, reduced inflammation, improved gut barrier integritySikiric 2018

Feedback intact?

—

No known endogenous receptor; mechanism still under investigation

Origin

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

Synthetic pentadecapeptide derived from a sequence in human gastric juice; first characterised by Sikiric et al.Sikiric 2018

Antibody development

—

02Dosage Protocols

Parameter

ACE-031

BPC-157

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 clinicalSikiric 2018 Hwang 2016

Half-life

Days to weeks (Fc-fusion typical kinetics)

IgG1-Fc domain confers extended circulation time.

~30 min plasma (estimated)

Tissue half-life longer; mechanism may explain durable effect.

Duration investigated

12–24 weeks (trial cut short)

—

Standard dose

—

250–500 mcg / dayHwang 2016

Anecdotal community range. Phase 2 trial used 1.0 mg PL-14736 IV/day.

Frequency

—

Once or twice daily

Split dosing reported anecdotally for chronic injury.

Lower / starter dose

—

200 mcg / day

Conservative starter for new users.

Duration

—

2–4 weeks (acute injury); 4–8 weeks (chronic)

Anecdotal; no long-term human safety data.

Reconstitution

—

Bacteriostatic water, 1–2 mL

Timing

—

Local SQ to injury site preferred (anecdotal)

Systemic SQ also used; oral bioavailability shown in animal studies.

04Side Effects & Safety

Parameter

ACE-031

BPC-157

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 irritation (anecdotal)

GI symptoms

—

None reported in PL-14736 Phase 2

Cardiovascular

—

Not reported

Cancer risk

—

Theoretical concern via VEGF angiogenesis pathwaySikiric 2018

Antibody formation

—

No data (no long-term human trials)

Pregnancy / OB

—

Avoid — insufficient safety data

Long-term safety

—

Unknown beyond Phase 2 trial duration

Drug interactions

—

None established

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

BPC-157

·Pregnancy / breastfeeding
·Known active malignancy (theoretical VEGF concern)

Relative Contraindications

ACE-031

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

BPC-157

·History of cancer
·Concurrent VEGF inhibitor therapy (theoretical)
·Acute thrombotic events

05Administration Protocol

Parameter

ACE-031

BPC-157

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 a 5 mg vial. Roll gently; do not shake. Solution should be clear and colourless.

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 near the injury site is the most common anecdotal route. Systemic SQ (abdomen) also used. 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

No strict timing requirement. Most users dose once or twice daily, often morning + evening.

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 2–8 °C, use within 30 days.

5. Needle

—

27–31G insulin syringe, 4–8 mm. Local injection allows finer 31G.

06Stack Synergy

ACE-031

— no documented stacks

BPC-157

+ TB-500

Strong

View TB-500 →

BPC-157 and TB-500 (Thymosin β-4) target distinct healing axes: BPC-157 upregulates VEGF-driven angiogenesis and fibroblast migration; TB-500 increases actin remodelling and cell migration via the actin-sequestering β-thymosin domain. Stacked, they cover both vascular (BPC) and structural (TB-500) regeneration pathways. Anecdotally favoured for tendon and ligament repair where both pathways contribute.

BPC-157: 250–500 mcg SQ · daily
TB-500: 2 mg SQ · 2× per week
Primary benefit: Tendon/ligament/muscle repair via complementary angiogenesis + migration