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

ARA 290vsTB-500

Side-by-side comparison across mechanism, dosage, evidence, side effects, administration, and stack synergies. Citations on every claim where available.

APhase 2HUMAN-REVIEWED17/59 cited
BPhase 2HUMAN-REVIEWED8/46 cited
ARA 290
EPO-Derived Peptide · Innate Repair Receptor Agonist
28 daysPhase 2 durationCulver 2017
Non-erythropoieticSafety profileBrines 2015Liu 2014
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
ARA 290
TB-500
Primary target
Innate repair receptor (EPO receptor / CD131 heterodimer)
G-actin (sequestering) + cell-surface integrinsGoldstein 2012
Pathway
EPO/CD131 → JAK2 activation → PI3K/AKT, MAPK signaling → anti-inflammatory, anti-apoptotic cascades
Actin remodelling → cell migration; integrin-linked signaling → angiogenesis; anti-inflammatory cytokine modulationGoldstein 2012Malinda 1999
Downstream effect
Tissue protection, nerve fiber regeneration, suppression of inflammatory macrophage activation, altered T-cell differentiation (↑Treg, ↑Th2, ↓Th1)Liu 2014Culver 2017
Accelerated wound healing, endothelial migration, hair follicle regeneration, cardiac repair (preclinical)Goldstein 2012
Feedback intact?
N/A — does not interact with hematopoietic EPO receptorLiu 2014
Endogenous protein at baseline; supplementation amplifies
Origin
11-amino-acid sequence from EPO helix B, engineered to eliminate hematopoietic activity while retaining tissue-protective properties
17-AA active fragment of endogenous 43-AA thymosin β4 (TMSB4X gene)Goldstein 2012
Antibody development
Not reported in clinical trials

02Dosage Protocols

Parameter
ARA 290
TB-500
Standard dose (Phase 2)
4 mg / dayBrines 2015Culver 2017
Sarcoidosis SFN and diabetic neuropathy trials.
Frequency
Once daily
Self-administered subcutaneously.
2× per week (loading); then 1× per week (maintenance)
Duration
28 days (Phase 2)Culver 2017
Corneal nerve improvements observed by day 28.
4–8 weeks loading; longer maintenance for chronic injury
Evidence basis
Phase 2 RCTsCulver 2017Brines 2015
64-subject sarcoidosis trial, type 2 diabetes trial.
Animal-strong + Phase 2 dermal/ocular trialsGoldstein 2012
Route
SubcutaneousBrines 2015
Timing
Any time of day
No circadian dependence reported.
Evening or pre-rest preferred (anecdotal)
Standard dose
2 mg per injectionGoldstein 2012
Anecdotal community range; clinical Phase 2 trials used 70–840 mcg/kg IV.
Lower / starter dose
1 mg per injection
Reconstitution
Bacteriostatic water, 1–2 mL per 5 mg vial
Half-life
~2 hours (estimated; tissue uptake longer)

03Metabolic / Fat Loss Evidence

Parameter
ARA 290
TB-500
Primary effect
Improved metabolic control (HbA1c, fasting glucose)Brines 2015
Secondary to neuropathy treatment; direct lipolytic effects not established.
HbA1c
Significant reduction vs placebo
Observed in type 2 diabetes + neuropathy trial.
Fasting glucose
Improved in ARA 290 group
Body composition
Not directly quantified
Fat loss not a primary endpoint; metabolic improvements may reflect insulin sensitivity.

04Side Effects & Safety

Parameter
ARA 290
TB-500
Injection site reaction
Mild, transient
Mild erythema, transient pain
Hematopoiesis
None — non-erythropoietic
Distinguishes ARA 290 from native EPO.
Cardiovascular
No thrombotic events or hypertension reported
Immunogenicity
No antibody formation reported
Tolerability
Well-tolerated in Phase 2 trialsCulver 2017Brines 2015
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
ARA 290
  • ·Hypersensitivity to ARA 290
TB-500
  • ·Active malignancy (theoretical angiogenesis concern)
  • ·Pregnancy / breastfeeding
Relative Contraindications
ARA 290
  • ·Active malignancy (theoretical EPO-axis concern; not observed in trials)
TB-500
  • ·Cancer history
  • ·Concurrent VEGF inhibitor therapy

05Administration Protocol

Parameter
ARA 290
TB-500
1. Preparation
Reconstitute lyophilised powder per manufacturer instructions. Use sterile technique.
Add 1–2 mL bacteriostatic water to 5 mg vial → 2.5–5 mg/mL. Roll gently.
2. Injection site
Subcutaneous — abdomen, thigh, or upper arm. Rotate sites to avoid lipohypertrophy.
SQ near injury site (preferred), or systemic SQ (abdomen). Rotate sites.
3. Timing
Once daily, any time of day. Self-administered in Phase 2 trials.Brines 2015
Evening or pre-sleep is most common anecdotal timing.
4. Dosing
4 mg daily for 28 days (Phase 2 protocol). Duration for chronic use not established.Culver 2017
Lyophilised: room temp, light-protected. Reconstituted: refrigerate, ≤30 days.
5. Storage
Lyophilised: store at controlled room temperature. Reconstituted: refrigerate, use within specified timeframe.
27–31G, 4–8 mm insulin syringe.

06Stack Synergy

ARA 290
+ BPC-157
Moderate
View BPC-157

ARA 290 targets the innate repair receptor (EPO/CD131) for nerve regeneration and anti-inflammatory signaling, while BPC-157 promotes angiogenesis and tissue repair through distinct mechanisms (likely involving VEGF, growth hormone receptor pathways). Combined, they may address both neuroinflammation and structural tissue repair in neuropathy or injury models. No direct clinical data; mechanistic overlap in tissue protection.

ARA 290
4 mg SQ · daily
BPC-157
250–500 mcg SQ · daily
Frequency
Once daily, same or separate injections
Primary benefit
Nerve regeneration, pain reduction, tissue healing
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