ARA-290

ARA-290 (also known as Cibinetide) is a synthetic 11-amino acid peptide derived from the helix-B domain of erythropoietin (EPO). It selectively activates the Innate Repair Receptor (IRR), a heterodimeric complex of the erythropoietin receptor (EPOR) and beta-common receptor (CD131), providing tissue-protective and anti-inflammatory effects without stimulating red blood cell production. Research focuses on neuroprotection, nerve regeneration, pain modulation, and metabolic regulation. For research use only.

Research Grade

Price range: $54.00 through $90.00

Confirm compounded formula & unique dosing are necessary for the patient

Research Profile

At a Glance

  • Type: Synthetic EPO-Derived Peptide (Helix-B Domain)
  • Also Known As: Cibinetide
  • Sequence: QEQLERALNSS (11 amino acids)
  • Molecular Weight: 1,257.3 Da
  • Primary Target: Innate Repair Receptor (EPOR/CD131 heterodimer)
  • Research Focus: Neuroprotection, nerve regeneration, anti-inflammatory, pain modulation
  • Regulatory Status: RUO (Research Use Only); FDA Orphan Drug Designation for sarcoidosis-induced neuropathic pain
  • Categories: Neuropathy Research; Inflammation Research; Tissue Repair; Metabolic Research

What Research Shows

  • Activates the Innate Repair Receptor (IRR) to reduce key inflammatory cytokines (TNF-α, IL-1β, IL-6) and suppress NF-κB signaling, supporting investigation into tissue protection and anti-inflammatory mechanisms.
  • Demonstrates neuroprotective effects in preclinical and human studies, including improvements in corneal nerve fiber density and reductions in neuropathic pain symptoms associated with small-fiber nerve damage.
  • Protects endothelial and microvascular systems in experimental models, reducing vascular leakage, supporting nitric-oxide–related vasodilation, and improving microcirculatory function after inflammatory or ischemic stress.
  • Enhances cellular survival and reduces tissue injury during ischemia/reperfusion events, indicating a potential role in research focused on organ and tissue recovery.
  • Shows exploratory benefits in autoimmune and systemic inflammatory conditions, with early studies noting reductions in inflammatory markers and symptom burden, though findings remain preliminary.

Mechanistic Notes

ARA-290’s activity centers on selective Innate Repair Receptor activation:
Core Mechanisms
  • Binds to the Innate Repair Receptor (IRR) – a heterodimer of EPOR and CD131 (β-common receptor)
  • Does NOT activate the EPOR homodimer responsible for erythropoiesis
  • Triggers anti-apoptotic and pro-survival signaling cascades
  • Reduces pro-inflammatory cytokines (TNF-α, IL-6)
  • Shifts immune cells toward repair phenotypes
Why ARA-290 Is Distinct from EPO
  • No stimulation of red blood cell production (no hematocrit increase)
  • No cardiovascular risks associated with EPO therapy (thrombosis, hypertension)
  • Selectively targets tissue repair pathways upregulated during injury
  • Well-tolerated safety profile in Phase II clinical trials
Downstream Effects Observed in Research
  • Promotes neurite outgrowth and nerve fiber regeneration
  • Enhances angiogenesis and microvascular function
  • Reduces oxidative stress and ischemic damage
  • Blocks TRPV1 channels for direct pain modulation
  • Suppresses spinal microglia response in neuropathic pain models

What Remains Unknown

  • Optimal dosing protocols for different research applications
  • Long-term durability of nerve regeneration effects
  • Full scope of IRR-mediated signaling pathways
  • Comparative efficacy across different neuropathy models
  • Potential synergistic effects with other neuroprotective compounds
  • All findings are research-only and preliminary.