Ara 290 (Cibinetide)
Tissue-Protective Peptide · Innate Repair Receptor Agonist
Overview
Ara 290 is an engineered 11-amino acid peptide activating the Innate Repair Receptor (IRR) to provide tissue-protective effects without red blood cell stimulation. Has FDA Orphan Drug status.
Activates IRR through EPOR/β-common receptor complex, triggering tissue-protective signaling without erythropoietic effects.
23% increase in corneal nerve fiber area with sustained pain improvement.
Nerve regeneration and metabolic improvements in Type 2 diabetes patients.
Crosses blood-brain barrier for stroke and TBI neuroprotection.
Improves epithelialization and angiogenesis via VEGF upregulation.
Mechanism
Ara 290 is an engineered 11-amino acid peptide activating the Innate Repair Receptor (IRR) to provide tissue-protective effects without red blood cell stimulation. Has FDA Orphan Drug status.
Activates IRR through EPOR/β-common receptor complex, triggering tissue-protective signaling without erythropoietic effects.
23% increase in corneal nerve fiber area with sustained pain improvement.
Research areas
- Ara 290 is an engineered 11-amino acid peptide activating the Innate Repair Receptor (IRR) to provide tissue-protective effects without red blood cell stimulation. Has FDA Orphan Drug status.
- Activates IRR through EPOR/β-common receptor complex, triggering tissue-protective signaling without erythropoietic effects.
- 23% increase in corneal nerve fiber area with sustained pain improvement.
- Nerve regeneration and metabolic improvements in Type 2 diabetes patients.
- Crosses blood-brain barrier for stroke and TBI neuroprotection.
- Improves epithelialization and angiogenesis via VEGF upregulation.
- Reduces infarct size in myocardial infarction models.
- Maintains cardiac function in aging models.
- Reduces TNF-α, IL-6, and IL-12 production.
- Reduces colitis severity in animal models.
- Improves graft survival and reduces rejection.
Research notes
- Excellent safety profile in clinical trials with no serious drug-related adverse events
- Severe injection site reactions
- Unexpected blood count changes
- Allergic reaction signs
- Worsening of underlying condition
- New neurological symptoms
- Any serious adverse events
- Recent anti-TNF therapy (within 6 months)
- EPO use (within 2 months)
- Pregnancy
- BMI > 34 kg/m²
References
- pubmed.ncbi.nlm.nih.gov/21545288/
- pubmed.ncbi.nlm.nih.gov/32674280/
- pubmed.ncbi.nlm.nih.gov/28475703/
- pubmed.ncbi.nlm.nih.gov/25387363/
- pubmed.ncbi.nlm.nih.gov/18676614/
FAQs
How does Ara-290 differ from erythropoietin (EPO) for neuroprotection?
Ara-290 is an engineered 11-amino acid peptide derived from EPO structure that activates the Innate Repair Receptor (IRR) without triggering erythropoiesis. It provides tissue protection and nerve regeneration like EPO but without red blood cell stimulation, polycythemia risk, or thrombotic complications.
What's the timeline for nerve regeneration with Ara-290 in diabetic neuropathy?
Phase 2 trials showed 23% increase in corneal nerve fiber area at 4mg daily for 28 days, with sustained pain improvements. Nerve fiber regeneration markers appeared within weeks 2-4, with peak therapeutic effects and maximum improvements by week 4-6. Benefits persist via molecular switch effects through month 2-6.
Can I combine Ara-290 with other neuroprotective peptides like BPC-157?
Yes. BPC-157 and Ara-290 target complementary tissue repair pathways with no known direct interactions. TB-500 is also synergistic. These combinations likely enhance recovery from injury, though clinical data on simultaneous use doesn't exist.
Why must I avoid anti-TNF biologics or recent EPO use before starting Ara-290?
Anti-TNF therapy requires 6-month washout before Ara-290 due to immune interaction risks. EPO use requires 2-month washout because both target related receptor pathways. These washout periods prevent unpredictable receptor interference and potential adverse immune effects from concurrent use.