About ARA-290
Non-hematopoietic EPO analogue; activates innate repair receptor (IRR/EPOR/CD131 complex) without erythropoietic effects; promotes tissue repair and nerve healing
ARA 290 (cibinetide) is a synthetic 11-amino-acid peptide derived from the helix B region of erythropoietin (EPO), engineered to activate the innate repair receptor (IRR) — a tissue-protective heteroreceptor complex comprising the EPO receptor and the β-common receptor (CD131) — without engaging the classical erythropoietic EpoR homodimer, thereby separating EPO's tissue-protective signaling from its hematopoietic effects. By selectively engaging the IRR rather than the erythropoietic receptor, cibinetide activates anti-inflammatory and anti-apoptotic intracellular pathways in neurons, endothelium, and other metabolically active tissues without causing erythrocytosis, hypertension, or thrombosis, making it a candidate for neuropathy and inflammatory tissue injury contexts. Randomized, double-blind Phase 2 clinical trials have demonstrated that cibinetide improves metabolic control and neuropathic symptom scores in patients with type 2 diabetes, and a separate study demonstrated improved corneal nerve fiber abundance in patients with sarcoidosis-associated small fiber neuropathy — providing human proof-of-concept for both diabetic and inflammatory peripheral neuropathy applications. Cibinetide (ARA 290) is an investigational compound that has not received FDA approval for any indication; Phase 2 data supports further investigation in peripheral neuropathies, but no Phase 3 completion or regulatory filing has occurred as of 2025.
ARA-290 Benefits & Research Areas
Research Signals
Population research notes
These signals reflect research interest areas, not treatment indications.
Regulatory & Evidence
Risk Profile
Generally considered lower risk in research contexts. Risk profile varies by individual — review contraindications before use.
Regulatory Status
- Availability Status
- Research Only
- FDA Status
- Investigational
Non-hematopoietic EPO analog (cibinetide) by Araim Pharma. Phase 3 for sarcoidosis peripheral neuropathy; Dutch conditional marketing authorisation applied for. No FDA approval. Investigational.
Regulatory status reflects publicly available information and may change. This is not legal or medical advice.
Research Sources
3 sources cited · 3 moderate
2 RCTs · 1 Cohort
Immunometabolic dysregulation drives selective executive cognitive dysfunction in male db/db mice.
Neurobiol Dis · 2026
# Summary Research found that ARA-290 improved insulin sensitivity and altered immune cell profiles in diabetic mice, but did not restore impaired executive cognitive flexibility—the selective cognitive deficit observed in the Type 2 diabetes model. This study demonstrated that the cognitive dysfunction associated with diabetes involves chronic inflammation in brain regions like the hippocampus, and that peripheral metabolic improvement alone is insufficient to rescue executive function deficits.
Cibinetide (ARA 290) reduces small nerve fiber pathology in sarcoidosis patients
Investigative Ophthalmology & Visual Science · 2017
Research in a phase 2b randomized trial of 64 sarcoidosis patients with small nerve fiber loss found that cibinetide 4 mg significantly increased corneal nerve fiber area (p=0.012) and improvements correlated with functional gains on the 6-minute walk test, demonstrating nerve regenerative potential for this tissue-protective peptide.
ARA 290, a non-hematopoietic erythropoietin analogue, improves metabolic control and neuropathic symptoms in patients with type 2 diabetes
Molecular Medicine · 2015
In a phase 2 randomized controlled trial, ARA 290 (cibinetide) administered over 28 days improved HbA1c, lipid profiles, PainDetect neuropathy scores, and corneal nerve fiber density in patients with type 2 diabetes, consistent with tissue-protective signaling through innate repair receptors independent of erythropoietic activity.
ARA-290 Side Effects & Safety Considerations
Generally considered lower risk in research contexts. Individual response varies — review all considerations before use.
Reported contraindications & considerations
Consult a qualified healthcare professional before making any health decisions. This information is educational only and does not constitute medical advice.
Where to Buy ARA-290 — Providers & Availability
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Questions to Ask Your Provider
Frequently Asked Questions — ARA-290
ARA 290 (cibinetide) is a synthetic 11-amino-acid peptide derived from the helix B region of erythropoietin (EPO), engineered to activate the innate repair receptor (IRR) — a tissue-protective heteroreceptor complex comprising the EPO receptor and the β-common receptor (CD131) — without engaging the classical erythropoietic EpoR homodimer, thereby separating EPO's tissue-protective signaling from its hematopoietic effects. By selectively engaging the IRR rather than the erythropoietic receptor, cibinetide activates anti-inflammatory and anti-apoptotic intracellular pathways in neurons, endothelium, and other metabolically active tissues without causing erythrocytosis, hypertension, or thrombosis, making it a candidate for neuropathy and inflammatory tissue injury contexts.
neuropathic pain relief, tissue repair, anti-inflammatory, metabolic improvement.
Research on ARA-290 primarily documents effects related to neuropathic pain relief and tissue repair and anti-inflammatory and metabolic improvement. These are areas covered in preclinical and clinical literature — individual response varies and effects depend on context of use.
Reported contraindications and considerations for ARA-290 include active erythrocytosis. This is educational information only — consult a qualified healthcare professional before use.
12 providers in the directory currently offer ARA-290.
# Summary Research found that ARA-290 improved insulin sensitivity and altered immune cell profiles in diabetic mice, but did not restore impaired executive cognitive flexibility—the selective cognitive deficit observed in the Type 2 diabetes model. This study demonstrated that the cognitive dysfunction associated with diabetes involves chronic inflammation in brain regions like the hippocampus, and that peripheral metabolic improvement alone is insufficient to rescue executive function deficits.