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.

For ARA-290, its FDA status is investigational (not FDA-approved), and it is designated for research use only. Regulatory status reflects publicly available information and may change. This is not legal or medical advice.

14 providers in the directory currently offer ARA-290.

Across 27 research vendors tracked on PeptideBase, ARA-290 has a median price of about $4.34 per mg, typically ranging $3.34–$5.00 per mg. This reflects research-use vendor pricing, not clinical or prescription costs.

# 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.