ARA-290

Where ARA-290 comes from.

ARA-290, also called cibinetide, is a synthetic 11-amino-acid peptide derived from the helix B region of the erythropoietin (EPO) protein. The native EPO protein is 165 amino acids long and is the principal regulator of red blood cell production through its action at the EPO receptor on bone-marrow erythroid progenitor cells. The published research that led to the development of ARA-290 identified that the tissue-protective effects of EPO observed in non-haematopoietic tissues operate through a different receptor (the innate repair receptor, IRR) than the canonical EPO receptor responsible for haematopoiesis.

The peptide was developed in the 2000s by a research group at the Feinstein Institute of Medical Research and at Araim Pharmaceuticals to dissociate the tissue-protective IRR-mediated activity of EPO from its haematopoietic receptor activity. The 11-residue helix B fragment retains binding to the IRR but does not engage the canonical EPO receptor, producing a research compound that probes the IRR pathway selectively. The peptide is built by Fmoc solid-phase peptide synthesis, purified by reversed-phase HPLC, and freeze-dried.

PubMed lists roughly 60 papers mentioning ARA-290 or cibinetide as of 2026. The published research is concentrated in animal models of neuropathy and tissue protection, with a smaller body of clinical work in neuropathic-pain research. The compound has been the subject of phase-two clinical investigation; the research-supply form is identical in sequence to the investigational pharmaceutical product but is supplied for laboratory research only.

What the research looks at.

ARA-290 mechanism research starts from the innate repair receptor (IRR), a heteromeric receptor complex composed of the EPO receptor and the common beta receptor (CD131). The IRR is expressed on non-haematopoietic tissues including neurons, vascular endothelium, and immune cells. Published cell-culture studies have characterised ARA-290 binding and signalling at the IRR, distinguishing it from the canonical EPO receptor that mediates haematopoiesis.

A second strand of research has examined the peptide in animal models of neuropathy. Published studies in chemotherapy-induced peripheral neuropathy and diabetic neuropathy models measure neurological endpoints, electrophysiological markers, and tissue-level inflammatory and apoptotic markers. The literature describes the peptide as producing tissue-protective effects through the IRR pathway, with the absence of haematopoietic activity confirmed by haematocrit measurements in the same animal designs.

"The dissociation of tissue-protective activity from haematopoietic activity is the defining feature of ARA-290 in the published research and is the reason for its development as a research tool."

A third line of research has examined the peptide in inflammatory-pathway contexts. Published cell-culture and animal studies measure inflammatory-cytokine production, immune-cell infiltration, and tissue-injury markers in inflammatory-disease model systems. The literature describes the IRR pathway as producing anti-inflammatory and tissue-protective effects through mechanisms distinct from the broader anti-inflammatory pharmacology of corticosteroids or NSAIDs.

Where the published research does not go in the research-supply context: laboratory research does not extend to administration to humans, off-label clinical use, or any therapeutic application. ARA-290 has been the subject of phase-two clinical investigation but has not advanced to product approval. The research-supply form is supplied for laboratory research only.