ARA-290
ARA-290 (cibinetide) is an erythropoietin-derived peptide engineered to promote nerve and tissue repair without erythropoietin's blood-producing side effect — one of the more clinically advanced compounds referenced on this site, despite not being part of KYIN's standard catalogue.
Not currently stocked, but available to order — see availability below.
What Is ARA-290?
ARA-290 is an 11-amino-acid peptide derived from the helix-B surface of erythropoietin (EPO) — the hormone best known for stimulating red blood cell production. Rather than acting through EPO's classic receptor pathway, ARA-290 was deliberately engineered to selectively activate a different target: the “innate repair receptor,” a heteromeric complex formed by the EPO receptor and CD131. This receptor is expressed on nerve, glial, and endothelial cells under conditions of stress or injury, which is why ARA-290's research has focused on nerve regeneration and tissue protection rather than blood production.
Mechanism & Research Focus
By selectively engaging the innate repair receptor while avoiding the classic EPO receptor pathway, ARA-290 avoids the erythropoietic side effects (increased red blood cell counts) that limit therapeutic use of EPO itself. This selectivity has pushed ARA-290's research toward small-fiber nerve regeneration and neuropathic pain — a mechanism distinct from the gastric-, actin-, and copper-based repair pathways studied for compounds like BPC-157, TB-500, and GHK-Cu, but conceptually adjacent as tissue-protective, anti-inflammatory research. See our Healing & Recovery research overview for how it fits alongside KYIN's stocked recovery-focused peptides.
Clinical & Preclinical Trial Data
Development of ARA-290 is further along than most compounds referenced on this site. A Phase 2 randomized, double-blind pilot trial (Dahan et al., Molecular Medicine, 2013; 36 sarcoidosis patients with small-fiber neuropathy) found ARA-290 significantly improved neuropathic pain scores and increased corneal nerve fiber density, a structural marker of nerve regeneration. A follow-up Phase 2b trial (Culver et al., Investigative Ophthalmology & Visual Science, 2017; n=64) replicated the corneal nerve fiber finding and additionally found increased regenerating intraepidermal nerve fibers. A separate 2015 trial in type 2 diabetes patients (4mg/day for 28 days) reported reduced neuropathic symptom scores alongside secondary reductions in HbA1c that persisted through a 56-day observation period.
No Phase 3 trial was initiated, and development stalled after the compound's sponsor, Araim Pharmaceuticals, shut down. ARA-290 holds FDA orphan drug status for neuropathic pain in sarcoidosis but has not received full FDA approval for any indication.
Availability
ARA-290 is not part of KYIN Peptides' standard catalogue, but it is available to order — contact us directly and we'll source it for you.
ARA-290 questions
What is ARA-290?
ARA-290 (cibinetide) is an 11-amino-acid peptide derived from the helix-B surface of erythropoietin, engineered to selectively activate the “innate repair receptor” — a heteromeric complex of the EPO receptor and CD131 — without triggering red blood cell production.
Does ARA-290 raise red blood cell counts like erythropoietin?
No. ARA-290 was specifically engineered to activate only the innate repair receptor found on nerve, glial, and endothelial cells, without engaging the classic EPO receptor pathway responsible for red blood cell production.
What has ARA-290 been studied for?
Primarily small-fiber nerve regeneration and neuropathic pain. Human trials have covered sarcoidosis-associated small-fiber neuropathy and type 2 diabetes-related neuropathic symptoms, with corneal and intraepidermal nerve fiber density used as structural markers of nerve regeneration.
Does KYIN Peptides sell ARA-290?
Not as part of our standard catalogue, but yes — it's available to order. Contact us directly and we'll source it for you.
Interested in sourcing ARA-290?
Contact us and we'll help you source it, or browse our stocked recovery-focused peptides.