ARA-290
clinical trialsAlso known as: Cibinetide
**Mechanism of Action** ARA-290 (cibinetide) is an 11-amino-acid peptide derived from the helix B domain of erythropoietin (EPO). It selectively binds the heterodimeric innate repair receptor (IRR), composed of the erythropoietin receptor (EPOR) and the β common receptor (CD131). This interaction activates tissue-protective and anti-inflammatory signaling pathways (e.g., PI3K/Akt, STAT3) without engaging the homodimeric EPOR, thereby avoiding erythropoiesis and associated thrombotic risks. The peptide primarily targets endothelial cells, neurons, and immune cells, promoting cytoprotection, angiogenesis, and resolution of inflammation. **Key Research Findings** In preclinical models, ARA-290 demonstrated efficacy in reducing neuropathic pain, improving wound healing, and attenuating ischemia-reperfusion injury. Clinical trials (Phase I–II) have shown significant reductions in pain scores and nerve fiber regeneration in patients with sarcoidosis-associated small fiber neuropathy. Additional studies reported improved cognitive function in type 2 diabetes and enhanced corneal nerve density in diabetic neuropathy. The peptide also reduced markers of systemic inflammation (e.g., TNF-α, IL-6) and oxidative stress in human trials. No serious adverse events related to erythropoiesis or hypertension were observed. **Clinical Relevance** ARA-290 is under investigation for chronic inflammatory and neuropathic conditions, including sarcoidosis, diabetic neuropathy, and post-surgical pain. Its ability to promote tissue repair without hematopoietic side effects positions it as a safer alternative to EPO for non-anemic indications. Ongoing Phase II/III trials are evaluating long-term safety and efficacy in diabetic kidney disease and chemotherapy-induced peripheral neuropathy. For research purposes only — not medical advice.
Key data
C51H84N16O21Research & studies
ARA 290 early treatment decelerated Aβ pathology and improved cognitive functions in young APP/PS1 mice.; ARA 290 increased total monocytes by stimulating generation of Ly6C Low patrolling subset, reducing brain Aβ burden.; ARA 290 was ineffective in aged APP/PS1 mice with advanced pathology and in chimeric mice with depleted patrolling monocytes.; The study suggests ARA 290 prevents AD-like progression via monocyte modulation, specifically increasing patrolling monocytes.
Radiolabeling purity exceeded 96% with in vitro stability of 85% up to 6 hours.; Binding of 99mTc-ARA-290 to hypoxic cells was 3 times higher than to normoxic cells at 1 hour.; SPECT imaging in cardiac ischemic rats showed a cardiac ischemic-to-lung ratio of 3.65 ID/g% at 0.5 hours.; The radiopeptide is a promising candidate for early diagnosis of cardiac ischemia.
Eight studies met inclusion criteria, evaluating infliximab, adalimumab, ARA 290, methylphenidate, armodafinil, and exercise programs.; Anti-TNF therapies (adalimumab, infliximab) and neurostimulants (methylphenidate, armodafinil) showed some evidence of treatment effect.; Five studies had high risk of bias in most domains; the remaining three had small sample sizes and short duration.; Trial evidence for treating sarcoidosis-associated fatigue is limited and requires further investigation.
ARA 290 protected pancreatic islets from cytokine-induced damage and apoptosis in vitro.; ARA 290 significantly inhibited secretion of pro-inflammatory cytokines (IL-6, IL-12, TNF-α) from macrophages.; ARA 290 treatment improved blood glucose levels after marginal islet transplantation in diabetic mice.; ARA 290 suppressed upregulation of MCP-1, MIP-1α, IL-1β, and IL-6 mRNA in the liver post-transplantation.
ARA 290 specifically inhibits TRPV1 channel activity.; ARA 290 relieves capsaicin-induced mechanical hypersensitivity.; ARA 290 may function as a novel TRPV1 channel antagonist.; The findings suggest integration between immune system and peripheral nervous system in pain modulation.
EPO's tissue-protective effects are mediated by the IRR (EPOR/cR heterodimer), not the EPOR homodimer responsible for erythropoiesis.; The IRR is induced by injury or inflammation and is not typically expressed in normal tissues.; pHBSP (ARA-290) is an 11-amino acid peptide modeled from EPO's helix B region that selectively activates the IRR.; Despite a ~2-minute plasma half-life, pHBSP produces long-lasting biological effects via a molecular switch mechanism.
Frequently asked questions
What is ARA-290?
**Mechanism of Action** ARA-290 (cibinetide) is an 11-amino-acid peptide derived from the helix B domain of erythropoietin (EPO). It selectively binds the heterodimeric innate repair receptor (IRR), composed of the erythropoietin receptor (EPOR) and the β common receptor (CD131). This interaction activates tissue-prote
How does ARA-290 work?
Erythropoietin-derived 11-aa peptide targeting the innate repair receptor (EPOR/CD131) for tissue protection without erythropoiesis.
What is the research status of ARA-290?
ARA-290 is currently classified as clinical trials, with 23 research references on record. This is for research purposes only and is not medical advice.
What is the molecular weight of ARA-290?
ARA-290 has a molecular weight of approximately 1257.3 g/mol (formula C51H84N16O21).
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