ARA-290 is a healing & repair research compound currently in stock directly from a verified Chinese manufacturer. Every batch is HPLC-verified and shipped with a Certificate of Analysis (COA). Sourcing is direct — no intermediaries. Minimum order value is $600 USD. International shipping available.
ARA-290, also known by the INN cibinetide, is a synthetic cyclic peptide derived from the helix B surface region of erythropoietin (EPO). Unlike full-length EPO — which stimulates erythropoiesis through homodimeric EPO receptor (EPOR) signalling — ARA-290 is designed to selectively activate the Innate Repair Receptor (IRR), a heterodimer of EPOR and the beta common receptor (βcR, CD131). This receptor complex is expressed in injured and stressed tissues including peripheral neurons, immune cells, and metabolic organs, but is absent from erythroid progenitors. Consequently, ARA-290 produces tissue-protective and anti-inflammatory effects without erythropoietic side effects — haematocrit, platelet count, and thromboembolic risk remain unaffected at research doses.
The majority of published preclinical research on ARA-290 addresses peripheral neuropathy, metabolic disorders, and inflammation. In rodent models of diabetic peripheral neuropathy (streptozotocin-induced diabetes), ARA-290 administration restores intraepidermal nerve fibre density and improves nerve conduction velocity — endpoints used in translational small fibre neuropathy research. Phase II clinical trials in sarcoidosis-associated small fibre neuropathy documented improvements in pain scores and corneal nerve fibre density (measured by confocal microscopy). The IRR-mediated mechanism involves activation of Akt and STAT3 survival pathways in sensory neurons, suppression of NF-κB-mediated neuroinflammation, and induction of neurotrophic factor expression in Schwann cells.
PeptidesFromChina.co supplies ARA-290 as lyophilized powder at ≥98% purity, verified by HPLC and confirmed by mass spectrometry. Certificates of Analysis available per batch. Wholesale quantities on request. For laboratory research use only.
| Chemical Class | EPO-derived Cyclic Peptide / IRR Agonist |
|---|---|
| INN | Cibinetide |
| CAS Number | 1160528-96-4 |
| Molecular Weight | ~1096 Da |
| Peptide Origin | Helix B surface of erythropoietin (EPO) |
| Receptor Target | IRR (EPOR/βcR heterodimer); not homodimeric EPOR |
| Key Feature | Non-erythropoietic — no haematopoietic activity at research doses |
| Synonyms | Cibinetide, ARA 290, Helix B Surface Peptide |
| Storage | -20°C lyophilized; 4°C reconstituted (up to 14 days) |
| Molecular Formula | N/A — 11-aa EPO helix B peptidomimetic; see COA |
| Sequence | HBSSLRALGAQ (modified; exact sequence on COA) |
| Name | Strength | Pack Size | Purity | Availability | Price (USD) |
|---|---|---|---|---|---|
| ARA-290 | 10 mg | 10 vials | ≥98% | In Stock | $82.00 |
Testing method: HPLC / LC-MS. Every batch is tested before shipment. Purity ≥99% confirmed per batch.
Certificate of Analysis (COA) is included with every order. Documentation covers purity, molecular weight, and batch identification.
ARA-290's primary studied application is in peripheral neuropathy, particularly models of small fibre neuropathy where intraepidermal nerve fibres (IENFs) are reduced. In streptozotocin (STZ)-diabetic rat models, ARA-290 restores IENF density and improves hot plate latency (thermal nociception) and nerve conduction velocity measurements — the standard preclinical endpoints for diabetic peripheral neuropathy. Dorsal root ganglion (DRG) neuron survival assays using primary DRG cultures under glucose toxicity conditions confirm dose-dependent neuroprotection via PI3K/Akt signalling. The βcR co-receptor is confirmed as required for this effect using βcR-knockout fibroblast and DRG models.
IRR activation by ARA-290 in macrophages and dendritic cells suppresses LPS-induced TNF-α, IL-6, and IL-12 production while modestly upregulating IL-10. Mechanistic studies using NF-κB reporter cell lines confirm that IRR agonism attenuates p65 nuclear translocation and IκB kinase activity. In animal models of endotoxaemia (LPS-challenged rodents), ARA-290 reduces cytokine storm markers and improves survival in dose-response studies. This anti-inflammatory profile is studied in the context of tissue protection in ischaemic, metabolic, and autoimmune injury models — all contexts where IRR-mediated inflammation suppression may play a cytoprotective role.
βcR is expressed in pancreatic beta-cells and adipocytes, implicating the IRR in metabolic regulation. Preclinical studies in high-fat diet (HFD) and STZ-diabetic rodent models show ARA-290 treatment associated with improved glucose tolerance, reduced fasting insulin, and improved HOMA-IR — measured by glucose tolerance tests (GTT) and insulin tolerance tests (ITT). Beta-cell survival assays (TUNEL staining in pancreatic sections, INS-1 cell apoptosis under glucolipotoxic conditions) show ARA-290's protective effects on beta-cell viability. These findings situate ARA-290 within the broader research on tissue-protective EPO axis signalling in metabolic disease.
Phase II clinical trials investigated ARA-290 in sarcoidosis-associated small fibre neuropathy — a condition characterised by corneal nerve loss and chronic neuropathic pain. The ESSN trial documented statistically significant improvements in corneal confocal microscopy nerve fibre density and reductions in autonomic and neuropathic pain scores versus placebo. Preclinical murine models of sarcoid granuloma formation and peripheral nerve involvement use ARA-290 to characterise the contribution of IRR-mediated neuroinflammation suppression to granuloma resolution and nerve fibre preservation. These models bridge basic IRR pharmacology with a defined clinical research indication.
Erythropoiesis is driven by EPO binding to a homodimeric EPOR complex on erythroid progenitors. ARA-290 is derived from the helix B surface of EPO — a region that does not engage the homodimeric EPOR binding site but does bind the Innate Repair Receptor (IRR), which is an EPOR/βcR heterodimer expressed in non-erythroid tissues. Because ARA-290 lacks the structural features required for homodimeric EPOR activation, it does not stimulate erythroid colony formation or elevate haematocrit in preclinical models at doses producing tissue-protective effects.
Target specificity is confirmed using βcR-knockout cell models (MEFs, macrophages, DRG neurons) where ARA-290's protective and anti-inflammatory effects are abolished — demonstrating that intact βcR is required for activity. Co-immunoprecipitation and proximity ligation assays confirm EPOR/βcR heterodimer formation in responsive non-erythroid cell types. Anti-βcR blocking antibodies in wild-type cells also attenuate ARA-290's effects, further validating the IRR as the pharmacological target.
Standard formats include: (1) DRG neuron survival assays under glucolipotoxic conditions (glucose + palmitate) with TUNEL and NeuN staining; (2) LPS-stimulated macrophage cytokine secretion assays (TNF-α, IL-6 ELISA); (3) NF-κB reporter assays in THP-1 or RAW264.7 cells; (4) corneal epithelial cell scratch-wound healing assays for nerve fibre regeneration modelling; (5) INS-1 or MIN6 beta-cell apoptosis assays. Working concentrations typically range from 1–100 nM.
Yes. ARA-290 is available through PeptidesFromChina.co on a B2B wholesale basis. Pricing and minimum order quantities are provided on request after account verification. Contact us via the Request page.
For laboratory research use only. Not for human or veterinary use. PeptidesFromChina.co is a B2B wholesale supplier operating under strict research-use-only terms. All products are sold exclusively for in vitro and preclinical research purposes.