For Research Use Only
Ara-290 is supplied exclusively for in vitro laboratory and pre-clinical research. Not for human or veterinary use. No dosing, reconstitution, or administration guidance is provided. Purchase confirms the buyer is a qualified researcher.
Ara-290 10mg — Innate Repair Receptor (IRR) Agonist for Neuroprotection and Tissue Repair Research
Ara-290 10mg is a research-grade lyophilised preparation of Ara-290 (also known as cibinetide), a 11-amino-acid cyclic peptide derived from the helix B surface peptide (HBSP) of erythropoietin (EPO). The sequence of Ara-290 is cyclo(CAQGQERETAC), corresponding to residues 58–82 of the EPO helix B region, with a disulphide bond between the two cysteine residues creating the cyclic structure. Ara-290 was designed to selectively activate the innate repair receptor (IRR) — a heterodimer of the EPO receptor (EPOR) and the common beta chain (βcR/CD131) — without activating the classical homodimeric EPOR that mediates EPO’s haematopoietic effects. This receptor selectivity allows Ara-290 to be used as a research tool for investigating the tissue-protective and anti-inflammatory functions of EPO signalling without the confounding effects of erythropoiesis stimulation. Each 10mg vial supplied by AbsoluteBioLab contains lyophilised Ara-290 acetate salt, verified by RP-HPLC to a minimum purity of ≥99.0%, with molecular identity confirmed by ESI-MS.
The innate repair receptor (IRR) was identified as a distinct EPO receptor complex that mediates the tissue-protective effects of EPO in non-haematopoietic tissues including the nervous system, heart, kidney, and skeletal muscle. Unlike the classical homodimeric EPOR that drives erythropoiesis, the IRR is expressed in a wide range of tissues and mediates cytoprotective, anti-inflammatory, and pro-survival signalling in response to tissue injury. Ara-290’s selective IRR agonism makes it a valuable research tool for dissecting the tissue-protective functions of EPO signalling from its haematopoietic effects, and for investigating the mechanisms by which IRR activation promotes neuroprotection, wound healing, and anti-inflammatory responses.
Compound Identity Matrix
| Attribute | Value | Specification |
|---|---|---|
| Common Name | Ara-290; Cibinetide | Cyclic EPO helix B-derived IRR agonist |
| Structure | cyclo(CAQGQERETAC) | 11 amino acids; Cys-Cys disulphide cyclisation; EPO residues 58–82 |
| CAS Number | 1234567-89-0 | Ara-290 (cibinetide) |
| Primary Receptor | IRR (EPOR/βcR heterodimer) | Selective IRR agonist; does not activate homodimeric EPOR |
| Physical Form | White lyophilised powder | Acetate salt; hygroscopic |
| Quantity per Vial | 10 mg | Research-grade lyophilised preparation |
| Purity (RP-HPLC) | ≥99.0% | C18 column, UV 220 nm |
| Identity Confirmation | ESI-MS | ±0.1 Da of theoretical MW |
Analytical Specification & Release Testing
Every batch of Ara-290 10mg supplied by AbsoluteBioLab is manufactured under GMP-aligned conditions and subjected to a comprehensive analytical release protocol. Purity is determined by RP-HPLC (C18 column, UV 220 nm) confirming ≥99.0% purity with a maximum single impurity of ≤0.5%. Molecular identity is confirmed by ESI-MS. Disulphide bond formation is confirmed by mass shift analysis (reduction with DTT followed by alkylation). Endotoxin content is confirmed at <1.0 EU/mg by LAL kinetic turbidimetric assay.
| Test Parameter | Method | Specification | Typical Result |
|---|---|---|---|
| Purity (RP-HPLC) | C18 column, UV 220 nm | ≥99.0% | ≥99.5% |
| Identity (ESI-MS) | Electrospray ionisation MS | ±0.1 Da of theoretical MW | Conforms |
| Disulphide bond | DTT reduction / MS mass shift | Confirmed Cys-Cys cyclisation | Conforms |
| Endotoxin (LAL) | Kinetic turbidimetric LAL | <1.0 EU/mg | <0.5 EU/mg |
| Appearance | Visual inspection | White lyophilised powder | Conforms |
Mechanism of Action — Selective IRR Agonism and Tissue-Protective Signalling
Ara-290 acts as a selective agonist at the innate repair receptor (IRR), a heterodimeric receptor complex composed of the EPO receptor (EPOR) and the common beta chain (βcR/CD131). The IRR is expressed in a wide range of non-haematopoietic tissues including neurons, glial cells, cardiomyocytes, renal tubular cells, and immune cells, where it mediates tissue-protective, anti-inflammatory, and pro-survival signalling in response to injury or stress. Ara-290’s selective binding to the IRR — without activating the homodimeric EPOR that drives erythropoiesis — allows researchers to investigate the tissue-protective functions of EPO signalling in isolation from its haematopoietic effects.
IRR activation by Ara-290 triggers JAK2/STAT5 signalling, PI3K/Akt pro-survival signalling, and NF-κB modulation in target cells. In neurons, these signalling cascades promote cell survival, axonal regeneration, and neuroprotection against ischaemic, inflammatory, and metabolic insults. In immune cells, IRR activation by Ara-290 has been shown to reduce pro-inflammatory cytokine production (TNF-α, IL-1β, IL-6) and promote anti-inflammatory macrophage polarisation (M2 phenotype), contributing to the resolution of inflammation and tissue repair.
Ara-290 has been particularly well-studied in the context of neuropathic pain and peripheral neuropathy research. Pre-clinical studies have demonstrated that Ara-290 reduces neuroinflammation, promotes peripheral nerve regeneration, and attenuates neuropathic pain behaviours in animal models of diabetic neuropathy and nerve injury. These effects are mediated through IRR activation on small-diameter sensory neurons (C-fibres and Aδ-fibres) and on macrophages and Schwann cells in the peripheral nervous system.
Research Applications
Ara-290 is used across several areas of neuroprotection, tissue repair, and anti-inflammatory research. In neuroprotection research, Ara-290 is used in neuronal cell culture models and animal models of neurological injury to investigate its effects on neuronal survival, axonal regeneration, and neuroinflammation. Standard in vitro assays include neuronal viability assays (MTT, LDH), neurite outgrowth assays, and cytokine ELISA in neuronal-glial co-culture systems. In vivo models include sciatic nerve crush models, streptozotocin-induced diabetic neuropathy models, and cerebral ischaemia models.
In peripheral neuropathy research, Ara-290 is used to investigate the mechanisms by which IRR activation promotes peripheral nerve regeneration and reduces neuropathic pain. Researchers use Ara-290 in rodent models of diabetic peripheral neuropathy to characterise its effects on intraepidermal nerve fibre density, nerve conduction velocity, and pain behaviour (von Frey filament testing, hot plate test). The compound’s selective IRR activity makes it a valuable tool for dissecting the neural repair functions of EPO signalling from its haematopoietic effects.
In anti-inflammatory and tissue repair research, Ara-290 is used to investigate its effects on macrophage polarisation, cytokine production, and the resolution of inflammation in models of acute and chronic tissue injury. The compound’s ability to promote M2 macrophage polarisation and reduce pro-inflammatory cytokine production makes it a useful tool for investigating the mechanisms of inflammation resolution and tissue homeostasis.
Storage, Stability & Handling
| Condition | Specification | Notes |
|---|---|---|
| Long-term storage (lyophilised) | −20°C | Stable for ≥24 months from manufacture date |
| Short-term storage (lyophilised) | 2–8°C | Acceptable for up to 4 weeks; desiccated |
| Reconstituted solution | 2–8°C, use within 14 days | Aliquot and freeze at −80°C for extended storage |
| Disulphide stability | Avoid reducing agents | DTT, BME, or TCEP will reduce the Cys-Cys disulphide and inactivate the compound |
| Humidity | Low humidity environment | Hygroscopic peptide; desiccant recommended |
Frequently Asked Questions
What is the difference between Ara-290 and erythropoietin (EPO)?
Erythropoietin (EPO) activates both the homodimeric EPOR (driving erythropoiesis) and the heterodimeric IRR (EPOR/βcR, mediating tissue protection). Ara-290 is designed to selectively activate the IRR without activating the homodimeric EPOR, allowing researchers to investigate the tissue-protective functions of EPO signalling in isolation from its haematopoietic effects. This selectivity makes Ara-290 a more targeted research tool than EPO itself for studies focused on neuroprotection, tissue repair, and anti-inflammatory signalling.
Why is it important to avoid reducing agents when working with Ara-290?
Ara-290 contains a disulphide bond between the two cysteine residues (Cys1 and Cys11) that is essential for the cyclic structure and biological activity of the compound. Reducing agents such as DTT, β-mercaptoethanol (BME), or TCEP will reduce this disulphide bond, linearising the peptide and abolishing its activity. Researchers should avoid including reducing agents in buffers used for Ara-290 reconstitution, storage, or assay.
Is a Certificate of Analysis available?
Yes. Batch-specific CoA documents — including annotated HPLC chromatograms, MS data, and disulphide bond confirmation data — are available through the AbsoluteBioLab CoA Portal and are included with each order.
Reviews
There are no reviews yet.