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Free U.S. shipping on orders over $150ARA 290, also known as Cibinetide, is a synthetic peptide derived from the structure of erythropoietin (EPO) but engineered to exclude EPO’s hematopoietic, red-blood-cell–stimulating effects [1].
Instead, ARA 290 selectively targets the innate repair receptor (IRR), a heteromeric EPOR/CD131 complex involved in cellular protection, inflammatory resolution, and tissue homeostasis [2].
By isolating the non-erythropoietic region of the EPO molecule, researchers created a peptide that retains EPO’s cytoprotective and pro-repair signaling without impacting hematocrit or erythropoiesis.
As a result, ARA 290 has gained significant attention as a research peptide used to study pathways related to cellular stress, microvascular function, and immune modulation.
ARA 290 has been studied for its influence on nerve integrity and health. Its activity centers on the innate repair receptor (IRR), a heteromeric EPOR/CD131 complex that becomes activated in response to cellular stress [2, 3].
IRR activation has been shown to modulate inflammatory cascades that contribute to neuronal hypersensitivity.
A Phase 2 RCT in adults with type 2 diabetes and painful small-fiber neuropathy evaluated whether ARA 290 can mitigate neuropathic pain [1].
This study followed a parallel timeline, where 48 participants first received ARA 290 4 mg subcutaneously (SC) daily for 28 days, or matched placebo, followed by 28 days of observation.
Results showed that ARA 290:
There were minimal significant adverse events, and no anti–ARA 290 antibodies detected.
These findings support ARA 290 as a potential disease-modifying agent for diabetic small-fiber neuropathy, with benefits extending to widespread metabolic regulation.
Similar neuroprotective effects of ARA290 have been found in models of radiation induced injury and peripheral nerve damage [4, 5].
Beyond its effects on neural pathways, ARA 290 has been investigated for its influence on metabolic and cardiovascular homeostasis through its selective activation of the innate repair receptor (IRR).
A randomized, controlled preclinical trial determined whether ARA290 could affect cardiac aging and function in 48 advanced-age Fischer x Brown Norway rats [6].
Rats were assigned to chronic ARA 290 or saline control from 18-33 months of age.
Results showed that ARA 290 administration:
Long-term administration of ARA290 attenuates multiple hallmarks of cardiac aging. By preserving cardiomyocyte function, ARA290 appears to extend healthspan and mitigate the systemic decline associated with advanced age.
ARA 290 plays a distinct role in immune modulation and tissue recovery through the activation of the IRR pathway, among others.
ARA290 activation influences macrophage polarization, encouraging a shift from pro-inflammatory M1 macrophages toward M2 macrophages that facilitate debris clearance, extracellular matrix organization, and overall tissue restoration [7].
An in vitro preclinical study evaluated whether using an elastin-like peptide (ELP) fusion can increase stability of ARA290 and enhance wound healing in a full-thickness diabetic wound model [8].
After establishing that ELP fusion preserved biological activity, results showed that:
Fusing ARA290 to elastin-like peptide generates stable, proteolytically resistant, bioactive therapeutics suitable for the harsh environment of chronic diabetic wounds.
ARA290 has also shown efficacy in non-diabetic injury models, including ischemic/reperfusion injury in kidney models and surface burns [9, 10]
Research Use Only. All findings described above are derived from preclinical studies (animal models and in vitro experiments). ARA290 is not approved by the FDA for any diagnostic or therapeutic use in humans. Genesis Peptides makes no claims regarding human clinical efficacy. This product is sold exclusively for laboratory research.
Every lot undergoes six independent assays before release. Results are published in the lot-specific Certificate of Analysis.
ARA 290, also called cibinetide, is an 11-amino acid linear nonhematopoietic peptide derived from the three-dimensional structure of helix B of erythropoietin (EPO). It is described as a prolonged peptide derived from erythropoietin and as an alternative to erythropoietin. ARA 290 is described as interacting selectively with the innate repair receptor (IRR), which arbitrates tissue protection. It is described as mediating tissue protection by reducing inflammation and fibrosis.
ARA 290, also called cibinetide, is a non-hematopoietic derivative of erythropoietin (EPO) that selectively activates the innate repair receptor (IRR). The cited studies describe its effects as tissue protection mediated through the IRR, a receptor pharmacologically distinct from the erythropoiesis-mediating receptor (EPO-R). Cibinetide has been described as a non-erythropoietic EPO analogue that exclusively binds the heteromeric receptor composed of EPOR and CD131, and this was examined in bone metabolism studies in vivo and in vitro.
In chronically stressed mice, ARA 290 had marginal effects on peripheral blood hemoglobin and red cells. In cerebral ischemic mice, ARA 290 provided a neuroprotective effect via the β-common receptor without causing erythropoiesis. ARA 290 is an EPO-derived helix-B peptide that has been reported to retain the anti-inflammatory and tissue-protective functions of erythropoietin without erythropoiesis-stimulating effects.
Cibinetide, another name for ARA 290, is described as a non-erythropoietic EPO analogue that exclusively binds the heteromeric receptor composed of EPOR and CD131, as shown in a study of bone metabolism in vivo and in vitro. In H9c2 cardiomyocyte cells, ARA290 is described in this paper as a CD131 agonist and was supplemented in mechanistic rescue experiments. In mice, the neuroprotective effect of ARA290 was significantly suppressed following injection of siRNA against the β-common receptor (βCR).
In mice with cerebral ischemia, ARA 290 significantly reduced neuronal apoptosis and the level of inflammatory cytokines in brain tissue. In cerebral ischemic mice, ARA 290 provided a neuroprotective effect via the β-common receptor (βCR) without causing erythropoiesis. In mice, the neuroprotective effect of ARA 290 was significantly suppressed after injection of siRNA against the β-common receptor (βCR).
In mice exposed to chronic unpredictable mild stress and chronic social defeat stress, daily ARA 290 given during stress induction ameliorated depression-like behavior, similarly to fluoxetine. ARA 290 also reversed chronic stress-induced microglia activation in mice, as fluoxetine did. The researchers concluded that ARA 290 ameliorated chronic stress-induced depression-like behavior in mice through, at least partially, its anti-inflammatory effects.
A narrative review that summarizes current evidence on regenerative peptides for chronic pain management includes cibinetide (ARA-290) among the compounds it covers. In human studies summarized by this review, cibinetide (ara290) is reported to show improvement in the Neuropathic score in diabetic neuropathy, together with acetyl-L-carnitine.
In mice with Stx-induced hemolytic uremic syndrome (HUS), ARA 290 (PHBSP) attenuated renal nitrosative stress and reduced tubular dedifferentiation. A rat study examined ARA 290 (PHBSP), an erythropoietin mimetic peptide, and infliximab for protective effects on ischemic renal reperfusion injury. In those rats with ischemia-reperfusion kidney injury treated with PHBSP and infliximab, blood creatinine and urea levels decreased significantly.
In animal studies, ARA 290 (also called PHBSP or ARA290) has been tested for recovery after nerve injury. In rats with sciatic nerve crush injury, it inhibited the early inflammatory response and promoted functional recovery. In Schwann cells in an animal study, ARA290 was reported to inhibit activation of the NLRP3 inflammasome by inhibiting NF-κB phosphorylation and reducing reactive oxygen species production.
In a rat cardiac ischemia model, the DOTA-(Lys-Dabcyl6, Phe7)-ARA-290 radiopeptide was studied for where it accumulated in the heart. Biodistribution and SPECT imaging of the DOTA-(Lys-Dabcyl6, Phe7)-ARA-290 radiopeptide showed that it considerably accumulated in the ischemic region. The cardiac ischemic-to-lung rate for the DOTA-(Lys-Dabcyl6, Phe7)-ARA-290 radiopeptide was 3.65 ID/g % at 0.5 hr. The DOTA-(Lys-Dabcyl6, Phe7)-ARA-290 form was designed and synthesized by Fmoc solid-phase peptide synthesis, and its radiolabeling purity was more than 96% by ITLC in vitro.
According to a review, the researchers modified ARA 290 with thioether cyclization to address its short half-life, producing a thioether cyclized helical B peptide (CHBP). A related form, DOTA-(Lys-Dabcyl6, Phe7)-ARA-290, was designed and synthesized by Fmoc solid-phase peptide synthesis, with Fmoc-Lys-(Dabcyl)-OH introduced as a lipophilic amino acid to improve serum stability.
FOR RESEARCH USE ONLY — Products are sold exclusively for in vitro and preclinical laboratory research. Not for human consumption or administration. Not intended for diagnostic or therapeutic use. These statements have not been evaluated by the FDA.