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ARA-290 / Cibinetide

10mg Vial
2 September 2026Updated 2 September 2026
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Full range of benefits for ARA-290 / Cibinetide

Activates the innate repair receptor (IRR) to mediate cytoprotection

Non-erythropoietic—does not increase red blood cell mass or hematocrit

Modulates inflammation and can reduce pro-inflammatory cytokine release

May reduce neuropathic pain symptoms observed in clinical studies

Promotes small-fiber nerve repair and regeneration in preclinical and clinical work

Improves corneal nerve fiber density on clinical imaging assessments

Protects tissues from ischemia-reperfusion injury in animal models

May improve sensory function and nerve conduction measures in neuropathy

Can produce relatively rapid symptomatic effects in short-term studies

This peptide's combination-safety and interaction data below always stays visible, regardless of membership.

Warning

Important information. The data compiled from scientific literature is provided for educational purposes. Dosage ranges reflect what is reported in studies and do not constitute a recommendation, prescription, or usage guidance. Health decisions should always be made with a qualified professional.

15 Published Studies

Scientific literature related to ARA-290 / Cibinetide and its potential applications.

Full text analysed

Retraction Note: Delayed administration of pyroglutamate helix B surface peptide (pHBSP), a novel nonerythropoietic analog of erythropoietin, attenuates acute kidney injury.

The 2012 study claiming that delayed administration of pHBSP (a nonerythropoietic erythropoietin analog) attenuates acute kidney injury has been retracted due to image/figure integrity issues; its data and conclusions are not reliable.

Acute kidney injuryNonerythropoietic erythropoietin analogs (pHBSP / ARA-290 / Cibinetide)Molecular signaling (blot-based assays) — image integrity concerns
Relevance
80%
Source
Europe PMC, PubMed
DOI: 10.1186/s10020-026-01439-y
Published
2026
Full text analysed

Phase-targeted erythropoietin derivatives for traumatic brain injury: bridging mechanisms to precision therapy.

ARA-290 (cibinetide/HBSP) is a short-lived, non-erythropoietic EPO-derived peptide that shows promising preclinical neuroprotection in rodent TBI models via βcR-biased anti-inflammatory and pro-survival signaling; early human safety data exist in other indications but clinical efficacy and safety in TBI patients remain unestablished.

High-resolution receptor biology to confirm EPOR–βcR (CD131) engagement by ARA-290 in human neural and vascular tissuesDose-ranging and PK/PD studies of ARA-290 in acute TBI patients, including brain exposure and target engagement biomarkersRandomized controlled trials in TBI testing timing (hyperacute administration), functional outcomes, and safety+2 more
Relevance
75%
Source
Europe PMC, PubMed
DOI: 10.3389/fneur.2025.1665405
Published
2025
Full text analysed

Co-treatment with erythropoietin derived HBSP and caspase-3 siRNA: A promising approach to prevent fibrosis after acute kidney injury.

In a mouse ischemia–reperfusion AKI model, early co-administration of HBSP (an EPO-derived, non-erythropoietic peptide) and CASP3siRNA produced greater preservation of kidney function and structure at 2 weeks and reduced markers of apoptosis and fibrosis compared with either treatment alone, supporting further preclinical investigation.

Preclinical evaluation of combined peptide (HBSP/ARA-290) and gene-silencing (CASP3siRNA) therapies for AKI-to-CKD progressionMechanistic studies on EPOR/βcR signalling in renal repair and fibrosisLong-term fibrosis and functional outcome studies after combined interventions+2 more
Relevance
95%
Source
Europe PMC, PubMed
DOI: 10.1111/jcmm.70082
Published
2024
Full text analysed

Renal protective effects of helix B surface polypeptide in rats with puromycin aminonucleoside nephropathy.

In a rat PAN nephropathy model, HBSP (8 nmol/kg i.p. given 4 h before PAN and daily for 7 days) reduced proteinuria, improved podocyte histology and further increased renal GDNF expression compared with PAN + vehicle; the authors propose GDNF upregulation as a potential mediator, but direct mechanistic proof is lacking.

Podocyte protection and proteinuriaHBSP (cibinetide) renal protective mechanismsGDNF involvement in renal/podocyte repair+1 more
Relevance
95%
Source
Europe PMC, PubMed
DOI: 10.1080/0886022x.2024.2394637
Published
2024
Full text analysed

HBSP inhibits tubular cell pyroptosis and apoptosis, promotes macrophage M2 polarization, and protects LPS-induced acute kidney injury.

In LPS-induced mouse AKI and in LPS-stimulated mouse renal epithelial cells, HBSP (cibinetide) reduced markers of pyroptosis and apoptosis in tubular epithelial cells, decreased systemic and renal inflammation, reduced macrophage infiltration and shifted macrophage phenotype toward M2, and lowered EPOR expression; these preclinical data support further mechanistic and translational studies but do not establish clinical efficacy or safety.

Mechanisms of HBSP-mediated reduction of pyroptosis and apoptosis in TECsHBSP effects on macrophage polarization and interactions with TECsRole and regulation of EPOR and EPOR/βcR in injury and repair in AKI+2 more
Relevance
95%
Source
Europe PMC, PubMed
DOI: 10.1111/jcmm.70202
Published
2024
Abstract analysed

The protective effect of erythropoietin and its novel derived peptides in peripheral nerve injury.

The review summarizes that EPO has neuroprotective effects but long-term EPO use is limited by side effects; ARA290 (cibinetide) shows neuroprotective promise but has a short half-life, and CHBP is a thioether-cyclized derivative developed to improve half-life — both ARA290 and CHBP are presented as promising peptide therapeutics with ongoing investigation into mechanisms.

Neuroprotection in peripheral nerve injuryDevelopment of EPO-derived peptide therapeutics (ARA290, CHBP)Peptide modification to improve pharmacokinetics (thioether cyclization)+1 more
Relevance
92%
Source
Europe PMC, PubMed
DOI: 10.1016/j.intimp.2024.112452
Published
2024
Abstract analysed

Mechanisms of ARA290 in counteracting cadmium-triggered neurotoxicity in PC12 cells.

In PC12 cells exposed to cadmium, ARA290 pretreatment was reported to reduce cytotoxicity, DNA damage, oxidative stress, apoptosis, and inflammatory cytokine levels, with proposed involvement of IRR activation; however, the evidence is limited to an incompletely reported in vitro study.

Neuroprotection against heavy metal (cadmium) toxicityMechanisms of non-hematopoietic EPO derivatives (ARA290) in neuronal cellsOxidative stress and antioxidant defense modulation+2 more
Relevance
100%
Source
Europe PMC, PubMed
DOI: 10.1093/toxres/tfaf023
Published
2025
Full text analysed

The Role of Erythropoietin in Metabolic Regulation.

ARA290 (Cibinetide), a non-erythropoietic EPOR agonist, mimics many metabolic benefits of EPO in preclinical models—improving glucose tolerance, insulin-related measures, reducing body weight and fat mass, and shifting lipid gene expression toward increased lipolysis and decreased lipogenesis—while not increasing erythropoiesis. Mechanistic data implicate EPOR:CD131 signaling and stabilization of RUNX1 (via decreased FBXW7) as mediators. Clinical evidence is referenced but not detailed; further rigorous human trials and safety assessment are needed.

Mechanistic studies of EPOR:CD131 (β-common receptor) signaling by ARA290 in metabolic tissuesDose–response, pharmacokinetics, and optimal administration parameters for ARA290 in metabolic indicationsRigorous clinical trials to assess efficacy and safety of ARA290 for metabolic outcomes (glucose tolerance, insulin sensitivity, body weight/fat mass) in humans+2 more
Relevance
95%
Source
Europe PMC, PubMed
DOI: 10.3390/cells14040280
Published
2025
Full text analysed

Multiple Mammalian Cytokines and Erythropoietin-Mimetic Peptides Protect Insect Neurons via Phylogenetically Conserved Cytokine Receptor-Like Factor 3 (CRLF3).

Short Epo-mimetic peptides (HBSP, P16, EMP1) and human thrombopoietin protect primary locust brain neurons from hypoxia-induced apoptosis via activation of the conserved receptor CRLF3; growth hormone and prolactin do not. These findings indicate CRLF3 can be activated by multiple vertebrate cytokines and small peptides, supporting its proposed role as a broadly ligandable, evolutionarily conserved neuroprotective receptor.

CRLF3 receptor ligand specificity and activationErythropoietin-mimetic peptide neuroprotection mechanismsEvolutionary biology of type I cytokine receptors+2 more
Relevance
95%
Source
Europe PMC, PubMed
DOI: 10.1111/jnc.70207
Published
2025
Abstract analysed

Exploring the EPO/EPOR-βCR/TLR9 pathways in sepsis-associated encephalopathy: Therapeutic implications of EPO and HBSP.

In a mixed clinical and preclinical analysis, higher serum EPO was associated with increased delirium in septic patients, while preclinical studies show a dose-dependent effect where low-dose EPO or HBSP (ARA-290/cibinetide) activates EPOR-βCR to suppress TLR9/MyD88/NF-κB signaling, promote anti-inflammatory microglial polarization, and reduce neuroinflammation and neuronal apoptosis; high-dose EPO had opposite, harmful effects in animal models.

Mechanisms of EPO/EPOR-βCR signaling in neuroinflammationRole of TLR9/MyD88/NF-κB signaling in sepsis-associated encephalopathyTherapeutic potential of non-hematopoietic EPO derivatives (HBSP/ARA-290/cibinetide) in SAE+2 more
Relevance
95%
Source
Europe PMC, PubMed
DOI: 10.1016/j.intimp.2025.116053
Published
2026