Research use only
Regenerative researchReference entry

ARA-290

CATALOG NO.
AR10
MOL. WEIGHT
1,257.3
CLASS
Peptide
Computed conformer
Overview

ARA-290 (cibinetide) is an 11-amino-acid peptide, beginning with a pyroglutamate residue, modelled on the aqueous-facing surface of helix B of erythropoietin rather than cut contiguously from its sequence. It reproduces erythropoietin's tissue-protective activity without stimulating red cell production, and is neither erythropoietic in vitro nor in vivo. It was developed by Araim Pharmaceuticals, whose officers, employees, consultants or shareholders are authors on 12 of the 14 papers cited here, including every clinical trial; the two exceptions are the two studies below that reported negative results.

Research-use-only note

Information on this page is provided for laboratory research reference. The compound is not a drug, supplement, or medical product, and is not for human or veterinary use, ingestion, or consumption.

Molecular characteristics
Catalog no.AR10
Research areaRegenerative
ClassPeptide
SequencePyr-Glu-Gln-Leu-Glu-Arg-Ala-Leu-Asn-Ser-Ser
Length11 aa
Molecular weight1,257.3 g/mol
Molecular formulaC51H84N16O21
FormLyophilized research material
AppearanceWhite to off-white powder
UseFor laboratory research use only
VerificationReference specifications pending COA verification
COA statusPending authentic product-specific COA
Measured results

No reviewed report has been published for this product family yet. The molecular values opposite are public reference data, not results measured on a CRX sample.

Browse published reports →
Sequence
PyrEQLERALNSS
Pyr
Pyroglutamic acid — N-terminal lactam of glutamate; blocks the free α-amine.
How it works

Erythropoietin's two activities run through two different receptors: red cell production through the EPO receptor homodimer, and tissue protection through a heterocomplex of the EPO receptor with the beta-common receptor (CD131), termed the innate repair receptor. That heterocomplex is typically not expressed by normal tissue and is rapidly induced by injury or inflammation. ARA-290 was designed to engage only the heterocomplex, which is why it protects tissue without raising haematocrit. In LPS-activated mouse macrophages the peptide's anti-inflammatory effect required both CD131 and JAK2 and worked by inhibiting NF-kappaB subunit p65. Its plasma half-life is roughly two minutes, yet in rats five doses over ten days relieved allodynia out to 20 weeks, so the peptide is described as flipping a molecular switch rather than acting by sustained occupancy.1,2,3,4

What the research shows12 findings · 15 sources · 6 from clinical trials

Recovery & repair

In a randomised, placebo-controlled trial in 38 adults with sarcoidosis-associated small nerve fibre loss (21 on ARA 290, 17 on placebo), 28 days of daily subcutaneous dosing raised median corneal nerve fibre area 14.5% within the treated arm (p = 0.022) while placebo fell 5.3% (p = 0.462); 6-minute walk distance rose 18.7 m versus a 15.1 m decline on placebo (between-group p = 0.049). A 2016 erratum rescales the paper's absolute areas, not these percentages.5,6

Clinical trialPhase phase 2 · 38 participants · 28 daysadults with sarcoidosis-associated small nerve fibre loss and neuropathic pain

In a 28-day phase 2b randomised trial in 64 adults with sarcoidosis-associated small nerve fibre loss, only one of three dose arms (4 mg) showed a significant placebo-corrected increase in corneal nerve fibre area (p = 0.012); the 1 mg and 8 mg arms did not, their confidence intervals spanning zero. Intraepidermal GAP-43+ regenerating fibres also rose at 4 mg (p = 0.035). Absolute areas are omitted: their measurement scale is unconfirmed.7

Clinical trialPhase phase 2b · 64 participants · 28 daysadults with sarcoidosis-associated small nerve fibre loss and neuropathic pain

In a phase 2 randomised trial in 48 adults with type 2 diabetes and painful neuropathy (24 per arm), 28 days of daily ARA 290 improved PainDetect symptom scores by 3.3 points versus 1.1 on placebo at day 28 (p = 0.037). In a subgroup with corneal nerve fibre density more than one standard deviation below normal, density rose within the treated arm only (+2.6 fibres/mm2, paired p = 0.02); placebo did not change.8

Clinical trialPhase phase 2 · 48 participants · 28 days dosing, 56 days observationadults with type 2 diabetes and painful neuropathy

In a single-arm phase 2 trial, nine patients with diabetic macular oedema self-administered cibinetide for 12 weeks, the longest human exposure published. There was no improvement from baseline in best-corrected visual acuity (-2.9 letters), central retinal thickness (+10 um), central retinal sensitivity or tear production; only a vision-related quality-of-life questionnaire score rose. Eight of nine completed, and the trial had no control group.9

Clinical trialPhase phase 2 · 9 participants · 12 weekspatients with diabetic macular oedema, single-arm and uncontrolled

Inflammation & immunity

In C57BL/6N mice with established dextran-sulphate-sodium colitis, cibinetide improved weight gain and survival compared with solvent-treated mice, as did erythropoietin itself, and preserved tissue integrity by reducing myeloid-cell infiltration and production of pro-inflammatory cytokines, chemokines and nitric oxide synthase-2. In LPS-activated primary mouse macrophages the effect depended on CD131 and JAK2 and ran through inhibition of NF-kappaB subunit p65.3

Animal studycourse of experimental colitisC57BL/6N mice with DSS-induced colitis, plus primary macrophage culture

In streptozotocin-diabetic C57BL/6N mice given BALB/c islet allografts, 14 days of cibinetide reduced liver inflammatory gene expression, improved glycaemic control immediately after transplantation and significantly delayed the onset of allograft loss; combined with low-dose tacrolimus it significantly improved long-term graft survival. In culture, cibinetide lowered bone-marrow-derived dendritic-cell maturation and the subsequent allogeneic T-cell response.10

Animal study14 days of dosing with long-term graft follow-upstreptozotocin-diabetic C57BL/6N mice transplanted with BALB/c islets, plus in vitro dendritic cell assays

In a 15-month randomised study in Fischer 344 x Brown Norway rats dosed from 18 months of age (48 longitudinal, 144 cross-sectional), chronic ARA290 versus saline mitigated age-related rises in cardiac non-myocyte to myocyte ratio, infiltrating leukocytes and monocytes, pro-inflammatory cytokines and NF-kappaB; it blunted the blood pressure rise, preserved ejection fraction, enhanced cardiomyocyte autophagy flux, reduced lipofuscin, desensitised the mitochondrial permeability transition pore to oxidant stress, and reduced frailty markers at 33 months.11

Animal study192 studies · 15 months (18 to 33 months of age)ageing Fischer 344 x Brown Norway rats, including isolated left ventricular myocytes

Focus & brain health

In rats with a spared nerve injury, ARA 290 given on five occasions over ten days produced a dose-dependent reduction in mechanical allodynia and reduced cold allodynia at all four doses tested, both sustained to 20 weeks versus vehicle. Spinal microglial reactivity (iba-1) was suppressed at both doses examined histologically at two weeks and at the higher of them at 20 weeks; astrocyte reactivity did not differ.4

Animal study5 doses over 10 days, followed to 20 weeksrats with spared nerve injury (neuropathic pain)

In young APP/PS1 mice, early systemic ARA 290 decelerated amyloid-beta pathology and improved cognitive function compared with untreated APP/PS1 mice, by expanding Ly6C-low patrolling monocytes; in chimeric mice in which that subset was selectively depleted the benefit was absent. In aged APP/PS1 mice with advanced pathology, ARA 290 failed to reverse amyloid-beta pathology or to raise circulating monocytes.12

Animal studynot stated in abstractyoung and aged APP/PS1 transgenic mice, including patrolling-monocyte-depleted chimeras

In 36 healthy human volunteers randomised to a single 2 mg dose of ARA290 or placebo and tested one week later, no effects were observed on mood or affective symptoms. ARA290 lowered neural response to happy faces in the fusiform gyrus and tended to reduce recognition of happy and disgust expressions; the authors concluded that the direction and strength of the effects do not unequivocally support an antidepressant-like profile.13

Clinical trialPhase experimental medicine · 36 participants · single dose, assessed at one weekhealthy volunteers, double-blind randomised parallel-group neuropsychological model of drug action

Fat loss & metabolism

In that same 48-subject phase 2 trial in adults with type 2 diabetes, HbA1c fell 0.16% at day 28 and 0.21% at day 56 on ARA 290 versus 0.01% and a 0.21% rise on placebo (p = 0.002, repeated-measures ANOVA restricted to the 42 subjects with complete serial measurements). Triglycerides fell (p = 0.043) and the cholesterol-to-HDL ratio improved (p = 0.039) relative to placebo.8

Clinical trialPhase phase 2 · 48 participants · 28 days dosing, 56 days observationadults with type 2 diabetes and painful neuropathy

In streptozotocin-diabetic mice given a deliberately marginal intraportal transplant of 185 pancreatic islets, ARA 290 dosed around the transplant improved blood glucose compared with untreated transplanted controls (p < 0.001), and suppressed liver upregulation of MCP-1, MIP-1beta, IL-1beta and IL-6 messenger RNA measured 12 hours after transplantation.14

Animal study12 hours to short-term follow-upstreptozotocin-induced diabetic C57BL/6J mice receiving marginal intraportal islet transplantation
Reported adverse events

What investigators recorded alongside the results above, at the rates their papers state.

Overall adverse event burden similar to placebo over 28 days of daily subcutaneous dosing in adults with type 2 diabetes8

54 mild, 9 moderate and 1 severe event on ARA 290 versus 61 mild and 5 moderate on placebo (24 subjects per arm)

Clinical trial

Serious adverse events, including one death, in the ARA 290 arm of the type 2 diabetes trial. A 70-year-old man developed severe cellulitis of the lower extremity requiring hospitalisation two weeks after his last dose and suffered a fatal myocardial infarction; the safety committee judged the event to be unrelated to ARA 290 treatment. Separately, pre-existing borderline renal insufficiency worsened slightly (creatinine 119 to 159 umol/L) in a subject whose furosemide dose had been increased, and dosing was stopped. No serious adverse events were reported in the placebo arm.8

4 serious adverse events in the ARA 290 arm, 2 judged possibly related and 2 judged unlikely to be associated; 1 death

Clinical trial

No pain or local irritation at the subcutaneous injection site in the upper leg or lower abdomen over 28 days of daily dosing, and no serious adverse events during dosing or within 12 weeks of follow-up. The single moderate event on ARA 290 was a 14 kg weight loss that the patient's medical history showed had begun before enrolment, of undetermined cause and persisting after dosing stopped; the placebo group's three moderate events (diarrhoea, irritability, light-headedness) resolved spontaneously.5

1 moderate event on ARA 290 (n = 21) versus 3 moderate events on placebo (n = 17)

Clinical trial

No clinically significant haematology or clinical chemistry changes at any sampled timepoint, and negative anti-ARA 290 titres at baseline and day 28. The peptide was engineered to be non-erythropoietic and is not erythropoietic in vitro or in vivo, so the haematocrit rise, platelet activation and thrombosis risk that limit recombinant erythropoietin are not expected; this has not been tested in a long-term human trial.1,2,8

no clinically significant change from baseline reported

Clinical trial

No serious adverse events or reactions and no anti-cibinetide antibodies detected after 12 weeks of daily self-administered dosing, the longest human exposure reported9

0 serious adverse events and 0 anti-drug antibody responses in 9 patients (8 completed), single-arm and uncontrolled

Clinical trial

Absence of evidence: no human safety data beyond 12 weeks of dosing, and no trial large enough to detect uncommon harms. The first published patient trial enrolled 22 sarcoidosis patients for 4 weeks and the largest randomised trial 64 subjects for 28 days; the only 12-week study was single-arm and enrolled 9 patients. Nothing is known about repeated or chronic courses in humans, and no phase 3 trial or marketing approval appears anywhere in the published record.7,9,15

not applicable; no data

Clinical trial
Sources
  1. 1.Nonerythropoietic, tissue-protective peptides derived from the tertiary structure of erythropoietin. · Proceedings of the National Academy of Sciences of the United States of America · 2008 · PMID 18676614
  2. 2.Flipping the molecular switch for innate protection and repair of tissues: Long-lasting effects of a non-erythropoietic small peptide engineered from erythropoietin. · Pharmacology & therapeutics · 2015 · PMID 25728128
  3. 3.Cibinetide dampens innate immune cell functions thus ameliorating the course of experimental colitis. · Scientific reports · 2017 · PMID 29026145
  4. 4.ARA 290, a peptide derived from the tertiary structure of erythropoietin, produces long-term relief of neuropathic pain coupled with suppression of the spinal microglia response. · Molecular pain · 2014 · PMID 24529189
  5. 5.ARA 290 improves symptoms in patients with sarcoidosis-associated small nerve fiber loss and increases corneal nerve fiber density. · Molecular medicine (Cambridge, Mass.) · 2013 · PMID 24136731
  6. 6.ERRATUM. · Molecular medicine (Cambridge, Mass.) · 2016 · PMID 28059429
  7. 7.Cibinetide Improves Corneal Nerve Fiber Abundance in Patients With Sarcoidosis-Associated Small Nerve Fiber Loss and Neuropathic Pain. · Investigative ophthalmology & visual science · 2017 · PMID 28475703
  8. 8.ARA 290, a nonerythropoietic peptide engineered from erythropoietin, improves metabolic control and neuropathic symptoms in patients with type 2 diabetes. · Molecular medicine (Cambridge, Mass.) · 2015 · PMID 25387363
  9. 9.A Phase 2 Clinical Trial on the Use of Cibinetide for the Treatment of Diabetic Macular Edema. · Journal of clinical medicine · 2020 · PMID 32674280
  10. 10.Improvement of Islet Allograft Function Using Cibinetide, an Innate Repair Receptor Ligand. · Transplantation · 2020 · PMID 32345869
  11. 11.A small erythropoietin derived non-hematopoietic peptide reduces cardiac inflammation, attenuates age associated declines in heart function and prolongs healthspan. · Frontiers in cardiovascular medicine · 2022 · PMID 36741836
  12. 12.Early monocyte modulation by the non-erythropoietic peptide ARA 290 decelerates AD-like pathology progression. · Brain, behavior, and immunity · 2022 · PMID 34343617
  13. 13.Testing the antidepressant properties of the peptide ARA290 in a human neuropsychological model of drug action. · European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology · 2015 · PMID 26431906
  14. 14.A Nonhematopoietic Erythropoietin Analogue, ARA 290, Inhibits Macrophage Activation and Prevents Damage to Transplanted Islets. · Transplantation · 2016 · PMID 26683514
  15. 15.Safety and efficacy of ARA 290 in sarcoidosis patients with symptoms of small fiber neuropathy: a randomized, double-blind pilot study. · Molecular medicine (Cambridge, Mass.) · 2012 · PMID 23168581
Public COA coverage
No reviewed public report is currently available for this product family. Molecular values above are reference information, not tested-sample results.

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