ARA-290
An 11-amino-acid peptide engineered from erythropoietin that retains tissue-protective effects without raising red blood cell count. Studied for neuropathic pain, small fiber neuropathy, and tissue repair.
ARA-290 (cibinetide) is an 11-amino-acid peptide built to copy erythropoietin's tissue-repair signalling while leaving out the red-blood-cell effect that makes EPO risky. Its best evidence is in small fiber neuropathy, where Phase 2 trials showed symptom improvement and measurable corneal nerve regrowth. It never reached Phase 3, and the programme appears to have wound down: the last trial was terminated because the drug supply expired with no replacement, and no human data has been published since 2017.
What is ARA-290?
ARA-290 (cibinetide) is an 11-amino-acid synthetic peptide modeled on helix B of the erythropoietin (EPO) molecule. It was designed to retain EPO's tissue-protective and anti-inflammatory effects while eliminating the erythropoietic activity (red blood cell stimulation) that causes EPO's cardiovascular side effects. ARA-290 activates the innate repair receptor (IRR) — a heteromer of the EPO receptor and the β-common receptor — which is transiently expressed on injured tissues to initiate repair, reduce inflammation, and protect cells from further damage. The peptide has advanced through multiple Phase 2 trials, most notably in sarcoidosis-associated small fiber neuropathy and type 2 diabetes neuropathy.
What ARA-290 Is Investigated For
ARA-290 (cibinetide) is investigated for small fiber neuropathy, diabetic peripheral neuropathy, corneal nerve regeneration, and tissue repair — all use cases built on its engineered ability to retain erythropoietin's tissue-protective effects without stimulating red blood cell production. The strongest evidence is in sarcoidosis-associated small fiber neuropathy, where a randomized, double-blind Phase 2 pilot trial showed significant improvement in neuropathic symptom scores and physical functioning over 4 weeks, followed by a larger 64-patient Phase 2b trial that measured corneal nerve fiber area by confocal microscopy and found a placebo-corrected mean increase of 697 square micrometres at the 4 mg dose (95% CI 159-1236, P = 0.012) — an objective regenerative endpoint that is unusual in the peripheral neuropathy literature. That trial also found regenerating intraepidermal nerve fibers increased at 4 mg, and that corneal nerve change correlated with both the skin-fiber marker and six-minute walk distance. Note that pain improved in every arm including placebo, with the 4 mg placebo-corrected difference not reaching significance. The caveats are real: sample sizes are small (22-64 patients), Phase 3 has never been conducted, and ARA-290 has orphan drug designation but no approval in any indication. Its mechanism — selective activation of the innate repair receptor expressed only on injured tissue — is well-characterized and differentiates it from broadly immunosuppressive therapies. The honest framing is a well-engineered molecule with small but methodologically solid Phase 2 evidence in a specific neuropathy niche, pending the Phase 3 development it has not yet received.
History & Discovery
ARA-290 (cibinetide) emerged from work mapping which surface of the erythropoietin (EPO) molecule is responsible for its tissue-protective effects versus its erythropoietic effects. Researchers identified helix B as the structural region engaging the innate repair receptor (IRR) — the heteromer of EPOR and the β-common receptor (CD131) that is transiently expressed on injured tissue. By synthesising an 11-amino-acid peptide modelled on the aqueous-facing surface of helix B (pyroglutamate-Glu-Gln-Leu-Glu-Arg-Ala-Leu-Asn-Ser-Ser), the program produced a molecule that retains EPO's cytoprotective and anti-inflammatory signalling while losing affinity for the homodimeric EPOR2 on erythroid precursors. The peptide was advanced into human trials by Araim Pharmaceuticals, anchored by the 2012 randomised, double-blind pilot study in sarcoidosis-associated small fiber neuropathy that remains the reference trial. Subsequent Phase 2 work extended the program into type 2 diabetic neuropathy and corneal nerve regeneration, and ARA-290 has received orphan drug designation for sarcoidosis-associated neuropathy. A 2026 Current Pain and Headache Reports review of regenerative-medicine peptides (Luansritisakul et al., PMID 42635865) is a recent example of cibinetide being included in cross-peptide surveys of tissue-repair and chronic-pain applications despite the still-modest late-phase footprint. The programme itself, however, appears to have ended rather than paused, and the page should say so plainly. Four trials were ever registered, all Phase 1 or 2, and the most recent to start did so in April 2016. That last one — a study of ARA290 in diabetic macular oedema run by the Belfast Health and Social Care Trust with Araim as collaborator — was terminated after enrolling nine patients, and the recorded reason is unusually revealing: expiry of study drug with no replacement available. In other words the sponsor could not supply more peptide. No results were posted. The last publication reporting new human interventional data appeared in 2017, with a re-analysis of previously collected corneal imaging in 2018. Everything since has been rodent and cell work, much of it from groups unconnected to the original developers, plus review articles. Araim Pharmaceuticals no longer maintains a working corporate website. Against that backdrop, describing ARA-290 as 'awaiting Phase 3' overstates the position: the molecule has a genuine and methodologically respectable Phase 2 record that was never followed up, which is a different and more common fate than failure.
How It Works
ARA-290 is a fragment of erythropoietin (EPO) — the hormone that stimulates red blood cell production — but redesigned to keep EPO's healing effects without boosting blood cells. It activates a special receptor (the innate repair receptor) that only appears on damaged tissues, telling them to repair, reduce inflammation, and protect against further damage. The most studied application is nerve pain, where ARA-290 appears to help damaged small nerve fibers regenerate.
ARA-290 (pyroglutamate-Glu-Gln-Leu-Glu-Arg-Ala-Leu-Asn-Ser-Ser) is derived from the aqueous-facing surface of helix B of erythropoietin. It is worth being precise about what that means, because the shorthand 'EPO fragment' misleads: the sequence is not a contiguous stretch of the EPO molecule at all. Helix B spans residues 58-82 of mature EPO, which read QQAVEVWQGLALLSEAVLRGQALLV — sharing only a two-residue run with ARA-290. What the peptide reproduces is the set of residues that point outward into solvent when EPO is folded and bound to the receptor homodimer, assembled into a new linear molecule. This is why the founding paper is titled for peptides derived from the tertiary structure of erythropoietin rather than from its sequence, and it explains why searching the EPO sequence for ARA-290 returns nothing. It does not activate the classical homodimeric EPOR2 receptor on erythroid precursors (explaining the absence of erythropoietic effects). Instead, it binds the innate repair receptor (IRR) — a heterocomplex of EPOR and the β-common receptor (βcR/CD131) that is transiently expressed on tissues undergoing injury or inflammation. IRR activation triggers JAK2/STAT3, PI3K/Akt, and MAPK pathways, leading to: inhibition of apoptotic signaling, suppression of pro-inflammatory cytokine production (TNF-α, IL-6, IL-1β), promotion of cell survival, enhanced nerve fiber regeneration, and reduced oxidative stress. In small fiber neuropathy, ARA-290 appears to restore unmyelinated C-fiber function and support epidermal and corneal nerve fiber regrowth. Because IRR is not expressed on healthy tissue, the anti-inflammatory and protective effects are localized to injury sites — a tissue-specific pharmacology that differentiates ARA-290 from broadly immunosuppressive therapies. The receptor assignment is not merely inferred from binding studies. In a neuropathic pain model, ARA290 relieved tactile and cold allodynia in wild-type mice but produced no effect whatsoever in mice lacking the beta-common receptor, the genetic test that establishes the beta-common subunit as necessary for the drug's action rather than incidental to it. The same work reported relief persisting as long as 15 weeks in rats, including in animals dosed only during the first two weeks — a durability that is unusual for an analgesic and is consistent with repair rather than symptomatic suppression.
Evidence Snapshot
Human Clinical Evidence
Moderate, and now historical. Three published Phase 2 trials: the 22-patient sarcoidosis small-fiber-neuropathy pilot, a 48-patient trial in type 2 diabetes with neuropathic symptoms, and a 64-patient Phase 2b that used corneal nerve fiber area as its primary endpoint and is the only one with results posted to ClinicalTrials.gov. Sample sizes are small (22-64 patients) and Phase 3 was never conducted. No human interventional data has been published since 2017.
Animal / Preclinical
Strong. Extensive preclinical work across diabetic neuropathy, retinopathy, ischemia-reperfusion, traumatic brain injury, myocardial infarction, and wound healing models.
Mechanistic Rationale
Strong. The innate repair receptor mechanism is well-characterized, and ARA-290's selectivity for IRR over classical EPOR has been demonstrated at the molecular level.
Research Gaps & Open Questions
What the current literature has not yet settled about ARA-290:
- 01Phase 3 trials have not been conducted in any indication, including the sarcoidosis-associated small fiber neuropathy lead program that has the strongest Phase 2 signal — and on current evidence none is planned. No trial has started since 2016, the last one terminated because study drug expired with no replacement, and no new human data has been published since 2017.
- 02Whether the corneal nerve fiber density increase observed at the 4 mg dose translates to durable functional improvement (sensory thresholds, neuropathic pain scores) over longer follow-up is unresolved.
- 03Optimal route (subcutaneous vs. intravenous), dose, and treatment duration for chronic neuropathy management have not been settled — trial protocols have varied across the program.
- 04Efficacy outside sarcoidosis and type 2 diabetes — for example in chemotherapy-induced peripheral neuropathy, chronic inflammatory demyelinating polyneuropathy, or idiopathic small fiber neuropathy — has not been tested in adequately powered trials.
- 05Whether nerve regeneration persists after discontinuation, or whether ongoing dosing is required to maintain benefit, is unknown.
- 06Long-term safety beyond the 4-week to several-month trial durations published to date has not been characterised.
Forms & Administration
ARA-290 has been studied via subcutaneous and intravenous administration. In the sarcoidosis SFN trial, dosing was 2 mg IV three times weekly for 4 weeks. Corneal nerve fiber studies used 4 mg doses. Subcutaneous administration is the more practical route for extended use. ARA-290 is not available as an FDA-approved therapy; access is restricted to research settings. As with any investigational peptide, use should only occur under qualified medical supervision in a research or specialty context.
Dosing & Protocols
The ranges below reflect protocols commonly discussed in the literature and by clinicians — not a prescription. Actual dosing for any individual should be determined by a qualified healthcare provider who knows the patient.
Typical Range
There is no approved dose, and no dose has been validated beyond Phase 2. Published human trials used three regimens: 2 mg intravenously in the 22-patient sarcoidosis pilot; 4 mg daily subcutaneously in the 48-patient type 2 diabetes trial; and 1, 4 or 8 mg daily in the 64-patient Phase 2b dose-ranging study, where 4 mg produced the significant corneal nerve effect and 8 mg did not do better. In rodent neuropathic pain work the effective range was roughly 3 to 60 micrograms per kilogram, with 30 micrograms per kilogram the most consistently effective.
Frequency
Three times weekly in the sarcoidosis pilot (intravenous), once daily in the subcutaneous trials. Treatment periods were 28 days in every published human study; nothing longer has been reported.
Timing Considerations
No specific timing requirements: can be administered at any time of day, with or without food, and is not tied to exercise timing. Consistency matters more than the specific clock — dose at roughly the same time each day (or same day each week, for weekly protocols) to keep exposure steady.
Cycle Length
Every published human trial ran 28 days. Whether benefit requires continuous dosing, responds to intermittent courses, or persists after a single course has not been established in humans. The rodent data hint at the last possibility — animals dosed only during the first two weeks retained relief for months — but that has never been tested in a person.
Protocol Notes
The striking feature of the dose-response is that it is not monotonic. In the Phase 2b dose-ranging trial the 4 mg arm met the primary endpoint while the 8 mg arm produced a smaller, non-significant effect. That pattern is consistent with the innate repair receptor pharmacology, where the receptor is transiently expressed on injured tissue and more drug does not create more receptor, but it means 'more is better' reasoning is specifically contradicted by the only dose-ranging data that exists. Both routes have been used. Intravenous dosing was used in the earliest trial; subcutaneous was used subsequently and is the more practical route for repeated administration. There is no published human pharmacokinetic profile, no bioavailability comparison between routes, and no guidance on dose adjustment for renal or hepatic impairment. Anything sold as ARA-290 outside a trial is a research chemical of unverified identity — and note that this is a peptide a sponsor with a GMP supply chain ultimately could not keep in stock, which should temper confidence in grey-market material.
ARA-290 is investigational and not approved anywhere. The doses above are drawn from completed Phase 2 trials, not from any established therapeutic protocol, and no regimen has been validated in a Phase 3 trial.
Timeline of Effects
Onset
In the published trials, symptom improvement was assessed at the end of a 28-day course rather than tracked continuously, so there is no fine-grained human onset curve. The sarcoidosis pilot reported a significant difference in the small-fiber neuropathy symptom score at week 4. Objective nerve-regrowth measures — corneal nerve fiber area and regenerating intraepidermal fibers — were also measured at day 28, so nerve structural change is detectable within a month of starting. Nerve regeneration is inherently slow, and nothing in this literature supports expecting a response within days.
Peak Effect
Unknown, because no human trial ran longer than 28 days or followed patients past the end of dosing. The 28-day timepoint is where every published effect was measured, not a demonstrated plateau. Whether longer courses produce greater nerve regrowth is one of the programme's unanswered questions.
After Discontinuation
This is the clearest gap in the human evidence. No published trial followed patients after stopping, so whether corneal and intraepidermal nerve regrowth persists, continues or reverses off-drug is simply unknown. The animal data are more encouraging than the absence of human data might suggest: in rats, relief of allodynia lasted as long as 15 to 20 weeks, including in animals dosed only during the first two weeks after nerve injury, which is what would be expected if the drug promotes repair rather than suppressing symptoms. Extrapolating that to humans is unjustified without follow-up data.
Monitoring & Measurement
Bloodwork & Labs
- •Hemoglobin and hematocrit — the central safety question for any EPO-derived molecule. Published trials consistently showed no increase, and a rise would suggest the material is not what it claims to be
- •Serum ferritin and iron studies — relevant only as context for interpreting any unexpected hemoglobin change
- •HbA1c and a lipid panel in anyone with diabetes — the type 2 diabetes trial reported improvement in both over 56 days, making them a reasonable secondary readout
- •C-reactive protein — a crude systemic inflammation marker; the mechanism predicts localised rather than systemic anti-inflammatory effect, so a large CRP drop would be unexpected
Functional & Performance Tests
- •Corneal confocal microscopy — the objective endpoint used in the Phase 2b trial, quantifying corneal nerve fiber area. Available at academic ophthalmology and diabetic-neuropathy centres rather than routine clinics
- •Skin biopsy for intraepidermal nerve fiber density, the standard diagnostic test for small fiber neuropathy and the measure most directly comparable to the trial endpoints
- •Quantitative sensory testing for thermal and vibration thresholds
- •A validated symptom instrument recorded at baseline and at four weeks — the trials used the small-fiber neuropathy symptom score and PainDetect
- •Six-minute walk test — a simple functional measure that correlated with corneal nerve change in the Phase 2b trial
When to Test
Baseline and 28 days, mirroring every published trial, with hemoglobin and hematocrit checked at both.
Interpretation & Notes
ARA-290 is unusual among research peptides in having genuinely objective, validated outcome measures attached to it — corneal confocal microscopy and intraepidermal nerve fiber density are the same endpoints used in the trials, and both detect structural nerve change rather than relying on how someone reports feeling. That is worth taking advantage of, because small fiber neuropathy symptoms fluctuate considerably and the published trials themselves found pain improving in placebo arms. Without a baseline nerve measurement there is no way to distinguish a real regenerative effect from the natural variability of the condition. The practical obstacle is access: corneal confocal microscopy is a research-grade technique available mainly through academic centres, and skin biopsy requires a neurology or neuromuscular service. Hemoglobin and hematocrit are the one genuinely easy and genuinely important measurement — they are the check that distinguishes a correctly manufactured non-erythropoietic peptide from EPO or an adulterated product, and no legitimate ARA-290 exposure should raise them.
Common Questions
How is ARA-290 different from EPO?
Full-length EPO stimulates red blood cell production by binding homodimeric EPO receptors on erythroid precursors — this is useful for anemia but causes elevated hematocrit and cardiovascular risks in non-anemic patients. ARA-290 does not activate these homodimeric receptors. Instead, it targets the innate repair receptor (IRR), a heteromer of EPOR and β-common receptor that's only expressed on damaged or stressed tissue. This gives ARA-290 EPO's protective effects without the erythropoietic activity.
What did the sarcoidosis neuropathy trial show?
A randomized, double-blind Phase 2 pilot in 22 sarcoidosis patients with small fiber neuropathy (12 on drug, 10 on placebo) found significant improvement in the small-fiber neuropathy symptom score versus placebo after 4 weeks of IV ARA-290 at 2 mg three times weekly. Two details are usually dropped: the improvement in pain and physical functioning on the SF-36 was a within-group change from baseline in the treated arm, not a difference versus placebo, and two other instruments (the Brief Pain Inventory and a fatigue scale) improved significantly but equally in both groups. A separate and larger 64-patient Phase 2b then measured corneal nerve fiber area by confocal microscopy and found a placebo-corrected increase of 697 square micrometres at 4 mg (P = 0.012) — an objective measure of nerve regrowth. A widely circulated '23% increase in corneal nerve fiber density' traces to a 2017 company press release, describes area rather than density, and does not appear in the peer-reviewed paper.
Is ARA-290 FDA-approved?
No. ARA-290 is investigational. It has received orphan drug designation for sarcoidosis-associated neuropathy and has progressed through multiple Phase 2 trials, but no Phase 3 program or regulatory approval exists yet.
What did the type 2 diabetes neuropathy trial show?
A randomized, placebo-controlled Phase 2 study in patients with type 2 diabetes and neuropathic symptoms reported that ARA-290 improved both metabolic control and neuropathic symptom scores over the treatment period — the second positive Phase 2 signal in the program after the sarcoidosis pilot. Sample size was modest (around 48 patients), and the result has not yet been replicated in a Phase 3 trial, so it should be read as a supporting signal rather than a confirmed efficacy finding. A 2026 Current Neuropharmacology review of diabetic-neuropathy pharmacotherapy (Alburghaif et al., PMID 42693836) positioned cibinetide among the emerging DPN targets pending late-phase confirmation.
Does ARA-290 raise red blood cell count like EPO?
No. That was the entire engineering goal. Across the published Phase 2 trials, ARA-290 did not elevate hemoglobin or hematocrit, consistent with its lack of activity at the homodimeric EPOR2 receptor on erythroid precursors. Its effects are confined to the innate repair receptor expressed on injured tissue, which is what separates it pharmacologically from full-length EPO and erythropoiesis-stimulating agents.
Does the nerve regeneration last after stopping ARA-290?
Unclear. The corneal nerve fiber density increase observed at the 4 mg dose was measured during or shortly after the treatment window, and published trials have not followed patients long enough to determine whether the regenerative effect persists off-drug or whether ongoing dosing is needed to maintain benefit. Durability of response after discontinuation is one of the program's open questions.
Who ARA-290 Is NOT For
- •Pregnancy and breastfeeding — no human safety data exist in these populations and ARA-290 has not been studied in either.
- •Children and adolescents — clinical trials have been conducted in adults; pediatric safety and pharmacology are unestablished.
- •Active malignancy — although ARA-290 lacks erythropoietic activity, the broader EPO/IRR signalling family has been linked to tumor-cell survival pathways in some preclinical work, and oncology patients have not been studied.
- •Anyone unable to access qualified medical supervision — ARA-290 is investigational and should only be used in a research or specialty context, not self-administered.
Drug & Supplement Interactions
No clinically documented drug-drug interactions have been reported for ARA-290 in the published Phase 2 trials, but the interaction profile has not been systematically studied. Theoretically, because ARA-290 acts on the innate repair receptor to suppress pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) and modulate JAK2/STAT3 signalling, additive effects with biologic immunomodulators (TNF inhibitors, IL-6 antagonists, JAK inhibitors) are plausible but unquantified. Unlike full-length EPO, ARA-290 does not raise hematocrit, so the cardiovascular-risk interactions associated with erythropoiesis-stimulating agents (with antihypertensives, anticoagulants, or in patients with iron-deficiency states) are not expected to apply. The honest framing is that interaction data are absent rather than reassuring — patients on complex regimens should review use with the prescribing investigator.
Safety Profile
Common Side Effects
Cautions
- • Not FDA-approved for any indication
- • Long-term safety beyond trial durations is unestablished
- • Clinical evidence is from relatively small Phase 2 studies
What We Don't Know
Whether ARA-290 produces durable nerve regeneration after discontinuation is unclear. Optimal treatment duration, dosing frequency for chronic use, and effects in non-sarcoidosis neuropathies need further study.
Legal Status
United States
Investigational, and no longer in active development. Not FDA-approved for any indication. ARA-290 has received US orphan drug designation in the sarcoidosis space, but no marketing application has ever followed and no trial has started since 2016. Cibinetide also appears on FDA's bulk drug substances list for pharmacy compounding under section 503A — specifically in Category 3, 'Bulk Drug Substances Nominated Without Adequate Support,' as of the list updated 14 May 2026. Category 3 means someone nominated it for compounding and FDA judged the nomination inadequately supported; it is not authorization to compound, and compounding pharmacies have no sanctioned route to it. Access outside a research setting is not legitimately available.
International
No regulatory approval in any major jurisdiction. The European Medicines Agency granted orphan designation EU/3/13/1191 on 7 October 2013 for the treatment of sarcoidosis, to Araim Pharmaceuticals Europe Limited of Dublin, and the designation is still listed with positive status — but an orphan designation is an incentive to develop a drug, not an approval, and no marketing authorisation application followed. Clinical development was conducted under research protocols rather than via marketed-drug pathways, and has not been active for roughly a decade.
Sports & Competition
Not named on the WADA Prohibited List, but the class is. The 2027 List prohibits 'innate repair receptor agonists' at S2.1.5, giving asialo EPO and carbamylated EPO as examples — ARA-290 is an innate repair receptor agonist, so it is caught by that class whether or not it appears by name. As an unapproved investigational compound it also falls under S0. Athletes should treat it as prohibited at all times.
Regulatory status changes over time. Verify current local rules with a qualified professional.
Myths & Misconceptions
Myth
ARA-290 is just a safer form of EPO that still boosts red blood cells.
Reality
ARA-290 was specifically engineered to lose erythropoietic activity. It does not activate the homodimeric EPOR2 receptor on erythroid precursors, and Phase 2 trials have consistently shown no elevation of hemoglobin or hematocrit. The point of the molecule is to retain EPO's tissue-protective signalling via the innate repair receptor while removing the red-blood-cell effects that drive EPO's cardiovascular risks.
Myth
ARA-290 is FDA-approved for neuropathy.
Reality
It is not approved for any indication anywhere. ARA-290 holds orphan drug designation for sarcoidosis-associated small fiber neuropathy and has advanced through multiple Phase 2 trials, but Phase 3 has not been conducted and no regulatory approval exists.
Myth
ARA-290 broadly suppresses the immune system like a steroid or biologic.
Reality
Its anti-inflammatory effects are tissue-localised. The innate repair receptor is only transiently expressed on injured or stressed tissue, so ARA-290's downregulation of TNF-α, IL-6, and IL-1β signalling concentrates at sites of damage rather than producing the systemic immunosuppression seen with corticosteroids or TNF inhibitors.
Myth
Because ARA-290 is not erythropoietic and is not named on the WADA list, athletes are in the clear.
Reality
This is backwards, and it is the most consequential misconception about this compound. The Prohibited List has a dedicated entry at S2.1.5 for 'innate repair receptor agonists,' giving asialo EPO and carbamylated EPO as examples — and both of those are themselves non-erythropoietic tissue-protective EPO derivatives. Lacking red-cell activity is precisely what that sub-section covers, not an exemption from it. ARA-290 is an innate repair receptor agonist by definition, so it is caught whether or not it appears by name, and the S2.1 heading explicitly extends to substances with similar structure or biological effect. Substances in S2.1 are non-Specified, and the prohibition applies at all times, in and out of competition. A WADA-accredited laboratory in Cologne has published metabolism work describing ARA-290 outright as a prohibited peptide and identifying its main metabolite. There is no 'clearing it with your federation' short of a therapeutic use exemption.
Published Research
11 studiesPharmacological Management of Diabetic Neuropathy: Current Evidence, Clinical Positioning, and Emerging Therapeutic Targets.
Peptides in Regenerative Medicine: A Comprehensive Review of Clinical Applications in Tissue Repair and Chronic Pain Management.
Targeting the innate repair receptor to treat neuropathy
Characterization of in vitro generated metabolites of selected peptides <2 kDa prohibited in sports.
Cibinetide Improves Corneal Nerve Fiber Abundance in Patients With Sarcoidosis-Associated Small Nerve Fiber Loss and Neuropathic Pain
ARA 290, a Nonerythropoietic Peptide Engineered from Erythropoietin, Improves Metabolic Control and Neuropathic Symptoms in Patients with Type 2 Diabetes
ARA 290 for treatment of small fiber neuropathy in sarcoidosis
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.
Safety and Efficacy of ARA 290 in Sarcoidosis Patients with Symptoms of Small Fiber Neuropathy: A Randomized, Double-Blind Pilot Study
The first randomized human trial of ARA 290 — established tolerability and preliminary neuropathic-symptom benefit in sarcoidosis-associated small fiber neuropathy, the anchor study for cibinetide's continued development in rare neuropathies.
ARA290, a peptide derived from the tertiary structure of erythropoietin, produces long-term relief of neuropathic pain: an experimental study in rats and β-common receptor knockout mice.
The genetic proof of mechanism. ARA290 relieved tactile and cold allodynia in rats for up to 15 weeks and in wild-type mice, but had no effect at all in mice lacking the beta-common receptor — establishing that the beta-common subunit of the innate repair receptor is required for the drug to work.
Nonerythropoietic, tissue-protective peptides derived from the tertiary structure of erythropoietin.
The founding paper for the whole molecule. It localised EPO's tissue-protective activity to helix B (residues 58-82), showed that an 11-amino-acid peptide reproducing the aqueous face of that helix is tissue-protective across ischemic stroke and renal ischemia-reperfusion models while accelerating wound healing and improving cognition, and confirmed that neither helix B nor the 11-mer is erythropoietic in vitro or in vivo. This is the paper that makes ARA-290 a structural mimic rather than an EPO fragment.
Quick Facts
- Class
- EPO-Derived Peptide
- Tier
- C
- Evidence
- Moderate
- Safety
- Moderate Data
- Updated
- Oct 2026
- Citations
- 11PubMed
Also known as
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Evidence Score
Clinical Trials
View Clinical TrialsLinks to ClinicalTrials.gov for reference. Listing does not imply endorsement.