ARA-290 (Cibinetide): The EPO-Derived Peptide Targeting Nerve Pain

ARA-290, also known as cibinetide, is an 11-amino-acid peptide engineered from erythropoietin (EPO) that aims to calm inflammation and repair damaged nerves without the red-blood-cell-boosting effect that makes EPO famous (and banned in sport). It is one of the more interesting compounds in this corner of research because it has more genuine human data than most peptides: it reached Phase 2 trials in people with nerve pain. The catch is that it stalled there, and it is not approved by any regulator.

If you have seen ARA-290 marketed as a "nerve pain peptide" or a "neuropathy" compound, or alongside the top peptides for recovery, this guide is the high-level map of the whole molecule. We cover what it actually is, how its innate-repair-receptor mechanism works, what the human trials really showed, the doses those trials used, the safety picture, and its investigational legal status. Each section is a clear overview; deeper subtopics point to dedicated guides so this page stays a clean hub.

Key Takeaways

• ARA-290 (cibinetide) is an 11-amino-acid peptide derived from erythropoietin, with the sequence pGlu-Glu-Gln-Leu-Glu-Arg-Ala-Leu-Asn-Ser-Ser, modeled on EPO's helix-B surface (Wikipedia, "Cibinetide", retrieved 2026-06-16).
• It targets the "innate repair receptor" (IRR), a heteromer of the EPO receptor and the beta-common receptor (CD131), to drive tissue protection and nerve repair (Brines et al., Molecular Medicine, 2015, retrieved 2026-06-16).
• It does not raise red blood cells. It was deliberately engineered to keep EPO's tissue-protective signaling while avoiding the classic erythropoietic receptor, so it carries none of EPO's blood-thickening risk (Brines et al., Molecular Medicine, 2015, retrieved 2026-06-16).
• It reached human Phase 2 trials, notably in sarcoidosis-associated small-fiber neuropathy (n=64) and type 2 diabetes neuropathy (n=48), where it improved nerve-fiber and neuropathic-pain measures at 4 mg subcutaneously daily (ClinicalTrials.gov NCT02039687, 2017; Brines et al., Molecular Medicine, 2015, retrieved 2026-06-16).
• It is investigational, not FDA-approved. It was developed by Araim Pharmaceuticals, holds orphan-drug designation for sarcoidosis neuropathic pain (a designation, not an approval), and has not completed Phase 3 (Wikipedia, "Cibinetide", retrieved 2026-06-16).
• The studied dose was 1 to 8 mg subcutaneously per day for 28 days, with 4 mg as the effective dose in trials. These are trial figures, not a recommendation, and there is no approved label.

What is ARA-290 (cibinetide)?

ARA-290 is a small synthetic peptide, just 11 amino acids long, designed from a specific surface of the erythropoietin (EPO) protein so it can switch on EPO's healing signals without switching on EPO's blood-building effect. Its formal drug name is cibinetide, and it is studied mostly for nerve pain and small-fiber neuropathy. It is not approved by any drug regulator.

Chemically, ARA-290 is an 11-amino-acid peptide (a hendecapeptide) with the sequence pGlu-Glu-Gln-Leu-Glu-Arg-Ala-Leu-Asn-Ser-Ser and the molecular formula C51H84N16O21 (Wikipedia, "Cibinetide", retrieved 2026-06-16). The key idea is that EPO does two very different jobs in the body: it tells bone marrow to make red blood cells, and, separately, it protects and repairs injured tissue. ARA-290 was engineered to mimic only the second, tissue-protective job. If injectable peptides are new to you, start with our how peptides work guide.

The single most important fact about ARA-290 is its status: it is investigational. It was developed by Araim Pharmaceuticals, was tested in human Phase 2 trials, and even holds an FDA orphan-drug designation for sarcoidosis-related neuropathic pain, but a designation is not an approval, no Phase 3 has been completed, and it is not approved for sale or prescription as a medicine (Wikipedia, "Cibinetide", retrieved 2026-06-16).

Citation capsule. ARA-290 (cibinetide) is an 11-amino-acid peptide (sequence pGlu-Glu-Gln-Leu-Glu-Arg-Ala-Leu-Asn-Ser-Ser, formula C51H84N16O21) derived from the helix-B surface of erythropoietin. It activates the innate repair receptor (an EPO-receptor / beta-common-receptor heteromer) for tissue protection without erythropoietic activity, was developed by Araim Pharmaceuticals, reached Phase 2 trials for neuropathic pain, and is not approved by any regulator. Source: Wikipedia, "Cibinetide," 2026; Brines et al., Molecular Medicine, 2015; CAS 1208243-50-8; PubChem CID 91810664; DrugBank DB13006.

How does ARA-290 work?

ARA-290 works by activating the "innate repair receptor" (IRR), a partnership between the erythropoietin receptor and the beta-common receptor (CD131), which switches on the body's own tissue-protection and nerve-repair program while leaving red-blood-cell production untouched. In plain terms, it borrows EPO's healing signal but not its blood-building signal. This mechanism is supported by laboratory and early human work.

The reason this matters is structural. Classic EPO drives red blood cell production by binding a receptor made of two identical EPO-receptor units (a homodimer). The tissue-protective effect runs through a different receptor: the EPO receptor paired with the beta-common receptor (CD131), a combination researchers call the innate repair receptor. ARA-290 was engineered to engage that innate repair receptor selectively. As the 2015 Molecular Medicine paper puts it, ARA-290 is a "nonerythropoietic peptide engineered from erythropoietin" that retains tissue protection without stimulating red blood cell production (Brines et al., Molecular Medicine, 2015, retrieved 2026-06-16).

Here is what each piece of the mechanism contributes, in simple terms:

• Innate repair receptor (EPOR + CD131): the target ARA-290 is designed to switch on, triggering anti-inflammatory and pro-repair signaling at sites of injury.
• Non-erythropoietic by design: because it does not activate the classic homodimeric EPO receptor, it does not raise hematocrit, red cell count, or blood viscosity, which is the safety problem that limits EPO itself.
• Small-fiber nerve repair: in trials, the downstream effect of interest was regrowth of small nerve fibers and reduced neuropathic pain, not muscle or tendon healing.
• Anti-inflammatory tilt: the innate repair receptor sits at the interface of inflammation and tissue repair, which is why ARA-290 is studied in inflammatory neuropathies.

The receptor-biology deep dive (how the heteromer assembles, how EPO splits its two jobs) is its own topic. We keep it at overview level here and link out to how peptides work for the foundations.

What is ARA-290 used for?

ARA-290 is studied mainly for neuropathic pain and small-fiber neuropathy, the nerve damage behind conditions like sarcoidosis-related nerve pain and diabetic neuropathy, with broader research interest in inflammation and tissue protection. None of these are FDA-approved uses; they are the directions its human and preclinical research has pointed.

The headline use is nerve pain. Small-fiber neuropathy damages the tiny nerve endings that carry pain and temperature signals, producing burning, tingling, and chronic pain that existing drugs treat poorly. ARA-290's repair-and-anti-inflammation mechanism is a logical fit, and that is exactly where its two main human trials focused: sarcoidosis-associated small-fiber neuropathy and type 2 diabetes neuropathy (ClinicalTrials.gov NCT02039687, 2017; Brines et al., Molecular Medicine, 2015, retrieved 2026-06-16). Beyond nerves, the innate repair receptor's role in inflammation has driven preclinical interest in kidney, cardiac, and metabolic protection, though those remain earlier-stage.

A quick overview of the areas ARA-290 is studied for, and where the evidence stands:

Because several of these are distinct future topics, we keep them brief here. The honest headline: ARA-290 has real, if small, human nerve-pain data, which already puts it ahead of most research peptides, but it has not been confirmed in large trials.

How strong is the evidence for ARA-290?

The evidence for ARA-290 is unusually mature for a research peptide, with two completed Phase 2 human trials, but it is still early: the trials were small, ran only 28 days, and no Phase 3 has been completed or published. Promising Phase 2 results are a real signal, not proof, and the program has not advanced to approval.

The most-cited trial is the sarcoidosis study, a Phase 2b double-blind randomized controlled trial (NCT02039687) of 64 patients given placebo or 1, 4, or 8 mg of ARA-290 subcutaneously per day for 28 days. The 4 mg dose increased corneal nerve fiber abundance by roughly 23% versus placebo and produced clinically meaningful pain reduction in patients with moderate-to-severe baseline pain (ClinicalTrials.gov NCT02039687, 2017, retrieved 2026-06-16). The earlier type 2 diabetes trial, with 48 completers on 4 mg daily for 28 days, reported an improved PainDetect neuropathic-pain score versus placebo (p=0.037) plus secondary metabolic improvements, including a fall in HbA1c (Brines et al., Molecular Medicine, 2015, retrieved 2026-06-16).

Why "Phase 2" is the key phrase

It helps to see exactly where ARA-290 sits on the drug-development ladder. Phase 2 trials test whether a drug shows a real effect and is reasonably safe in a few dozen to a few hundred patients; they are not the large, long, confirmatory Phase 3 trials that regulators require for approval. ARA-290's two main trials each enrolled fewer than 70 people and lasted 28 days, which is enough to generate a promising signal but not enough to establish lasting efficacy or rare-but-serious risks. No completed Phase 3 trial of ARA-290 has been published, development for some other indications (such as depressive disorders) was discontinued, and the orphan-drug designation it holds for sarcoidosis neuropathic pain is a regulatory incentive, not evidence that it works (Wikipedia, "Cibinetide", retrieved 2026-06-16).

This matters for a practical reason. ARA-290 has cleared a bar that compounds like BPC-157 never have, namely a randomized, placebo-controlled human trial with objective nerve-imaging endpoints. That is genuinely more than most peptides sold for research can claim. But "better evidence than most peptides" is a low bar, and it is not the same as "proven." The honest reading is that ARA-290 is a promising Phase 2 compound whose development appears to have stalled before the trials that would confirm it.

Our take: The most common mistake we see is the opposite of the usual peptide problem. With most research peptides people overstate thin animal data; with ARA-290 the temptation is to treat real Phase 2 trials as if approval were a formality. It is not. Stalled-at-Phase-2 is its own warning sign, and a 64-person, 28-day study cannot tell you about long-term outcomes.

What doses of ARA-290 were studied?

There is no approved dose for ARA-290, but the human Phase 2 trials studied 1 to 8 mg given subcutaneously once daily for 28 days, with 4 mg emerging as the effective dose. These are figures from published trials, framed as "studied in trials," not an established or recommended dose, and there is no approved label to anchor them.

In the sarcoidosis trial, patients received 1, 4, or 8 mg subcutaneously per day, and the 4 mg arm gave the best nerve-fiber and pain results, so 4 mg per day is the most commonly cited research dose (ClinicalTrials.gov NCT02039687, 2017, retrieved 2026-06-16). The type 2 diabetes trial used the same 4 mg daily subcutaneous dose over 28 days (Brines et al., Molecular Medicine, 2015, retrieved 2026-06-16). Both trials used short, daily subcutaneous courses rather than long-term dosing, so even the trial data say nothing about safe or effective use beyond a month. We label all of this as trial-studied because no regulator has reviewed or approved a dose for general use.

The detailed reconstitution math, injection technique, and how research doses are framed are a dedicated future topic. We cover only the high-level framing here and link out to the general how peptides work guide.

For orientation only, here is how the trials described the studied regimen (not a recommendation):

Our take: It is easy to read "4 mg daily worked in a trial" as a protocol. It is not one. These doses come from short, small, supervised studies with objective monitoring, not from approval-grade dose-finding, and nothing in the published record speaks to using ARA-290 for longer than 28 days.

How much does the ProtocolPlus community track ARA-290?

ARA-290 is a small, niche compound in the ProtocolPlus app: 144 people have logged about 900 doses, a tiny slice of total activity, which fits its status as an investigational nerve-pain peptide rather than a mainstream one. These figures are shown to give an honest sense of scale, not a clinical signal.

Within the app's overall tracking window of September 2024 to June 2026, ProtocolPlus has recorded 233,668 logged doses across 27,272 unique trackers. ARA-290's 900 logged doses are roughly 0.4% of that total, placing it among the least-tracked compounds we cover, in line with peptides like FOXO4-DRI and follistatin rather than the heavily tracked GLP-1 family. A typical reconstituted ARA-290 vial is finished in about 21 days of use by the people tracking it. All of these numbers trace to our canonical dataset.

What are the side effects of ARA-290?

In its Phase 2 trials ARA-290 was generally well tolerated, with no significant treatment-related safety problems reported and, importantly, no rise in red blood cells; but those trials were small and only 28 days long, so the true long-term side-effect profile is still unknown. "Well tolerated in short trials" is the honest headline, not "proven safe."

The sarcoidosis trial reported no significant safety issues in any treatment group, and the type 2 diabetes trial reported no clinically significant ARA-290-related adverse events, with two serious events judged possibly related but likely confounded (ClinicalTrials.gov NCT02039687, 2017; Brines et al., Molecular Medicine, 2015, retrieved 2026-06-16). A notable safety point in ARA-290's favor: unlike EPO, it did not raise hematocrit or red cell counts, which is consistent with its non-erythropoietic design and removes EPO's main blood-thickening danger.

A hub-level overview of what is reported and what remains unknown:

• Reported in trials (mild): generally well tolerated; injection-site reactions are the expected issue with any subcutaneous peptide.
• Reassuring signal: no increase in red blood cells or hematocrit, unlike EPO, so no associated clotting or blood-thickening risk was seen.
• Quality-related risks: because ARA-290 sold outside trials comes from an unregulated market, contamination, mislabeled potency, or impurities are real concerns independent of the peptide itself.
• Unknown: safety beyond 28 days, in larger populations, and over repeated courses, because the long-horizon human data simply do not exist.

This is the hub-level summary. The deeper safety discussion belongs with how to evaluate any unapproved compound: see how to vet peptide quality.

How does ARA-290 compare to EPO and other peptides?

ARA-290 is best understood as "EPO's healing half without its blood-building half," which sets it apart from both erythropoietin and the popular tissue-repair peptides like BPC-157: it targets nerves and inflammation through the innate repair receptor rather than building red cells or driving angiogenesis. All of these are different tools, and ARA-290 alone has Phase 2 nerve-pain data.

Against EPO, the contrast is the whole point of the molecule. EPO is an approved drug that raises red blood cells (and is banned in sport for that reason), but its tissue-protective potential is hard to use because of the clotting risk that comes with thicker blood. ARA-290 keeps the tissue protection and drops the red-cell effect (Brines et al., Molecular Medicine, 2015, retrieved 2026-06-16). Against the common "healing peptides," ARA-290 is aimed at a different problem: where BPC-157 is associated with angiogenesis and musculoskeletal repair, ARA-290's human data are specifically about small-fiber nerves and neuropathic pain. They are not interchangeable, and stacking claims are not supported by trials.

That is the hub-level contrast, kept deliberately brief to avoid overlapping future dedicated comparisons. The shared honest caveat applies to all of them: ARA-290 is investigational, and outside its short Phase 2 trials there is no validated protocol.

Is ARA-290 legal and approved?

ARA-290 is not approved by the FDA or any other regulator, so there is no approved medical use, and the products sold online are unapproved research chemicals rather than a prescribable medicine. Its investigational status, even with real trial data behind it, is the most important thing to understand before considering it.

On the regulatory picture, ARA-290 (cibinetide) was developed by Araim Pharmaceuticals, advanced through Phase 2 trials, and holds an FDA orphan-drug designation for sarcoidosis-associated neuropathic pain, but an orphan-drug designation is an incentive to develop a drug for a rare disease, not an approval to market it (Wikipedia, "Cibinetide", retrieved 2026-06-16). No completed Phase 3 trial has been published, and development for some indications was discontinued, so as of 2026 it remains an unapproved, investigational compound. Anything sold as ARA-290 outside a clinical trial is an unapproved research chemical with no regulatory oversight of identity, purity, or sterility. For the broader legal framing and how to evaluate a vendor, see are peptides legal and how to vet peptide quality.

Our take: ARA-290 sits in an unusual spot: it has better human evidence than most research peptides, yet it is still an unapproved drug that stalled in development. Both facts are true at once. Real Phase 2 data does not make a research-chemical vial a vetted medicine, and "more studied than BPC-157" is not the same as "approved" or "safe for unsupervised use."

How do people obtain ARA-290?

Because ARA-290 is investigational and unapproved, there is no legitimate prescription route outside a clinical trial; the main way people access it is by buying unapproved "research chemical" vials online, which is a legal and safety gray market. This is a description of what happens, not an endorsement.

The research-peptide market is where most online searches end up: vendors sell lyophilized ARA-290 "for research use only," typically in 5 mg or larger vials, and buyers reconstitute and use it off-label. That market carries real risks of mislabeled potency, impurities, and non-sterile product, with no regulatory oversight and none of the monitoring that the actual trials had.

If you are researching that path despite the risks, the responsible groundwork is the same as for any investigational peptide:

1. Confirm the legal status for your country and situation, including any sport or workplace rules. See are peptides legal.
2. Demand a certificate of analysis (COA) from independent third-party testing, and learn to read it for identity and purity. See how to vet peptide quality.
3. Understand the science first. Know what the trials did and did not show before assuming a research-chemical vial reproduces them. See how peptides work.
4. Talk to a qualified clinician who can weigh your specific health situation, interactions, and contraindications.

We are describing what people do, not recommending it. Using an unapproved drug means accepting unknown risks with no regulatory safety net.

Frequently Asked Questions

The bottom line

ARA-290 (cibinetide) is one of the more scientifically credible compounds in the research-peptide world. The core idea is elegant: take erythropoietin, keep its tissue-protective and nerve-repairing signal through the innate repair receptor, and discard the red-blood-cell effect that limits EPO. And unlike most peptides marketed online, ARA-290 actually reached human Phase 2 trials, where 4 mg daily improved small nerve fibers and neuropathic pain over 28 days. That is real evidence, and it is more than most peptides can show.

The other half of the story is discipline. ARA-290 is still investigational, its trials were small and short, no Phase 3 has been completed, and development appears to have stalled. The vials sold online are unapproved research chemicals, not the monitored trial drug. The honest label is promising-but-unproven, and "more studied than its peers" is not the same as approved or safe for unsupervised use. From here, the natural next reads are how peptides work, are peptides legal, and how to vet peptide quality.

Sources

• Wikipedia. "Cibinetide." Retrieved 2026-06-16. https://en.wikipedia.org/wiki/Cibinetide
• Brines M, Dunne AN, van Velzen M, et al. "ARA 290, a Nonerythropoietic Peptide Engineered from Erythropoietin, Improves Metabolic Control and Neuropathic Symptoms in Patients with Type 2 Diabetes." Molecular Medicine / PMC, 2015. Retrieved 2026-06-16. https://pmc.ncbi.nlm.nih.gov/articles/PMC4365069/
• ClinicalTrials.gov. "Efficacy and Safety Study of ARA 290 to Treat Neuropathic Symptoms in Patients With Sarcoidosis (NCT02039687)." 2017. Retrieved 2026-06-16. https://clinicaltrials.gov/study/NCT02039687
• U.S. National Library of Medicine, PubMed. "Cibinetide Improves Corneal Nerve Fiber Abundance in Patients With Sarcoidosis-Associated Small Nerve Fiber Loss and Neuropathic Pain" (PMID 28475703). 2017. Retrieved 2026-06-16. https://pubmed.ncbi.nlm.nih.gov/28475703/
• PubChem. "Cibinetide, CID 91810664." Retrieved 2026-06-16. https://pubchem.ncbi.nlm.nih.gov/compound/91810664
• DrugBank. "Cibinetide (DB13006)." Retrieved 2026-06-16. https://go.drugbank.com/drugs/DB13006
• Araim Pharmaceuticals / PR Newswire. "Araim Pharmaceuticals' Cibinetide (ARA-290) Regenerates Small Nerve Fibers and Improves Neuropathic Clinical Symptoms in the Orphan Disease of Sarcoidosis." 2017. Retrieved 2026-06-16. https://www.prnewswire.com/news-releases/araim-pharmaceuticals-cibinetide-ara-290-regenerates-small-nerve-fibers-and-improves-neuropathic-clinical-symptoms-in-the-orphan-disease-of-sarcoidosis-300452818.html