The ARA-290 peptide, also called cibinetide or ARA 290, is an investigational 11-amino-acid compound being studied for neuropathy and tissue repair. Its potential is unusual: it might reduce nerve pain while also helping repair the damaged small nerve fibers that contribute to the pain.
The short answer on ARA-290 dosage is that human trials used several different research regimens. These included 2 mg by intravenous infusion three times weekly and 1 mg, 4 mg, or 8 mg by subcutaneous injection once daily, usually for 28 days. The most repeated neuropathy regimen was 4 mg subcutaneously each day for 28 days.
That does not make 4 mg an approved or recommended dose. ARA-290 is not FDA-approved, and the trials do not establish a consumer protocol.
That would make it different from the drugs most people with neuropathy are offered today.
Medicines such as gabapentin, pregabalin, and duloxetine can reduce neuropathic pain signals. They can be valuable when they work. They are not established treatments for rebuilding lost small nerve fibers.
ARA-290 is being studied as a possible disease-modifying approach. Instead of only changing how pain is perceived, researchers want to know whether it can affect the inflammatory and repair pathways behind the nerve damage.
That possibility is supported by early human findings. It is not proven as a long-term fix.
ARA-290 dosage in human trials
The table below reports what researchers administered. It is not a dosage guide.
| Human study | Trial dose | Treatment period |
|---|---|---|
| Sarcoidosis pilot, 22 participants | 2 mg IV three times weekly | 4 weeks |
| NERVARA sarcoidosis trial, 38 participants | 4 mg SC once daily | 28 days |
| Type 2 diabetes and neuropathic symptoms, 49 participants | 4 mg SC once daily | 28 days |
| Phase 2b sarcoidosis dose-ranging trial, 64 participants | 1 mg, 4 mg, or 8 mg SC once daily | 28 days |
| Diabetic macular edema pilot, 9 participants | 4 mg SC once daily | 12 weeks |
The 64-person Phase 2b study provides the most useful dose-response result. Only the 4 mg group had a statistically significant placebo-corrected increase in the primary corneal nerve-fiber-area endpoint. The 1 mg and 8 mg groups did not. That finding is a reason to study 4 mg further; it is not evidence that more is better or that 4 mg is a safe dose outside a controlled trial.
The studies used a defined investigational product, medical monitoring, and study-specific preparation. They did not establish a “beginner dose,” a self-treatment cycle, or a universal method for mixing a research-vendor vial. A common online reconstitution convention should not be mistaken for a protocol validated by these trials.
What small-fiber neuropathy means
Peripheral nerves carry information between the brain, spinal cord, skin, muscles, and organs.
Small sensory nerve fibers help detect pain and temperature. Small autonomic fibers also help control functions such as sweating, blood pressure, heart rate, and digestion. Damage can produce burning, tingling, numbness, abnormal temperature sensation, or pain from light contact such as bedsheets.
Large-fiber problems can affect vibration, position sense, balance, strength, and reflexes. A person can have small-fiber symptoms even when standard nerve-conduction testing is normal.
Diabetes is one cause of peripheral neuropathy. Autoimmune and inflammatory disease, infections, toxins, nutritional problems, some medicines, and inherited conditions can also damage nerves. Some cases remain unexplained. The National Institute of Neurological Disorders and Stroke provides a useful overview.
This matters because pain is only one part of the problem. If small fibers are damaged, suppressing pain does not necessarily restore temperature sensation, autonomic function, or the damaged nerve structure.
There are also few established treatments that directly restore small nerve fibers. Treatment usually focuses on the underlying cause, when one can be found, and on controlling symptoms. This is the gap ARA-290 research is trying to address.
Most ARA-290 human neuropathy data come from people with sarcoidosis or type 2 diabetes. The findings cannot automatically be applied to every cause of neuropathy.
ARA-290 peptide at a glance
| Question | Evidence-based answer |
|---|---|
| What is it? | An investigational 11-amino-acid peptide also called cibinetide. |
| Other names | ARA 290, ARA290, cibinetide, pHBSP, and pyroglutamate helix B surface peptide. |
| Where did it come from? | It was designed from a tissue-protective surface of erythropoietin, or EPO. |
| What has been studied most? | Sarcoidosis-associated small-fiber neuropathy and neuropathic symptoms in type 2 diabetes. |
| Is it FDA-approved? | No. It remains investigational. |
What ARA-290 is designed to do
ARA-290 is a linear peptide with 11 amino acids. Its generic name is cibinetide. Researchers designed it to reproduce a tissue-protective surface on helix B of erythropoietin.
Full-length EPO stimulates red-blood-cell production through the classical EPO receptor. ARA-290 was designed to avoid that pathway. It is proposed to act through a different signaling complex called the innate repair receptor, often described as a combination of an EPO receptor component and the beta-common receptor CD131.
“Emergency repair system” is a useful metaphor for this pathway. Activation of the proposed receptor can trigger anti-inflammatory, cell-survival, and tissue-repair signals in experimental models.
That mechanism is what makes ARA-290 different from a conventional pain suppressant. The goal is not only to turn down the pain signal. The goal is to change the environment around an injured nerve and support repair.
A mechanism is still not a clinical outcome. The human evidence must show whether those signals produce measurable nerve changes.
ARA-290 also leaves the blood quickly. In the type 2 diabetes study, researchers cited a terminal plasma half-life of about 20 minutes after a 4 mg subcutaneous dose. The biological hypothesis is that a brief receptor signal can start longer downstream effects. A short half-life does not establish either benefit or safety.
Does ARA-290 “repair nerves” instead of masking pain?
This is the most important question around ARA-290.
The human studies did not rely only on pain questionnaires. Researchers also measured small nerve fibers in the cornea and skin.
In one 38-person sarcoidosis trial, 28 days of 4 mg subcutaneous ARA-290 was associated with a 14.5% median increase in corneal nerve-fiber area. The placebo group had a nonsignificant decrease.
In a later 64-person Phase 2b study, the 4 mg group had a statistically significant placebo-corrected increase in corneal nerve-fiber area. A marker of regenerating skin fibers also increased. The 1 mg and 8 mg groups did not meet the main corneal endpoint.
In the type 2 diabetes study, PainDetect scores improved versus placebo. Corneal nerve-fiber density increased in the subgroup that began with low density. The overall study groups did not show a significant density change.
Corneal nerve-fiber area, corneal nerve-fiber density, and GAP-43-positive skin fibers are useful biological measures. They may show nerve loss or regeneration. They are still surrogate endpoints. A change in a surrogate does not automatically mean durable restoration of sensation, autonomic function, mobility, or quality of life.
The studies lasted weeks, not years. They enrolled small groups. Several papers included authors affiliated with the company developing ARA-290. Independent replication and a larger confirmatory trial would make the conclusion stronger.
There is no head-to-head study against gabapentin. The meaningful contrast is between research goals: gabapentin is used to control neuropathic pain, while ARA-290 is being studied for possible disease modification and nerve repair.
The early objective findings make that possibility credible enough to study. They do not establish a permanent repair.
Is ARA-290 available? Live vendors and pricing
ARA-290 is not an approved prescription medicine. It is sold by research vendors, which is a different market from the investigational product used in clinical trials.
PeptidePrices tracks those listings and normalizes different vial sizes to a common 10 mg basis.
On August 11, 2026, the site tracked 25 in-stock ARA-290 listings. Twenty-four had enough quantity data for normalization.
| Pricing measure | August 11 snapshot |
|---|---|
| Lowest 10 mg-equivalent price | $33.33 |
| Median 10 mg-equivalent price | $54.99 |
| Highest 10 mg-equivalent price | $88.00 |
| Most recent listing check | August 10, 2026 |
See the live ARA-290 vendor and price comparison for current stock, vial size, vendor evidence, and price changes.
Price is not evidence of identity, purity, or sterile manufacture. Match any certificate to the exact compound, lot, and vial strength. Our COA verification guide explains the checks.
Could ARA-290 become a long-term fix for neuropathy?
Potentially, but the current trials cannot answer that yet.
The studies lasted about four weeks. They were designed to find biological and symptom signals, not to prove permanent recovery or prevention of future nerve loss.
A real long-term answer would require a larger trial with longer follow-up. It would need to show that objective nerve changes persist and translate into better sensation, autonomic function, mobility, and quality of life.
ARA-290 has crossed an important early threshold: selected trials found measurable small-fiber changes in people, not only animals. It has not crossed the threshold from promising disease-modifying candidate to proven therapy.
Claims that move beyond the human evidence
Concussion and traumatic brain injury
No human ARA-290 trial for concussion or traumatic brain injury was identified. Animal and cell findings cannot establish brain repair after repeated concussions.
The human brain-related study gave one intravenous dose to healthy volunteers and measured emotional processing one week later. It did not test people with brain injury and did not show nerve regeneration.
Chemotherapy-induced neuropathy
Preclinical toxin-injury models are sometimes used to support this claim. No completed human ARA-290 trial for chemotherapy-induced peripheral neuropathy was identified in the reviewed evidence.
Broad chronic inflammation
ARA-290 was designed around anti-inflammatory and tissue-protective signaling. That does not make “chronic inflammation” a proven human indication. The clinical studies tested specific populations, mainly people with sarcoidosis or type 2 diabetes.
Safety, approval, and other countries
The short clinical studies did not reveal a consistent major safety signal. They also cannot establish long-term safety.
In the type 2 diabetes trial, one participant stopped on day 15 after borderline renal insufficiency worsened. The participant was also taking furosemide and had a dose increase. The investigators did not identify a broader drug-related renal signal, but a small trial cannot exclude uncommon harms.
ARA-290 is not FDA-approved. No national marketing authorization was identified in the reviewed United States or European Union sources.
FDA's substance database recognizes cibinetide and records orphan-drug designations. The European Union has also granted an orphan designation for a transplant-related indication. These designations support development. They are not approval. The European Medicines Agency's orphan-designation page states that quality, safety, and efficacy still must be demonstrated before marketing authorization.
FDA also lists cibinetide in 503A Category 3, meaning it was nominated for compounding without adequate support for evaluation. This is not an approval pathway.
Short trial safety data for a controlled investigational product also cannot authenticate research-market vials. Identity, amount, endotoxin control, sterility, and storage can differ.
The bottom line
Most current neuropathy drugs are used to manage symptoms. ARA-290 is interesting because researchers are asking a harder question: can a treatment change the damaged nerve process itself?
Small early trials found changes in neuropathy questionnaires and selected objective small-fiber measures in sarcoidosis and type 2 diabetes. Those findings support the possibility of nerve repair.
They do not prove durable nerve restoration or a long-term fix. The 2 mg and 4 mg protocols describe human research, not consumer dosing.
ARA-290 is a serious disease-modifying candidate. It remains investigational, and the research-vendor market is not equivalent to the product used in clinical trials.
Primary sources
- Heij et al. Randomized pilot in sarcoidosis-associated small-fiber neuropathy, Molecular Medicine, 2012.
- Dahan et al. NERVARA sarcoidosis trial, Molecular Medicine, 2013.
- Brines et al. Type 2 diabetes and neuropathic symptoms trial, Molecular Medicine, 2015.
- Culver et al. Phase 2b sarcoidosis dose-ranging trial, Investigative Ophthalmology & Visual Science, 2017.
- ClinicalTrials.gov record NCT02039687 for the Phase 2b dose-ranging study.
- Cerit et al. Healthy-volunteer emotional-processing study, European Neuropsychopharmacology, 2015.
- Lois et al. Diabetic macular edema pilot, Journal of Clinical Medicine, 2020.
- NINDS peripheral neuropathy overview.
This article is for education and research comparison. It is not medical advice or a dosing protocol. ARA-290/cibinetide is investigational and is not FDA-approved.