An 11-amino-acid piece of erythropoietin that does not raise red blood cells, tested in small trials for nerve pain and nerve loss.
Also called Cibinetide, pHBSP, Pyroglutamate helix B surface peptide, ARA 290
ARA-290 (cibinetide) was built from the surface of erythropoietin (EPO), the kidney hormone that makes red blood cells. EPO also protects injured tissue, but its blood-thickening effect makes it unsafe to use for that purpose. ARA-290 keeps the tissue-protection signal and drops the red-blood-cell signal, because it binds a different receptor that only shows up on stressed or inflamed tissue.
Almost all of the human data comes from one sponsor, Araim Pharmaceuticals, and one academic group at Leiden University. In four small placebo-controlled trials (22 to 64 people, 28 days each), people with sarcoidosis or type 2 diabetes who had small-fiber nerve damage reported less burning and tingling, and corneal scans showed more nerve fibers. The largest trial hit its primary endpoint only at the 4 mg dose, not at 1 mg or 8 mg.
It has never gone past phase 2 and is not approved anywhere. The EU granted it orphan status for sarcoidosis in 2013, and no trial has been registered as active in years. What you see sold online as ARA-290 is a research chemical with no quality control, and its mechanism falls under WADA's ban on innate repair receptor agonists.
What it binds to, and what happens inside the body after that, step by step.
EPO makes red blood cells through a receptor made of two EPO receptor units. Injured or inflamed tissue switches on a second receptor, the innate repair receptor, made of one EPO receptor unit paired with the beta common receptor (CD131). ARA-290 binds only the second one, so it signals tissue protection and calms inflammation without raising hematocrit. It leaves the blood within minutes, but the downstream effects in animal and human studies lasted weeks.
Human results and animal results are kept apart below. A result in rats tells you a mechanism is plausible. It does not tell you what happens in a person.
Four small placebo-controlled trials in people with small-fiber neuropathy (sarcoidosis or type 2 diabetes) showed lower symptom scores and more corneal nerve fibers after 28 days, with no safety signal. The trials were short, sponsored by the developer, and the largest one was positive only at one of three doses. The broader claims about kidney, heart, brain and bone protection come from rodent studies only.
64 adults with sarcoidosis-associated small nerve fiber loss and neuropathic pain
Placebo-corrected corneal nerve fiber area rose by 697 square micrometers at 4 mg/day (P = 0.012); the 1 mg and 8 mg groups did not reach significance, and pain improved in every group including placebo.
Read the study38 adults with sarcoidosis and small nerve fiber loss
28 days of daily subcutaneous ARA-290 improved neuropathy symptom scores versus placebo and was associated with higher corneal nerve fiber density and a longer 6-minute walk.
Read the study48 adults with type 2 diabetes and painful neuropathy
HbA1c fell 0.21 percentage points by day 56 on ARA-290 while it rose 0.21 on placebo (P = 0.002 across the 56-day course); PainDetect neuropathy scores also improved.
Read the study22 adults with sarcoidosis and small fiber neuropathy (12 ARA-290, 10 placebo)
Small fiber neuropathy screening score dropped 11.5 points on ARA-290 versus 2.9 on placebo at week 4 (P < 0.05); pain inventory scores improved equally in both groups.
Read the study9 adults with diabetic macular edema (8 completed)
12 weeks of 4 mg/day produced no average improvement in visual acuity or retinal thickness; no serious adverse events and no anti-drug antibodies.
Read the study36 healthy volunteers
A single 2 mg dose changed some measures of emotional processing but had no effect on mood, and the pattern did not look like an antidepressant.
Read the studyRats, spared nerve injury model
Five doses over 10 days reduced mechanical and cold allodynia for up to 20 weeks and blunted spinal microglia activation.
Read the studyThese are questions the published research has not answered.
No product containing ARA-290 is approved as a medicine by the FDA.
Investigational drug that stalled after phase 2. The European Commission granted orphan designation EU/3/13/1191 for sarcoidosis on 7 October 2013 (sponsor transferred to Araim Pharmaceuticals Europe Limited, Ireland, in 2019). Orphan designation is a development incentive, not an approval. No ClinicalTrials.gov study is currently recruiting. WADA's 2026 list bans innate repair receptor agonists under S2.1.5; ARA-290 acts on that receptor and anti-doping labs treat it as prohibited.
How much of ARA-290 is left after a single dose
Simple first-order model from the published half-life. Real clearance varies with dose, route, kidney and liver function and formulation. This is not a dosing schedule.
This table records the doses that trials and approved labels used, with the source for each row. It is a record of research, not a recommendation, and it is open to free members.
Which symptoms are expected and which mean stop and get help: side effects and red flags.
Tap a claim to see what the studies found.
It was built specifically not to raise red blood cells, so it has no oxygen-carrying benefit. WADA still bans it because it acts on an EPO-related receptor.
Corneal and skin biopsies showed more small nerve fibers after 28 days in small trials of people with sarcoidosis or diabetes. That is a surrogate marker in small, sponsor-run studies, not proof of lasting repair.
One 48-person trial found HbA1c 0.21 points lower by day 56 versus a rise on placebo. That is a small change from a single trial and has not been repeated.
A 36-person study in healthy volunteers found no effect on mood, and the changes it saw in emotional processing did not match the pattern antidepressants produce.
Those effects come from rat and mouse injury models. No human trial has tested them.
These pairings come up often. Almost none have been tested together in a trial, and the evidence note on each says so plainly.
No approved product exists, so there is no label storage guidance. Trial drug was supplied by the sponsor; research-chemical vials are typically kept frozen and away from light.
No published stability data for reconstituted peptide outside the trial setting. The molecule is broken down quickly by blood enzymes, so stability once dissolved is unknown.
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