Peptide LexiconAll compounds

ARA-290: Real Trials, and the Numbers Nobody Reads

ARA-290 has what almost nothing else in this library has — a randomized, placebo-controlled, quadruple-masked phase 2 with posted results. Reading those results is the point: the middle dose beat the highest, and on one nerve measure placebo beat all three.

PeptideRandomized human trials completedNo approved product

Caroline S · Published 2026-09-13

Length

11 amino acids

Sequence

A short peptide derived from a region of erythropoietin that is not involved in making red blood cells, described in the literature as the helix B surface peptide

Origin

Developed by Araim Pharmaceuticals from work on erythropoietin's tissue-protective signalling, with the aim of separating that effect from the blood-forming effect.

Last reviewed

2026-09-13

What is it good for?

It is investigated for small-fibre nerve damage and the pain that comes with it — in sarcoidosis and in diabetes — and sold on the broader claim of tissue repair and reduced inflammation. Its registered trials are about nerves and eyes, not recovery or performance.

Illustration: A glass tube lying on its side on a white bench, half filled with a dark green and copper swirl, a copper dish blurred behind.
Illustration

What it is

ARA-290, generic name cibinetide, is a peptide of eleven amino acids lifted from a specific region of erythropoietin — the hormone that tells the marrow to make red blood cells.

The design idea is a good one, and it is worth understanding because it is not marketing. Erythropoietin does two quite separate things: it drives red cell production, and it protects tissue and nerves from injury. The second effect is desirable in its own right, but you cannot exploit it by giving erythropoietin, because the first effect thickens the blood and raises the risk of clots. ARA-290 is taken from a surface of the molecule involved in the protective signalling and not in the blood-forming one — an attempt to keep half of a hormone's behaviour and discard the other half.

It was developed by Araim Pharmaceuticals and investigated for small-fibre neuropathy: damage to the fine nerves that carry pain and temperature, in sarcoidosis and in diabetes.

It has a real trial programme

This entry is unusual for this library, so the distinction should be stated clearly. Most compounds here have a literature and no trials, or trials that predate registration, or registrations filed by people who never ran anything. ARA-290 has four interventional registrations on ClinicalTrials.gov as of 2026-09-13:

Registration Sponsor Phase n Status
NCT02070783 — cognitive and neural effects Leiden University Medical Center 1/2 36 Completed
NCT02039687 — corneal nerve fibre density and neuropathic symptoms in sarcoidosis Araim Pharmaceuticals 2 64 Completed, results posted
NCT01933529 — prediabetes and type 2 diabetes Claes-Göran Östenson 2 24 Unknown
NCT06626971 — diabetic macular oedema Belfast Health and Social Care Trust 2 9 Terminated

62 PubMed records name the compound, four of them carrying the randomized-controlled-trial publication type.

That is a genuinely better starting position than almost anything else in this library. Which is precisely why the next section matters.

The posted results, read rather than counted

NCT02039687 is the trial that decides how this compound should be described. It is randomized, quadruple-masked, placebo-controlled, with 64 participants in four arms of sixteen — 1 mg, 4 mg or 8 mg of ARA-290 given subcutaneously each day for 28 consecutive days, against a formulation-buffer placebo. (Those figures are the protocol's, reported here as the registry records them.)

Its results are posted on ClinicalTrials.gov, which is rare enough to be worth saying twice. Here is the primary outcome — change in corneal nerve fibre area, in µm², over 28 days, mean with standard deviation:

Arm Mean change SD
1 mg/day −64.3 759.9
4 mg/day +533.8 1110.02
8 mg/day +203.8 641.2
Placebo −170.0 633.0

Three things are visible in that table and none of them appear on a vendor page.

There is no dose-response. The 4 mg arm changed most; the 8 mg arm changed less than half as much; the 1 mg arm went the same way as placebo. If the compound were driving the effect, doubling the dose should not halve the result.

The variation dwarfs the effect. Every standard deviation is larger than its own arm's mean change, and in the 4 mg arm the spread is about twice the average. Individual participants were moving in both directions by hundreds of µm².

No p-value is posted for the primary outcome. There is no analysis in the record turning these numbers into a statistical claim.

The secondary outcomes point in different directions

Intra-epidermal nerve fibre density — the skin-biopsy count of the same small nerve fibres, and the more established of the two measures — came out as follows, in fibres per millimetre: placebo +0.8, 1 mg +0.5, 4 mg +0.4, 8 mg −0.3. On this measure placebo did better than every drug arm.

The six-minute walk test is the trial's most favourable number and deserves to be given fairly: +19.3, +17.7 and +18.2 metres in the three drug arms against +1.2 metres on placebo. That is a consistent pattern across all three doses, which is the opposite of what the primary outcome showed. It is also a secondary outcome, in a trial whose primary did not separate, with standard deviations of 38 to 79 metres and no posted analysis.

One more line in the participant-flow data is worth noting: withdrawals rose with the dose — 0 of 16 at 1 mg, 1 of 16 at 4 mg, 3 of 16 at 8 mg, and 0 of 16 on placebo. With numbers this small that is not evidence of harm, but it is the direction one would watch in a larger study.

The trial that stopped, and why the reason is interesting

The Belfast diabetic macular oedema study, NCT06626971, is recorded as terminated with this explanation: expiry of study drug — no replacement available. Nine participants had enrolled.

Registries seldom state a reason that concrete. It is not a safety termination and not a futility termination; it is a supply failure. A trial that ends because nobody could provide more of the drug describes the compound's commercial position more honestly than any press release: somewhere between an active research programme and a shelved one.

Where it stands

There is no approved product. Drugs@FDA and DailyMed both returned nothing for cibinetide on 2026-09-13. No phase 3 appears in the registry, roughly a decade after the phase 2 completed.

The fair summary is narrower than either the marketing or the cynical reading. ARA-290 is a rationally designed peptide that reached properly controlled human trials and reported its numbers — and those numbers did not show what they needed to show. That is a more respectable place to be than most of this library, and it is still not evidence of benefit.

For the other compounds sold on repair and anti-inflammatory claims, see BPC-157, LL-37 and the licensed immune peptide thymosin alpha-1; for the broader question these entries keep returning to, peptides for joints and tendons.

What the research shows

Has registered, randomized human trials

Four interventional registrations; the largest is randomized, quadruple-masked and placebo-controlled with 64 participants

Has posted trial results that anyone can read

NCT02039687 has results posted on ClinicalTrials.gov — rare in this library

Improved its primary outcome in a dose-dependent way

No. The 4 mg arm changed most, the 8 mg arm less than half as much, the 1 mg arm moved in the same direction as placebo, and every standard deviation exceeded its own mean

Improved the skin-biopsy measure of the same nerve biology

No. On intra-epidermal nerve fibre density, placebo recorded the largest gain of the four arms

Has an approved use anywhere

No approval and no product record in the United States

Bars show how much of the evidence is in humans, not how well anything works.

Where it stands

United States

No approved product. Drugs@FDA and DailyMed returned no record for cibinetide on 2026-09-13.

Published record

62 PubMed records name ARA-290 or cibinetide as of 2026-09-13, of which 4 carry the randomized-controlled-trial publication type.

Trial registry

4 interventional registrations on ClinicalTrials.gov (2026-09-13): a phase 1/2 cognitive and neural study at Leiden (n=36, completed), a phase 2 in sarcoidosis neuropathy sponsored by Araim (n=64, completed, results posted), a phase 2 in prediabetes and type 2 diabetes (n=24, status unknown), and a phase 2 in diabetic macular oedema in Belfast (n=9, terminated).

Dosing reported in the registry

The phase 2 in sarcoidosis administered 1 mg, 4 mg or 8 mg subcutaneously each day for 28 consecutive days, against a buffer placebo. These are trial protocol figures, reported as such.

Why one trial stopped

The Belfast macular oedema study is recorded as terminated for the expiry of the study drug with no replacement available — nine participants enrolled.

Frequently asked questions

What is ARA-290?

A peptide of eleven amino acids, also called cibinetide, copied from a region of the hormone erythropoietin that is not responsible for making red blood cells. The idea behind it is to capture erythropoietin's protective effect on tissue and nerves while leaving out the blood-thickening effect that makes erythropoietin itself risky to give for that purpose.

What does the research actually show?

That it has been properly tested, which is more than most compounds here can say, and that the clearest result available is ambiguous. Its one placebo-controlled phase 2 with posted results, in 64 people with sarcoidosis nerve damage, showed the middle dose changing the primary measure most, the highest dose changing it less than half as much, and the lowest dose moving in the same direction as placebo — with variation in every arm larger than the average change.

Is this a better evidence base than the other peptides in this library?

Structurally, yes. Four registered interventional trials, a randomized quadruple-masked design, a company sponsor and posted results put it in a different class from compounds whose entire file is cell culture or 1990s physiology. That is exactly why the numbers are worth reading rather than counting. A strong study design is what makes a null or noisy result informative instead of meaningless.

What does 'no dose-response' mean and why does it matter?

If a compound is producing an effect, more of it usually produces more of that effect, at least until a ceiling. Here the 4 mg arm recorded +533.8 µm² and the 8 mg arm +203.8 — the larger dose did less. That pattern is what noise looks like in a small trial, and it is the single most common way a promising early result fails to reproduce. It does not prove the compound does nothing; it does mean this trial did not demonstrate that it does something.

Placebo beat the drug on one measure. How should that be read?

Carefully, and in both directions. Intra-epidermal nerve fibre density is measured from a skin biopsy and it is the more established of the two nerve measures in the trial. Placebo recorded +0.8 fibres per millimetre against +0.5, +0.4 and −0.3 in the drug arms. With 16 people per arm none of these differences is likely to be distinguishable from chance, which is the point: the trial is too small to settle the question either way, and nothing in its posted results supports a claim of nerve regeneration.

What about the six-minute walk result?

It is the most favourable number in the trial and deserves to be reported as such: all three drug arms gained 17 to 19 metres while placebo gained 1.2. It is also a secondary outcome in a trial whose primary outcome did not separate, with standard deviations of 38 to 79 metres, and no posted analysis. A secondary outcome that looks better than the primary is a reason to run another trial, not a result.

Why did one of the trials stop?

The Belfast diabetic macular oedema study is recorded as terminated because the study drug expired and no replacement was available. Nine people had enrolled. Registries rarely state a reason that concrete, and it describes a supply problem rather than a safety or efficacy one — which tells you something about where the compound sits commercially.

What would change the picture?

A larger trial with a single dose chosen in advance and a posted analysis. The phase 2 has already done the hard part by being properly designed and reporting its numbers; what it has not done is produce a signal clear enough to act on. After a decade, no phase 3 appears in the registry.