Ara-290: what the studies show, status and safety

Summary

Ara-290, also called cibinetide, is a designed eleven-unit peptide copying one surface of erythropoietin, a surface with no role in making red blood cells. In small studies in sarcoidosis it increased the nerve fibre measured in the cornea. The largest of those studies missed its pain endpoint, no country has approved it, and the receptor it was built for is unconfirmed.

Key findings at a glance

• The largest study missed the endpoint patients feel. In 64 patients, pain improved in every group including placebo. The placebo-corrected fall in pain intensity reached p = 0.157, which is not a statistically significant difference ^[1], ^[2].
• What it did meet was a measurement in the eye. The primary endpoint was the amount of nerve fibre in the cornea, and only the middle of three dose levels reached significance. The highest level did not. More substance did not mean more effect ^[1].
• The receptor the whole idea rests on was not confirmed. An independent group tested whether the two proteins said to form it actually bind each other. They do not, with or without the peptide present ^[3].
• A supporting preclinical paper was withdrawn in 2026. A 2012 study on kidney injury, long used as a standard reference for organ protection, was retracted in February 2026. Its results can no longer be cited as findings ^[4], ^[5].
• Six orphan designations, zero approvals. Four were granted in the United States between 2009 and 2016, two in the European Union in 2013 and 2016. Every American record carries the line Not FDA Approved for Orphan Indication ^[6], ^[7], ^[8].
• The only product ever sold outside a trial was recalled. A Texas compounding pharmacy shipped a prescription-labelled injection nationwide. In April 2022 the FDA classified the recall as Class II for lack of assurance of sterility ^[9].
• It is prohibited in sport at all times. The 2026 list does not name it, but the category it heads covers it, and the 2016 list named it outright ^[10], ^[11].
• Three registered studies have never published a result. Two Dutch studies and one Swedish study are registered and silent, so the published record cannot be weighed against the complete one ^[12], ^[13].
• It does not raise red blood cells, by design. The founding paper states that the eleven-unit peptide is not erythropoietic, in cells or in animals. That effect was removed on purpose ^[14].
• Development stopped quietly in 2017. The last study closed early, and the register gives the reason as expiry of the study drug with no replacement available ^[15].

What it is

Ara-290 is a synthetic peptide of eleven amino acids. It is not a natural fragment of anything, and it is not a hormone. It is a deliberate copy of one small part of a much larger molecule.

That larger molecule is erythropoietin, the hormone that tells the bone marrow to make red blood cells. Erythropoietin also appears to protect tissue after injury, and researchers wanted the second effect without the first.

They narrowed the protective part down to one helix, then copied only the side of that helix which faces the surrounding water when erythropoietin sits in its receptor. That side takes no part in the blood-forming grip ^[14].

One chemical change was added on purpose. The first amino acid was closed into a ring, which slows the enzymes that chew peptides from the end. Even so, the molecule survives in blood for about two minutes ^[14], ^[16].

The naming is a genuine obstacle to research. pHBSP is the descriptive laboratory name, ARA 290 the development code from the company that ran the trials, and cibinetide the name assigned by the World Health Organization. A search under one name misses part of the record ^[17], ^[18].

One more trap sits in the letters. Written in single-letter code the sequence reads UEQLERALNSS, and the U there stands for the ring-closed first building block, not for the rare amino acid selenocysteine that the letter normally means. Pasted into a search tool without that knowledge, the string describes a different molecule ^[18].

Quick facts

How it works

The proposed idea is narrow and, if true, elegant: a signal that only exists where tissue is already damaged. Whether that signal exists in the form described is the open question of this whole substance.

• The intended target is a pair of receptors working together. The developers describe a complex of the erythropoietin receptor and a second chain called CD131, which they named the innate repair receptor ^[14], ^[21].
• It is not supposed to touch the blood-forming receptor. That one is a pair of identical erythropoietin receptors, and the copied surface has no grip on it. This is why the peptide does not raise haemoglobin ^[14].
• The target is said to appear only after damage. The developers write that the complex is usually absent from normal tissue and appears quickly after injury or inflammation. That is their hypothesis, not an independent finding ^[16].
• An independent group could not find the interaction. Australian researchers measured whether the outer parts of the two receptors bind each other, with and without the peptide. They concluded that they do not directly interact ^[3].
• At least one effect runs through a different route entirely. In cell and behavioural experiments the peptide blocked a pain-sensing channel called TRPV1, which would explain part of the pain results without the repair receptor ^[22].
• The timing is unexplained. Minutes in the blood, but effects lasting weeks in animals. The developers call this a molecular switch. No independent work has confirmed that model ^[16].

This is where Ara-290 sits apart from most peptides listed near it. Growth hormone releasers and appetite peptides act on receptors that are present in healthy tissue. Here the claim is the reverse, and the receptor itself is disputed ^[3], ^[14].

What the studies found

Six studies in people have been published. Together they enrolled 217 participants, of whom roughly 130 received the substance and the rest a placebo. Every one of them is small, and the endpoints are mostly questionnaires and microscope measurements rather than events ^[19].

Symptoms in sarcoidosis

Phase 2 pilot The first study randomised 22 patients with sarcoidosis and symptoms of small nerve fibre damage, twelve to the substance and ten to placebo, over four weeks. The symptom questionnaire improved more in the treated group, a change of −11.5 against −2.9, the two figures carrying a margin of error of 3.04 and 3.34, with p below 0.05 ^[23].

Phase 2 pilot The same study found no separation on two other measures. Scores on the Brief Pain Inventory and on a fatigue scale improved significantly in both groups equally, and a depression questionnaire did not move at all. Within the treated group two parts of a general quality-of-life questionnaire also shifted, pain by −23.4 and physical functioning by −14.6, with margins of error of 5.5 and 3.9, but those are movements against each patient's own starting value rather than against placebo. No safety concerns were raised in that study by clinical or laboratory assessments ^[23].

Phase 2 RCT A blinded study in 38 patients, 21 treated and 17 on placebo, ran for 28 days with twelve weeks of follow-up. The symptom score fell 12.2 points against 3.8 on placebo. That is about 28 per cent below the starting value against about 9 per cent, with a group difference of p = 0.005 ^[24].

Phase 2 RCT Two further measures in that study separated as well. The way the skin of the hand sensed temperature also shifted, with p = 0.027 for the threshold at which cold became painful, p = 0.032 for the same threshold with heat, and p = 0.008 for the smallest temperature difference patients could still tell apart. In a six-minute walking test the treated group covered 18.7 metres more than at the start, while the placebo group covered 15.1 metres less, a group difference of p = 0.049 ^[24].

Nerve fibres in the cornea

Phase 2 RCT The cornea is used as a window onto small nerves, because they can be photographed there without a biopsy. In the 38-patient study the nerve fibre area rose by a median 14.5 per cent, or 185 square micrometres, at p = 0.022. On placebo it fell by a median 5.3 per cent, or 64 square micrometres, a change well inside the range of chance at p = 0.462 ^[24].

Phase 2b RCT The largest study, 64 patients over 28 days, made this measurement its primary endpoint and tested three dose levels against placebo. The placebo-corrected change was 109 square micrometres at the lowest level, 697 at the middle level with p = 0.012, and 431 at the highest ^[1], ^[2].

Phase 2b RCT Two other findings from that study support the measurement rather than a benefit. Regenerating fibres in the skin increased at the middle level, p = 0.035. The change in nerve fibre area moved together with both those fibres, rho = 0.575 at p = 0.025, and with walking distance, rho = 0.645 at p = 0.009, where a rho of 1 would mean the two measures rise and fall in lockstep ^[1].

Method study The measurement itself was validated by the same author group, including the sponsor. Fibre area, density, branching and length separate patients from healthy people about equally well. This is a methods paper, so it adds no evidence of effect ^[25].

Pain, the endpoint that was missed

Phase 2b RCT This is the central negative result. Pain improved significantly in all groups, and for participants with moderate to severe pain the placebo-corrected fall at the middle level reached p = 0.157. A value that high means the gap to placebo lies well inside what chance alone produces, so the study cannot claim an effect on pain ^[1].

Phase 2 RCT The earlier study pointed the same way. Pain intensity fell by about 9 per cent in both arms, a mean drop of 3.4 points at p = 0.01 within each group. Between the groups there was no significant difference ^[24].

Phase 2 RCT What did separate in that study was how much the pain interfered with daily life. That score fell 36 per cent under the substance against 16 per cent on placebo, at p below 0.02 ^[24].

Blood sugar in type 2 diabetes

Phase 2 RCT Forty-eight participants with diabetes and painful limb complaints were analysed. HbA1c, which reflects the average blood sugar of the preceding weeks, fell 0.16 percentage points by day 28 and 0.21 by day 56, at p = 0.002. On placebo it barely moved by day 28, 0.01 points down, and had risen 0.21 points by day 56. A change of that size sits below what is usually treated as clinically meaningful ^[26].

Phase 2 RCT Other measures in the same study were mixed. The ratio of total cholesterol to HDL improved, p = 0.039, and triglycerides fell, p = 0.043, while the HDL rise itself missed significance at p = 0.066. Several authors were employees or shareholders of the sponsor ^[26].

Phase 2 RCT The nerve measures in that study moved in the same modest way. A questionnaire for nerve pain improved by 3.3 points by day 28 and by 4.2 points by day 56 under the substance, against 1.1 and 0.74 points on placebo, at p = 0.037. Among the participants whose corneal nerve density was clearly below normal at the start, density rose by 2.6 fibres per square millimetre in the 18 treated, at p = 0.02, against 0.7 fibres in the 19 on placebo, which was not significant ^[26].

Diabetic macular oedema

Phase 2, single arm This is the clearest negative study. Nine patients were recruited between May 2016 and April 2017 and followed over twelve weeks, the longest exposure ever documented, and eight of them completed it. None of the objective endpoints improved. Visual acuity fell by 2.9 letters on the eye chart, the retina at its centre thickened by 10 micrometres, its sensitivity fell by 0.53 decibels and tear production fell by 0.13 millimetres ^[27].

Phase 2, single arm The study also ended early, and the reason recorded in the register is worth quoting: expiry of study drug, no replacement available. Only a questionnaire score moved upward, by 2.7 points on a scale for vision-related quality of life. No serious adverse events and no antibodies against the substance were seen ^[15], ^[27].

Mood and emotion processing

Phase 1 or 2 RCT A single dose was given to 36 healthy volunteers, double-blind against placebo, with brain imaging and cognitive tests a week later. Responses to happy faces in one visual region were lower under the substance, the opposite direction to an antidepressant pattern, and the recognition of happy and disgusted expressions tended to drop as well. Two smaller measures pointed the other way, a faster sorting of positive against negative words and more attention to positive pictures. On mood and emotional symptoms there was no effect at all ^[28].

Animal studies

Animal data In rats given a heart attack by tying off an artery, a single injection immediately afterwards cut cell death in the threatened area by 80 per cent. Inflammation fell by 34 per cent and the damaged area by 50 per cent, and two weeks later that area was still 25 per cent smaller, an effect that held throughout the six weeks the animals were followed. Timing mattered more than quantity: the same injection given 24 hours after the artery was tied did nothing, while a sixtieth of it still worked when given at once ^[29].

Animal data In a mouse model of Alzheimer's disease the result splits by age. Young animals treated early showed slower plaque build-up and better cognition. In old animals with advanced disease the same treatment failed completely, both on plaques and on circulating monocytes ^[30].

Animal data In mice with a crushed sciatic nerve the substance relieved mechanical and cold hypersensitivity, but not in mice lacking the CD131 chain. The authors read that as evidence the effect runs through the proposed receptor ^[31].

What is still unknown

• How the body handles it. Only the two-minute half-life is published, and that comes from a review written by the developers. Bioavailability, peak level and clearance have never been reported for any route ^[16].
• Whether the mechanism is real. The direct binding of the two receptor parts could not be demonstrated by an independent group, and no alternative model has been established ^[3].
• What three registered studies found. Studies in rheumatoid arthritis, in complex regional pain syndrome and in prediabetes are registered with no published result. Two still show an obviously outdated status of ongoing ^[12], ^[13].
• Anything beyond twelve weeks. The longest documented exposure covered nine people over twelve weeks. There is nothing longer, nothing in healthy people beyond one dose, and nothing in pregnancy or in minors ^[27].
• Basic toxicology. No published toxicology study for this peptide was found. Whether such data exist inside regulatory dossiers cannot be checked from outside ^[19].
• What is in grey-market material. No laboratory analysis of traded material has been published. The one official quality finding on material actually sold is a recall for lack of sterility assurance ^[9].

Side effects and safety

There is no safety record that would carry use outside a study. About 130 people have received the substance, all under close supervision, and most of them for 28 days or for a single dose. Within those limits the substance was described as well tolerated ^[19].

• Two serious events were judged possibly related to it. Both came from the diabetes study, which recorded four serious events in the treated arm and none on placebo. In one of them a participant was already taking the diuretic furosemide, that treatment was stepped up after the second week, and an already borderline kidney function worsened, with creatinine rising from 119 to 159 micromoles per litre. The safety committee stopped the study drug in that person. The report sets out that case in detail and does not say which event was the second of the two ^[26].
• A further serious event in the same arm was fatal. A man of 70 developed a severe lower leg infection two weeks after his last dose, was admitted to hospital and suffered a fatal heart attack. The safety committee assessed that event as not connected to the treatment ^[26].
• Milder events were common in both arms. The same study recorded 54 mild, 9 moderate and 1 severe categorisation under the substance, against 61 mild and 5 moderate under placebo ^[26].
• One unexplained event in the sarcoidosis study. A long-term weight loss of 14 kilograms over several months was rated moderate and then stabilised. Its cause stayed unclear. Three moderate events in the same study occurred on placebo ^[24].
• No antibody response was detected. Three studies tested for antibodies against the substance and found none. All of them tested over 28 days or twelve weeks, in small groups ^[24], ^[26], ^[27].
• The safety data for the largest study are not public. The full text was unavailable, and the only statement on safety in that study comes from a sponsor press release. That is not a peer-reviewed finding ^[1], ^[32].
• Kidney biology deserves attention, not reassurance. The retracted 2012 paper was about kidney injury, the one possibly related serious event was renal, and no toxicology is published. None of this proves harm; all of it means the question is open ^[4], ^[26].
• It is not haematologically inert. It does not raise red cells, but in the Alzheimer mouse model it raised circulating monocytes and their precursors in the bone marrow. In the human studies the blood counts and general blood chemistry showed no medically significant deviations, but none of those studies set out to look for shifts in immune cell populations, and there are no systematic human data on that under longer use ^[24], ^[30].

Two structural problems sit behind all of the above. Most of the safety assessment rests on papers co-authored by employees and shareholders of the sponsor, and three registered studies were never published. The size of any publication bias cannot be estimated ^[12], ^[26].

Material traded online carries only the seller's own labelling. The American regulator has written, in letters to other peptide traders, that a research use only label does not change what a product legally is ^[33].

Why this page lists no doses

This page gives no amounts for Ara-290, in any unit, for people or for animals. No health authority anywhere has ever assessed an amount for this peptide, because none has ever reviewed it for approval ^[19].

The one preparation ever sold outside a trial shows why a figure here would mislead. A compounding pharmacy shipped it as a prescription-labelled injection, and the FDA classified the recall as Class II because sterility could not be assured ^[9].

The dose-response relationship is also not orderly, which is unusual and important. In the largest study the middle of three levels met the primary endpoint and the highest did not. A number on a reference page would suggest a logic the data do not support ^[1].

The amounts used in the published studies were given to defined patient groups under close clinical and laboratory monitoring, with a safety committee able to stop the study drug. In one case it did exactly that. None of that framework exists outside a hospital ^[26].

Development and approval status

Ara-290 has never been approved in any market and has never entered a phase 3 study. Register checks on 15 September 2026 found no authorised product anywhere, and no marketing application in any register consulted ^[19].

• 2008 the eleven-unit copy is published, together with the finding that it does not make red blood cells ^[14].
• 2009 to 2016 four American orphan designations are granted, for a transplant setting, for nerve pain in sarcoidosis, for sarcoidosis itself and for islet transplantation ^[6].
• 2012 to 2015 the human studies run, all of them small, most of them at one Dutch university hospital ^[23], ^[24], ^[26].
• October 2013 and August 2016 two European orphan designations are granted, both transferred to an Irish company in April 2019 ^[7], ^[8].
• May 2017 the sponsor announces a next step after a meeting with the American regulator. That step appears in no register ^[32].
• August 2017 the last study closes early because the study drug expired and could not be replaced ^[15].
• Since 2017 no new study has been registered anywhere, and three older registrations remain without results ^[12], ^[13].

The European pages spell out what a designation is and is not. The sarcoidosis designation followed a positive committee opinion of 4 September 2013, for a condition then affecting about 2 in 10 000 people in the Union, and the islet transplantation designation of August 2016 covered a condition affecting fewer than 0.01 in 10 000, which is under 500 people. Both pages carry the same sentence, that an orphan designation is not a marketing authorisation ^[7], ^[8].

Five of these entries rest on register queries run with a control substance in the same database. A blank result there means absence, not a broken query ^[19], ^[34], ^[35], ^[36].

Two entries are weaker and are marked as such. The British register could not be queried at all, and the European search tool returned an authorisation error, so both statuses rest on inference from the worldwide picture ^[37], ^[38].

One finding cuts against a common assumption. Ara-290 appears on no American list of bulk substances nominated for pharmacy compounding, unlike BPC-157, ipamorelin or AOD-9604. Without such a listing, compounding it was never lawful in the first place ^[39].

The wider legal picture is under are peptides legal and FDA-approved peptides.

Anti-doping

Ara-290 is prohibited at all times, in and out of competition. The 2026 prohibited list does not name it. It falls under section S2.1.5, which covers innate repair receptor agonists, and Ara-290 is the prototype of that category ^[10].

The class heading closes the gap explicitly. It prohibits the listed substances and other substances with similar chemical structure or similar biological effect. Everything in class S2 is a non-specified substance, which affects how a sanction is measured ^[10].

The 2016 list named it outright as item 1.2 of the same class, under the heading non-erythropoietic EPO-receptor agonists. The category was later renamed and its examples shortened. A renamed category does not release the substance that gave it its name ^[11].

Detection is not a theoretical problem. One published urine method covers Ara-290 alongside seventeen other prohibited small peptides. Its detection limits run from 50 to 500 picograms per millilitre, comfortably below the 2 nanograms per millilitre that anti-doping laboratories must be able to reach. The method's imprecision stayed under 20 per cent and its readings held proportional across the range from 0 to 10 nanograms per millilitre. The same study settled a practical point for the laboratories, that urine samples for this class of peptide keep best at minus 20 degrees Celsius ^[40].

A second study identified its main breakdown product, a shortened form called PyrEQLERALN, as an additional target. In blood samples and with a purified enzyme that study found the peptide cut back from its ends unusually fast, faster than two comparison peptides of similar size, which is precisely why the breakdown product matters for testing ^[41].

The German anti-doping statute is a separate matter and a common source of confusion. Its annex does not name Ara-290, and has no category for these agonists at all. That is a gap in a closed list, not a permission, and the sporting rules apply regardless ^[42], ^[10].

There is one honest oddity here. Ara-290 is not expected to improve endurance, because it does not raise red cells. The list is built by substance class, not by proven advantage, so using it for recovery breaks the rules exactly as blood doping would ^[10], ^[14]. The full picture is at peptides banned in sport.

Compared with related peptides

A 2026 review of peptides in regenerative medicine places cibinetide in exactly this company, next to BPC-157, TB-500 and GHK-Cu. It closes by noting that most of these remain unapproved ^[43].

Within that group Ara-290 is the one with the most orderly clinical paperwork. It has registered, blinded, placebo-controlled studies with pre-specified endpoints, which BPC-157 and TB-500 do not. That is a real difference in quality of evidence.

It is also the group member whose proposed mechanism has been tested hardest and held up worst. Being studied properly and being shown to work are not the same thing, and here the better paperwork produced a clearer negative ^[1], ^[3].

A separate 2026 review of the grey market for unapproved peptides in sports medicine covers twelve substances, including AOD-9604 and SS-31, and does not mention Ara-290 at all ^[44].

Common misconceptions

• "Ara-290 is a safer form of EPO for endurance." The founding paper removed the blood-forming effect on purpose and states that the peptide is not erythropoietic. There is no haematocrit gain to be had ^[14].
• "The 2026 list does not name it, so sport permits it." The category it heads covers it, and the class heading covers similar biological effects. The 2016 list named it outright, and validated detection methods exist ^[10], ^[11], ^[40].
• "Six designations mean regulators have accepted it." A designation is a development incentive granted for the rarity of a condition. All four American records read Not FDA Approved for Orphan Indication ^[6], ^[7].
• "The phase 2b study was positive, so it is nearly finished." It met a microscope measurement at one of three dose levels and missed pain at p = 0.157. No phase 3, no application and no new registration followed ^[1].
• "It was labelled Rx only in America, so it is an approved prescription medicine." That label came from a compounding pharmacy, not a regulator. Compounded material is by definition unapproved, and this batch was recalled ^[9], ^[39].
• "The preclinical base for organ protection is solid." One standard reference was retracted in February 2026, and the proposed receptor could not be confirmed by an independent group. The observed effects are not disproved; the explanation is ^[3], ^[4].
• "A two-minute half-life means it is harmless." The developers themselves argue that effects last for weeks. A short blood half-life therefore gives no dosing logic and no self-limiting safety margin ^[16].
• "It is not in the German anti-doping act, so it is unproblematic." Two separate rulebooks. The annex to that act names neither the substance nor any category for these agonists, and it cannot be stretched to cover it, because the substance does not stimulate red cell production. The sporting rules apply to anyone under an anti-doping code regardless, and medicines law is a third question again ^[42], ^[10].
• "It is a peptide for mood." That hope was tested directly and not confirmed. In 36 healthy volunteers a single dose lowered the brain response to happy faces rather than raising it, and mood and emotional symptoms did not change at all ^[28].
• "The sarcoidosis results transfer to nerve damage generally." In diabetes the effect was much smaller and in macular oedema it was absent. In old mice with advanced disease it disappeared entirely ^[26], ^[27], ^[30].

Frequently asked questions

What is Ara-290?

Ara-290 is a synthetic peptide of eleven amino acids, also known as cibinetide and as pHBSP. It copies the water-facing side of one helix of erythropoietin, the hormone that drives red blood cell production. That side was chosen precisely because it takes no part in the blood-forming signal. The molecule is a laboratory design, not a natural fragment found in the body.

Is Ara-290 approved as a medicine anywhere?

No. Register checks on 15 September 2026 found no authorised product in the United States, the European Union, Germany, the United Kingdom, Australia, Canada or Switzerland. There is no ATC code and no pharmacopoeia monograph. What exists are six orphan designations, which are development incentives for rare diseases, and no approval anywhere.

Did the largest trial of Ara-290 succeed?

Partly, and the part it failed is the part patients notice. The 64-patient study met its primary endpoint, the amount of nerve fibre measured in the cornea, but only at the middle of three dose levels. Pain improved in every group including placebo, and the placebo-corrected difference reached p = 0.157, which is not statistically significant.

Is Ara-290 a form of EPO that boosts endurance?

No, and the opposite was the design goal. The molecule copies the face of erythropoietin that points into the surrounding water and is not involved in binding the blood-forming receptor. The founding paper states plainly that the eleven-unit peptide is not erythropoietic in vitro or in vivo. Anyone hoping for a haematocrit effect has chosen the molecule that had that effect deliberately removed.

Is Ara-290 banned in sport?

Yes, at all times, in and out of competition. The 2026 prohibited list does not name it, but section S2.1.5 covers innate repair receptor agonists, and Ara-290 is the prototype of that category. The 2016 list named it outright. Validated urine and serum detection methods are published, including one for its main breakdown product.

Why does this page list no doses for Ara-290?

Because the substance is unapproved everywhere and was sold in the United States as a prescription-labelled compounded injection that the FDA recalled for lack of sterility assurance. No authority has ever assessed an amount for this peptide. On top of that, the dose-response relationship in the largest study was not orderly: the middle level worked on the primary endpoint and the highest did not.

What do the orphan designations for Ara-290 mean?

They are development incentives, not verdicts on whether the substance works. Four American and two European designations were granted between 2009 and 2016 for rare conditions. All four American records carry the line Not FDA Approved for Orphan Indication. The European page for the sarcoidosis designation records that the medicine was not authorised anywhere in the European Union for that condition.

Is Ara-290 the same substance as pHBSP and cibinetide?

They are three naming layers for one molecule. pHBSP is the descriptive laboratory name, ARA 290 the development code, and cibinetide the name assigned by the World Health Organization. All three point to the same registry identifiers. The split matters in practice: a search of the European trial register for cibinetide returns nothing, while ARA 290 returns six registrations.

What happened to the development of Ara-290?

It stopped without an announcement. The last study ended in 2017, and the register gives the reason as expiry of the study drug with no replacement available. No phase 3 study, no marketing application and no new registration has appeared since. Three registered studies have never published results, so the published picture cannot be checked against the full one.

What is known about the safety of Ara-290?

Little, and only under supervision. About 130 people have received the substance across six small studies, the longest run lasting twelve weeks in nine patients. Those studies described it as well tolerated. Two serious events in one study were judged possibly related to the substance, one of them a worsening of borderline kidney function. There are no long-term data and none in healthy people beyond a single dose.

Cite this page

The facts on this page were checked on 15 September 2026, and every register behind the status table was queried on that day. Three things could still move: the British and European entries rest on inference rather than a document, the full text of the largest study was not accessible, and three registered studies could still publish.

myPeptides Research & Editing. (2026). Ara-290: what the studies show, status and safety. Version 1.0, 15 September 2026. myPeptides Peptide Register. Retrieved from https://mypep.app/peptides/ara-290

How pages in this register are compiled and graded is described under methodology; the full register is at peptides. Storage questions in general are covered under peptide storage.

Last verified: 15 September 2026. Next review: on any publication from the three silent registrations, on any new registered study, or on any change to the anti-doping classification.