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ARA-290

Also known as cibinetide, helix B surface peptide, HBSP

Non-erythropoietic EPO-derived 11-peptide that repairs small nerve fibres; development halted after phase 2.

early-clinical Recovery & tissue research chemical

At a glance

Category
Recovery & tissue
Status
research chemical
Route
subcutaneous (intravenous in the first pilot study)
Half-life
approximately 20 minutes (human); peak plasma concentration approximately 3 ng/ml after 4 mg subcutaneously. The pharmacodynamic effect persists considerably longer than the plasma exposure
Onset
the studies treated over 28 days, with effects on corneal nerve fibre measures detectable at the end of that period - corneal nerve fibre area rose 14.5% (median) against -5.3% on placebo, p=0.022 2
Molecular weight
approximately 1257 g/mol
Sequence
pGlu-Glu-Gln-Leu-Glu-Arg-Ala-Leu-Asn-Ser-Ser (eleven residues, with N-terminal pyroglutamate)

Not approved anywhere. Received a European orphan medicine designation for cibinetide, EU/3/13/1191, designated 7 October 2013 for the treatment of sarcoidosis 5, and in the US an orphan drug and Fast Track status for neuropathic pain in sarcoidosis. Development by Araim Pharmaceuticals was discontinued after phase 2; there is no active programme.

Doping status: Not listed by WADA

Checked against the WADA 2026 Prohibited List. For a specific product and country, Global DRO is the lookup athletes are expected to use — the List names substances, not brand names.

Mechanism of action

ARA-290 is derived from the externally exposed part of helix B of human erythropoietin (EPO). It does not bind to any meaningful extent to the homodimeric EPO receptor and therefore has no erythropoietic action: the studies saw no rise in haemoglobin or haematocrit and no reticulocytosis.

Instead it is a selective agonist of the so-called innate repair receptor (IRR), a heteromer of the EPO receptor and the beta-common receptor (CD131). This receptor is expressed on damaged and inflamed tissue.

Downstream come suppression of pro-inflammatory cytokine production, anti-apoptotic signalling and regeneration of small nerve fibres. This is why clinical development focused on small fiber neuropathy.

Because the erythropoietic activity is absent, the known EPO risks of thrombosis and hypertension fall away — and indeed they were not observed in the studies performed.

What the research shows

ARA-290 has a small but methodologically decent clinical dossier: four randomised, placebo-controlled studies in roughly 170 participants in total, with consistent effects on objective measures of nerve fibre repair. The evidence is therefore early-clinical and unconfirmed in phase 3; that was never carried out. The developer no longer exists.

Research in humans

Pilot study (Molecular Medicine, 2012): 22 sarcoidosis patients with small fiber neuropathy, 2 mg intravenously three times a week for four weeks; significant improvement on the SFN Screening List compared with placebo 1. Follow-up study (Molecular Medicine, 2013): 38 patients, 4 mg subcutaneously per day for 28 days; corneal nerve fibre area +14.5% median versus -5.3% with placebo (p=0.022), SFNSL -28% versus -9% (p=0.005), no serious side effects 2. In type 2 diabetes (Molecular Medicine, 2015): 48 patients, 4 mg subcutaneously per day for 28 days; improvement on PainDetect, an increase in corneal nerve fibre density in the subgroup with an abnormal baseline value, and a difference in HbA1c of -0.21% versus +0.21% at day 56 3. A dose-finding study in 64 patients with painful sarcoidosis neuropathy (1, 4 or 8 mg per day for 28 days) met the primary endpoint at 4 mg, with an approximately 23% increase in corneal nerve fibre area — strikingly, not at 8 mg.

Animal and lab research

The preclinical literature on ARA-290 and the related helix B peptide covers protection against ischaemia-reperfusion injury (heart, kidney, brain), models of diabetic and chemotherapy-induced neuropathy, wound healing and preservation of islet transplants — consistently showing tissue protection without erythropoiesis.

Caveats. All studies lasted 28 days; nothing is known about longer use. The numbers are small (22 to 64 participants) and a confirmatory phase 3 study was never performed. The dose-response relationship is not monotonic: 4 mg worked, 8 mg did not. Pain intensity improved equally strongly in the placebo group in several studies, which points to a substantial placebo effect; the objective nerve fibre measures are the most convincing. Because development has been discontinued, there is no approved formulation and no package insert.

What it is used for

  • Small fiber neuropathy in sarcoidosis - the best-studied indication, and the one carrying the EU orphan designation 125
  • Diabetic peripheral neuropathy - studied in 48 patients with type 2 diabetes over 28 days 3
  • Neuropathic pain in sarcoidosis, the endpoint of the 64-patient dose-finding study 4
  • Also offered on the grey market for general tissue protection and anti-inflammatory effect, for which no clinical substantiation exists

Dosing

Dose
4 mg per day subcutaneously (study dose); tested range 1-8 mg. The pilot study used 2 mg intravenously
Frequency
Once daily subcutaneously; in the pilot 3 times a week intravenously
Route
subcutaneous
Duration
28 days in all studies performed
  • 4 mg per day is the only dose with a positive result on the primary endpoint; the dose-finding study in 64 patients tested 1, 4 and 8 mg per day and met its endpoint at 4 mg but not at 8 mg 4.
  • There are no data on treatment longer than 28 days; every published trial ran for 28 days or four weeks 1234.
  • Material sold on the grey market is not a medicine and carries no guarantee of identity, purity, sterility or endotoxin content.
  • Beyond the trial dose, a small grey-market practice self-injects ARA-290 at 1-4 mg for neuropathy and general 'recovery' on open-ended courses. That circulating pattern is described under Protocols; it diverges from the trials, which ran 28 days at exactly 4 mg.

These figures describe what the literature and published protocols report. They are not advice and not a dosing instruction.

Protocols

Sarcoidosis-associated small fibre neuropathy (28-day subcutaneous course)

published trial

Source: Molecular Medicine, 2013

Days 1-284 mg once daily, subcutaneously
After day 28nothing: no study has run longer

4 mg daily is the only dose that produced a positive result on a primary endpoint. 8 mg daily was no better, and in the dose-finding work it was ineffective, so this is not a schedule that can be scaled up.

Sarcoidosis pilot study (intravenous)

published trial

Source: Molecular Medicine, 2012

Weeks 1-42 mg intravenously, three times per week

A small pilot, and intravenous rather than subcutaneous. The later 4 mg subcutaneous schedule is not a route conversion of this one; the two were arrived at separately.

Grey-market 'recovery peptide' course (user-reported)

user protocol — not validated

Source: Research-chemical vendor labelling and peptide forum reports

This is not a validated schedule. It is a pattern that circulates among users and sellers, reproduced because it is what people actually follow — not because it has been tested. No trial established these doses, this interval or this duration, and nobody is checking what is in the vial. Treat every number below as an assertion, not a finding.

Reported daily amountaround 1-4 mg subcutaneously, at or below the single studied 4 mg dose
Reported course lengthopen-ended, or run in long cycles well beyond the 28 days every trial used
Reported usesneuropathy, general tissue recovery and anti-inflammatory effect, often stacked with BPC-157 or TB-500

Every published trial ran for exactly 28 days at 4 mg daily, and 4 mg was the only dose that worked — 8 mg did not — so the studied regimen is unusually narrow. What circulates is open-ended self-injection at 1-4 mg for neuropathy and general 'recovery', indications and durations that were never studied, using grey-market vials sold beside other healing peptides. There is no published basis for use beyond 28 days or for the anti-inflammatory and recovery claims, and because the developer no longer exists and no medicine was ever formulated, grey-market powder has no reference product to be compared against. The scene is small and self-reported, and it is confounded by the other compounds usually run alongside; no bad reports from it are evidence of safety.

Schedules are reproduced as their source states them. Units, IU and milligrams explains why the figures are not interchangeable between products.

Reconstitution

Vial sizes
5 mg, 10 mg, 16 mg
Solvent
bacteriostatic water (0.9% benzyl alcohol)
Storage
Reconstituted 2-8 °C. In practice roughly four weeks is assumed; that is a general rule of thumb for bacteriostatic water and not a stability study for this peptide. Powder cool and dark.

Worked example

10 mg vial + 2 ml bacteriostatic water = 5 mg/ml. 4 mg = 0.8 ml, or 80 units on a U100 insulin syringe.

These vial sizes and instructions come exclusively from grey-market suppliers. The study material was a sponsor-supplied formulation whose specification is not public.

Work it out for ARA-290

Safety

Side effects

  • Across all studies performed (approximately 170 participants) no serious safety signals attributable to the compound were seen
  • No changes in haematology: no rise in haemoglobin or haematocrit, no reticulocytosis 2
  • No relevant abnormalities in clinical chemistry 2
  • In the diabetes study four serious adverse events occurred, two of which were judged 'possibly related', with no recognisable pattern 3
  • Injection site reactions were not reported as limiting

Do not use if

  • There are no formally established contraindications, because the compound has never been approved
  • Active malignancy: theoretical concern because of EPO receptor and CD131 signalling in tumour biology; not studied
  • Pregnancy and breastfeeding: no data
  • Use for longer than 28 days: never studied - all four randomised trials ran 28 days or four weeks 1234

Interactions

Not systematically studied; no interaction studies exist. Because ARA-290 does not activate the classical EPO receptor, the interactions that apply to erythropoiesis-stimulating agents do not automatically apply here.

Sources