ARA-290 (Cibinetide)
Also known as: Cibinetide, ARA290, Helix B surface peptide, pHBSP, EPO helix-B peptide
Lower numbers = closer to natural. Higher numbers = more enhanced.
Why this rating?
ARA-290 is an 11-amino-acid peptide derived from the helix-B region of erythropoietin (EPO) that selectively activates the innate repair receptor (IRR) to deliver EPO's tissue-protective, anti-inflammatory, and repair effects WITHOUT stimulating red blood cell production. It is used for neuropathic pain, inflammation, and tissue repair, not muscle growth or hormonal enhancement. Because it does not raise hematocrit, it is not an EPO-style blood-doping agent, but it IS classified by WADA as an "innate repair receptor agonist" (S2.1.5), a mechanism-based ban that applies regardless of erythropoietic effect. It is rated 1 (basically natty) on the muscular/physique/performance scale: it is a non-hormonal, non-anabolic anti-inflammatory and nerve/tissue-repair peptide that at most restores tissue toward baseline function. It does not build muscle, burn fat, or raise anabolic hormones, so it does not move the natural ceiling.
Overview
An 11-amino-acid peptide engineered from the helix-B surface of erythropoietin (EPO). EPO has two separable activities: raising red blood cells, and protecting/repairing tissue. ARA-290 was designed to trigger only the second. It selectively activates the innate repair receptor without engaging the classical EPO receptor that drives erythropoiesis. The result is EPO's anti-inflammatory, anti-apoptotic, and regenerative signalling with none of the hematocrit rise (and none of the clotting/cardiovascular risk) that makes EPO a dangerous doping agent.
Purpose & Use Cases
Neuropathic Pain / Small-Fiber Neuropathy
Its most-studied use: a Phase II RCT in sarcoidosis-associated small-fiber neuropathy showed improved pain thresholds and regrowth of corneal nerve fibers.
Anti-Inflammatory / Tissue Protection
Activating the IRR reduces inflammatory signalling and protects tissue from injury and apoptosis, of interest across inflammatory and ischemic conditions.
Tissue & Nerve Repair
Promotes regeneration (e.g. nerve-fiber density recovery), overlapping conceptually with recovery peptides but via a distinct receptor.
Metabolic / Autoimmune Interest
Explored in diabetic and autoimmune contexts for its anti-inflammatory, tissue-protective profile.
Benefits
- Delivers EPO's tissue-protective/anti-inflammatory effects without raising red blood cells
- No polycythemia, clotting, or blood-pressure risk of classic EPO
- Real human Phase II evidence for nerve repair (improved pain thresholds, corneal nerve density)
- Anti-inflammatory via IRR / reduced TNF-alpha signalling
- Non-hormonal: no PCT, no aromatization, no androgenic effects
- Well tolerated across repeat-dose human trials, including a 12-week course, with no serious adverse events reported
Good to Know
EPO-derived but it does NOT thicken your blood
This is the whole point of the molecule. ARA-290 keeps EPO's tissue-protective, anti-inflammatory side while deliberately dropping the red-blood-cell-raising side. Across human studies hemoglobin and hematocrit stayed unchanged, so it carries none of EPO's polycythemia/clotting danger and is not a blood-doping agent.
WADA-prohibited as an "innate repair receptor agonist" (S2.1.5), even without raising hematocrit
ARA-290 does not stimulate erythropoiesis, so it avoids EPO's polycythemia/clotting risk, but the WADA Prohibited List's S2.1.5 category ("Innate repair receptor agonists, e.g. asialo EPO; carbamylated EPO (CEPO)") is defined by IRR-agonist mechanism, not by hematocrit effect, and is prohibited at all times. ARA-290 was purpose-built to be an IRR agonist, so it falls within this category even though it is not named as one of the two listed examples. Tested athletes should not assume the non-erythropoietic profile exempts it.
It has real human data, but development stalled
The pivotal Phase II RCT in sarcoidosis small-fiber neuropathy (Dahan et al. 2013) showed genuine benefits: improved pain thresholds and increased corneal nerve-fiber density suggesting actual regeneration. It holds FDA Orphan Drug and Fast Track status, but no Phase III was completed and the developer has been largely dormant, so it remains investigational, not approved.
Not anabolic or androgenic
ARA-290 does not build muscle, aromatize, convert to DHT, or affect testosterone. No AI, no finasteride considerations, and no PCT apply. It is an anti-inflammatory/tissue-repair peptide.
Dosage Guidelines
| Experience Level | Dosage Range |
|---|---|
| Beginner | 1 – 2 mg/day |
| Intermediate | 2 – 4 mg/day |
| Advanced | 4 – 8 mg/day |
The trial-anchored dose is 4mg subcutaneous once daily, used across most Phase 2 studies (Dahan et al. 2013 in sarcoidosis small-fiber neuropathy, 28 days; Brines et al. 2015 in type 2 diabetes, 28 days; Lois et al. 2020 in diabetic macular edema, 12 weeks). A dose-ranging Phase 2b trial (Culver et al. 2017) tested 1mg, 4mg, and 8mg/day for 28 days and found 4mg produced the largest improvement in corneal nerve fiber regeneration. 8mg was NOT more effective than 4mg, so higher doses do not appear to add benefit (a plateau/non-monotonic dose-response). Community protocols generally mirror the 4mg/day trial dose and ~4-week course length; there is no validated general-use human dose outside the trial setting. Reconstitute with bacteriostatic water and refrigerate.
Plasma half-life is very short (minutes), but the tissue-protective effects outlast the measurable peptide.
Side Effects
Injection Site Reaction
commonRedness or irritation at the subcutaneous injection site.
Rotate injection sites; sterile technique.
Mild Headache / Fatigue
uncommonOccasional headache or tiredness reported; the drug was otherwise well tolerated in trials with no serious adverse events.
Usually transient; stay hydrated.
Sourcing / Purity Risk
commonAs an unapproved research peptide, purity and actual content vary by supplier.
Use a tested product with a certificate of analysis.
General Mitigation Strategies
ARA-290 was well tolerated in human trials with no serious adverse events reported and, importantly, no rise in hematocrit, so it lacks EPO's blood-thickening danger. Injection-site reactions are the main complaint. As with any research peptide, product quality is the primary practical risk.
Post Cycle Therapy (PCT)
Not hormonal. Does not affect the HPTA or testosterone. No PCT required.
How It Works
Native EPO acts through two receptor systems: the classical homodimeric EPO receptor (EPOR/EPOR), which drives red-blood-cell production, and a heteromeric "innate repair receptor" (IRR) formed by the EPO receptor together with the beta-common receptor (CD131), which mediates tissue protection and repair. ARA-290 (cibinetide) is shaped after EPO's helix-B region so that it binds and activates the IRR but does not engage the erythropoiesis-driving homodimer. Through the IRR it dampens pro-inflammatory signalling (including TNF-alpha), reduces apoptosis, and promotes tissue and small-nerve-fiber repair. In human studies, hemoglobin and hematocrit were unchanged, confirming the erythropoietic and tissue-protective functions were successfully dissociated.
Fundamentals
Reference on the practices relevant to ARA-290 (Cibinetide): how they are done and where they go wrong. Not a recommendation to use it.
Common Stacks
- ARA-290 + BPC-157/TB-500 - Anti-inflammatory nerve/tissue repair stack
- ARA-290 + KPV - Layered anti-inflammatory protocol (IRR + NF-kB)
- ARA-290 + Thymosin Alpha-1 - Immune/inflammation modulation for recovery
Legal Status
Investigational / research chemical (USA). Holds FDA Orphan Drug and Fast Track designation for sarcoidosis small-fiber neuropathy but is not approved for marketing.
Legal status varies by country and changes over time. This is a general summary, not legal advice.
WADA Status
The WADA Prohibited List bans "Innate repair receptor agonists, e.g. asialo EPO; carbamylated EPO (CEPO)" under S2.1.5, prohibited at all times (in- and out-of-competition). ARA-290/cibinetide was engineered specifically to activate the innate repair receptor (IRR), so it fits this mechanism-defined category even though it is not one of the two named examples, the "e.g." list is illustrative, not exhaustive. It is non-erythropoietic (does not raise hematocrit), so the blood-doping rationale behind other S2.1 entries does not apply the same way, but that does not remove it from the category. Marked uncertain here because no WADA technical document or sanction case explicitly names ARA-290/cibinetide; tested athletes should treat it as prohibited and seek current, sport-specific guidance rather than relying on this summary.
References
- Dahan et al. 2013: ARA-290 improves symptoms in sarcoidosis small-fiber neuropathy and increases corneal nerve fiber density (Mol Med, PMC3883966)
- Wang et al. 2024: Erythropoietin-derived peptide ARA290 mediates brain tissue protection through the beta-common receptor in mice with cerebral ischemic stroke (CNS Neurosci Ther; PMC10941562)
- Culver et al. 2017, Dose-ranging trial (1/4/8mg/day x28 days): cibinetide improves corneal nerve fiber abundance in sarcoidosis-associated small nerve fiber loss, 4mg most effective (Invest Ophthalmol Vis Sci, PMID 28475703)
- WADA Prohibited List: S2.1.5 Innate Repair Receptor Agonists (prohibited at all times)