ARA290 · Cibinetide
ARA-290 (Cibinetide) is a synthetic 11-amino acid peptide derived from the B helix of erythropoietin (EPO) that selectively activates the innate repair receptor (IRR), a heterodimer of the EPO receptor (EPOR) and the beta common receptor (CD131). Unlike EPO itself, ARA-290 does not stimulate erythropoiesis (red blood cell production) or affect hematocrit, which eliminates the thrombotic and cardiovascular risks associated with EPO use. ARA-290 promotes tissue repair, reduces inflammation, and provides neuroprotection through the IRR pathway, which is distinct from the classical EPO receptor responsible for erythropoiesis. It has been studied in Phase 2 clinical trials for diabetic neuropathy and sarcoidosis-related neuropathy.
Can be taken any time. No fasting required. 28-day cycle protocol.
Start here. Every protocol below is ordered lowest-first. Begin at the smallest effective dose, hold about a week to assess tolerance, and step up only if needed.
ARA-290 binds to and activates the innate repair receptor (IRR), which is a heterodimer of EPOR and CD131 (beta common receptor). This receptor is expressed on neurons, endothelial cells, and immune cells and is upregulated in response to tissue injury and inflammation. IRR activation triggers anti-apoptotic signaling (preventing cell death at injury sites), anti-inflammatory cytokine modulation, neural repair and remyelination signaling, endothelial protection and vascular repair, and macrophage phenotype switching from pro-inflammatory M1 to reparative M2. Critically, ARA-290 does NOT activate the classical EPOR homodimer responsible for erythropoiesis. This selectivity means ARA-290 provides tissue protective effects without increasing red blood cell production, hematocrit, or thrombotic risk.
Days 1-7: No significant changes expected. IRR activation initiates repair signaling but neural repair is a slow process.
Weeks 2-4: Neuropathic symptoms may begin to improve. Phase 2 trial showed measurable improvements at 28 days. Anti-inflammatory effects accumulate.
Weeks 4-12: Nerve fiber density improvements (measured by corneal confocal microscopy in clinical trials). Sustained tissue repair effects. Best assessed through symptom tracking and objective nerve function testing.
Each reference below was re-fetched from its PubMed record, and the quoted sentence was confirmed to appear in that abstract and to support the claim it sits under. Follow any of them to read the source.
Dose-response: a human trial compared 1, 4, and 8 mg/day cibinetide with placebo.
Cibinetide (1, 4, or 8 mg/day) was compared to placebo.
Evidence scope. Human, sarcoidosis-associated small-nerve-fiber-loss patients (n=64); route of administration not stated in this abstract.
Mechanism: cibinetide activation of the innate repair receptor produced anti-inflammatory effects in a mouse colitis model.
Cibinetide activation of the IRR exerts potent anti-inflammatory effects, especially within the myeloid population, reduces disease activity and mortality in mice.
Evidence scope. Animal (mouse DSS-induced colitis model); preclinical mechanism only, no human IBD data.
Dose/route: patients self-administered 4 mg/day cibinetide subcutaneously for 12 weeks, matching the top of the card’s 2-4 mg/day range.
Patients self-administered cibinetide 4 mg/day subcutaneously for 12 weeks.
A Phase 2 Clinical Trial on the Use of Cibinetide for the Treatment of Diabetic Macular Edema.
Evidence scope. Human, diabetic macular edema patients (n=9); dose/route fact only, disease context not implied to generalize.
Primary safety: the 4 mg/day SubQ study reported no serious adverse events/reactions or anti-cibinetide antibodies.
No serious adverse events/reactions or anti-cibinetide antibodies were seen.
A Phase 2 Clinical Trial on the Use of Cibinetide for the Treatment of Diabetic Macular Edema.
Evidence scope. Human, n=9 single-arm safety observation, 12 weeks; too small to establish a general safety profile.
Non-erythropoietic tissue repair
Confirmed. ARA-290 selectively activates IRR without activating the classical EPO receptor. No effect on hematocrit or RBC production in clinical trials. This is its primary design advantage over EPO.
Phase 2 data shows objective nerve fiber density improvement (corneal confocal microscopy). Neuropathic pain reduction. The best-supported clinical claim for ARA-290.
Macrophage M1-to-M2 polarization documented. Distinct from classical anti-inflammatory pathways (NSAIDs, steroids). Complementary to other anti-inflammatory peptides.
Two different questions: what is documented about running these together, and what is documented about drawing them into the same syringe. A good pharmacological partner can still have to be pinned separately.
Check any specific pair in the Stack & Interaction Checker, which answers both questions separately. Absence of a documented conflict is not evidence of safety.
SubQ
IRR-mediated anti-apoptotic and repair signaling persists
Enzymatic degradation (peptidases); renal excretion
Storage. Store unreconstituted vials frozen (-20C) or refrigerated (2-8C). After reconstitution with BAC water, refrigerate at 2-8C. Stable for 28 days. Protect from light. EPO-derived structure but no special handling beyond standard peptide care.
ARA-290 (Cibinetide) is an investigational drug. Phase 2 clinical trials completed by Araim Pharmaceuticals. Not yet approved by FDA or any regulatory agency. Available as a research peptide. WADA status: Not specifically listed but may fall under S0.
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