$89.99
Buy ARA-290 Peptide 16 mg Online from SourceTides. Cibinetide | CAS 1208243-50-8 | pGlu-Glu-Gln-Leu-Glu-Arg-Ala-Leu-Asn-Ser-Ser-OH | MW 1,257.324 g/mol | C₅₁H₈₄N₁₆O₂₁ | ≥99% HPLC (pGlu cyclisation confirmed; −17 Da MS) | Endotoxin <1 EU/mg (LAL) | Full CoA | Lyophilised | Dry-ice cold chain.
11-AA helix B surface peptide of EPO. Selective Innate Repair Receptor (IRR = EPOR/CD131 heterodimer) agonist — zero erythropoietic/hematopoietic activity. TRPV1 antagonism (secondary mechanism). FDA Orphan Drug Designation for sarcoidosis neuropathy. Phase 2b: ~23% corneal nerve fibre area increase vs placebo (64 patients; IOVS 2017). Not WADA-prohibited. For in-vitro laboratory research use only. Not for human consumption.
Buy ARA-290 Peptide 16 mg Online | Cibinetide | Helix B Surface Peptide | Innate Repair Receptor | ≥99% Purity | CoA | SourceTides
Buy ARA-290 Peptide 16 mg Online from SourceTides.
ARA-290 (INN: Cibinetide; also pHBSP; Pyroglutamate Helix B Surface Peptide; CAS 1208243-50-8) is a synthetic 11-amino acid peptide derived from the tissue-protective helix B surface domain of erythropoietin (EPO), engineered by Araim Pharmaceuticals researchers Anthony Cerami and Michael Brines.
Unlike full-length EPO — which binds the classical erythropoietin receptor (EPOR) homodimer to drive red blood cell production, raising haematocrit with associated thrombotic and cardiovascular risk — ARA-290 binds only the Innate Repair Receptor (IRR): a heteromeric complex of EPOR and CD131 (β-common receptor) that is upregulated in injured tissues and mediates tissue-protective, anti-inflammatory, and nerve-regenerative effects.
ARA-290 produces zero erythropoietic, hematopoietic, or thrombotic activity at any dose studied.
The clinical evidence base is substantial and human.
Multiple Phase 2 randomised, placebo-controlled trials have been completed — most critically, a Phase 2b study in 64 patients with sarcoidosis-associated small fibre neuropathy (IOVS 2017) demonstrating ~23% increase in corneal nerve fibre area vs placebo, significant intraepidermal nerve fibre length increase, pain reduction, and improved functional capacity — with no significant safety issues at any dose.
ARA-290 holds FDA Orphan Drug Designation for neuropathic pain in sarcoidosis.
The 16 mg vial format supports the standard published research protocol (4 mg SC daily × 28 days = 112 mg total) scaled down to four days of single-dose equivalent — or longer protocols when lower doses are studied.
Every SourceTides vial is lyophilised, tested at ≥99% HPLC purity, and ships with a full lot-specific Certificate of Analysis.
For in-vitro laboratory research use only. Not for human consumption.
ARA-290 Peptide 16 mg — Technical Specifications
| Parameter | Specification |
|---|---|
| INN / Common Name | Cibinetide |
| Synonyms | ARA-290; ARA290; pHBSP; PHBSP; Pyroglutamate Helix B Surface Peptide; Helix B Surface Peptide; UEQLERALNSS (single-letter sequence code) |
| CAS Number | 1208243-50-8 |
| PubChem CID | 91810664 |
| DrugBank | DB13006 |
| Molecular Formula | C₅₁H₈₄N₁₆O₂₁ |
| Molecular Weight | 1,257.324 g/mol |
| Peptide Length | 11 amino acids; linear; no disulfide bonds; N-terminal pyroglutamate (pGlu); free C-terminal carboxylic acid (–OH) |
| Full Sequence | pGlu-Glu-Gln-Leu-Glu-Arg-Ala-Leu-Asn-Ser-Ser-OH (one-letter: UEQLERALNSS; U = pyroglutamate) |
| Critical Structural Feature | N-terminal pyroglutamate (pGlu): cyclised glutamine/glutamate that blocks aminopeptidase N-terminal degradation; derived from helix B surface loop of erythropoietin (residues ~58–82 of EPO) |
| Origin | Derived from the surface-exposed helix B domain of human erythropoietin — the tissue-protective domain physically distinct from the hematopoietic receptor-binding domain on helix A |
| Developer | Araim Pharmaceuticals Inc. (Tarrytown, NY); Anthony Cerami, Michael Brines; developed to isolate EPO’s tissue-protective activity from its erythropoietic activity |
| Receptor | Innate Repair Receptor (IRR) = EPOR/CD131 heteromeric complex (CD131 = β-common receptor; βc; IL-3Rβ; GM-CSFR subunit); does NOT bind the EPOR homodimer — zero erythropoietic/hematopoietic activity |
| Secondary Mechanism | TRPV1 (Transient Receptor Potential Vanilloid 1) antagonism — direct peripheral nociceptor modulation independent of IRR; confirmed by Zhang et al. (Peptides 2016) |
| Plasma Half-Life | ~20 minutes (rapid clearance); biological effects persist far beyond clearance via “molecular switch” mechanism — IRR activation initiates a sustained tissue repair programme that continues after peptide has cleared |
| Erythropoietic/Hematopoietic Activity | None — confirmed in all clinical trials; haematocrit and haemoglobin unaffected at any dose; no thrombotic risk; no EPO doping potential |
| Physical Form | White lyophilised powder; hygroscopic |
| Purity | ≥99% (RP-HPLC); identity confirmed by ESI-MS (MW 1257.32 Da; pGlu N-terminus confirmed); pyroglutamate cyclisation confirmed |
| Endotoxin | <1 EU/mg (LAL chromogenic assay) |
| Solubility | Freely soluble in sterile water and PBS pH 7.4; 4 mg/mL stock (matching clinical trial concentration); no organic solvent required |
| Storage — Lyophilised | −20°C long-term (stable 24 months); 2–8°C short-term; protect from moisture and light; equilibrate sealed vial to room temperature before opening |
| Storage — Reconstituted | 2–8°C for up to 7 days; −20°C for longer; aliquot for single use; avoid freeze-thaw |
| Vial Size Note | 16 mg vial; clinical research protocol used 4 mg SC daily × 28 days (112 mg/28-day course); 16 mg supports 4 days at clinical dose, or extended lower-dose research protocols; use single vial for consistent lot quality across a study |
| Certificate of Analysis | Lot-specific CoA with every order; HPLC + ESI-MS (1257.32 Da; pGlu confirmed) + endotoxin |
| Regulatory Status | Not FDA, EMA, TGA, or Health Canada approved; FDA Orphan Drug Designation for neuropathic pain in sarcoidosis; multiple Phase 2 clinical trials completed; research compound only |
| WADA Status | Not listed on 2024–2025 WADA Prohibited List; zero erythropoietic activity confirmed — not an EPO doping agent; not prohibited |
What Is ARA-290?
Erythropoietin (EPO) has two biological personalities.
As the haematopoietic hormone, it drives red blood cell production in bone marrow via the EPOR homodimer receptor — a function exploited by doping athletes and restricted by WADA.
As a tissue-protective molecule, it activates the Innate Repair Receptor (IRR) in injured tissues, driving anti-inflammatory, anti-apoptotic, and regenerative responses in neurons, endothelial cells, and immune cells.
The two activities reside in physically different domains of the EPO molecule.
The haematopoietic activity requires the extended binding surface of the full EPO protein, particularly helices A and C that engage the EPOR homodimer.
The tissue-protective activity can be reproduced by the surface-exposed loop region of helix B — a small structural element that contacts the IRR heterodimer (EPOR/CD131) without activating the EPOR homodimer.
ARA-290 is the 11-amino acid peptide corresponding to that helix B surface — engineered to be the tissue-protective signal of EPO with none of the haematopoietic liability.
Developed by Araim Pharmaceuticals researchers Anthony Cerami and Michael Brines, it was designed as the definitive test of whether EPO’s tissue protection and EPO’s blood production could be separated into independent molecules.
The answer confirmed in multiple human clinical trials is yes — completely.
The research context for ARA-290 is unusually strong for a non-approved peptide.
Multiple peer-reviewed Phase 2 clinical trials have been published in top journals (Nature PNAS, Molecular Medicine, Investigative Ophthalmology & Visual Science).
The FDA Orphan Drug Designation for sarcoidosis neuropathy places ARA-290 in a rare category: a non-approved peptide with formal regulatory recognition and extensive human safety data.
When you buy ARA-290 Peptide 16 mg from SourceTides, you access one of the most human-validated neuroprotective research peptides available.
The Innate Repair Receptor: The Key to ARA-290’s Biology
What the IRR Is and Why It Matters
The Innate Repair Receptor (IRR) is a heteromeric receptor complex consisting of the erythropoietin receptor (EPOR) and CD131 (β-common receptor; βc; also the shared signalling subunit of GM-CSF, IL-3, and IL-5 receptors).
It was characterised by Brines and Cerami as a receptor that mediates tissue protection independently of the haematopoietic EPOR homodimer.
The IRR has a critical spatial and temporal expression pattern: it is upregulated in injured, hypoxic, or inflamed tissue — including damaged peripheral nerves, ischaemic endothelium, injured kidney, and inflamed gut.
Normal, healthy tissue has minimal IRR expression.
This injury-induced upregulation means ARA-290’s activity is preferentially targeted to where damage is happening — an elegant built-in tissue selectivity that receptor-constitutively-expressed compounds cannot replicate.
IRR activation by ARA-290 initiates a downstream signalling cascade through JAK2-STAT5, PI3K-Akt, and MAPK pathways — driving pro-survival, anti-apoptotic, anti-inflammatory, and regenerative gene expression in target cells.
The result is a “molecular switch” that turns on tissue repair programmes and turns off inflammatory destruction cycles.
Critically, because IRR does not couple to the haematopoietic GATA-1 transcription factor pathway activated by the EPOR homodimer, ARA-290 produces none of the erythropoietic downstream effects.
TRPV1 Antagonism: The Secondary Analgesic Mechanism
In addition to the IRR-mediated tissue protective mechanism, ARA-290 directly antagonises TRPV1 (Transient Receptor Potential Vanilloid 1) — the primary peripheral nociceptor responsible for thermal and inflammatory pain signalling.
Zhang et al. (Peptides 2016) confirmed that ARA-290 blocks TRPV1 channel activity in peripheral nociceptors, independent of the IRR pathway.
This dual mechanism — IRR-mediated disease modification (nerve regeneration, inflammation suppression) combined with TRPV1 direct analgesic activity — explains why ARA-290 produces both symptom relief and objective nerve fibre regeneration in clinical trials.
Most analgesics (opioids, gabapentinoids) work only on the symptom.
ARA-290 works on the symptom (TRPV1 blockade) and the underlying pathology (IRR-driven nerve regeneration) simultaneously.
ARA-290 vs Full-Length EPO: The Critical Distinction
| Property | Full-Length EPO | ARA-290 (Cibinetide) |
|---|---|---|
| Receptor | EPOR homodimer (haematopoietic) + IRR (tissue protective) | IRR only (EPOR/CD131 heterodimer) — does not bind EPOR homodimer |
| Erythropoiesis | Yes — drives RBC production; raises haematocrit | None — confirmed in all human trials; haematocrit unaffected |
| Thrombotic risk | Yes — thrombosis, stroke, MI at high doses; major safety limitation | None documented — no safety issues in any trial |
| Tissue protective activity | Yes — via IRR; but inseparable from haematopoietic effects at clinical doses | Yes — same IRR-mediated protection, without haematopoietic liability |
| Nerve fibre regeneration (clinical) | Not well-characterised for neuropathy at safe doses | ~23% corneal nerve fibre area increase vs placebo (Phase 2b; 64 patients) |
| WADA status | WADA S2 prohibited (erythropoiesis-stimulating agent) | Not prohibited — no erythropoietic activity |
| Regulatory status | FDA-approved (Epogen, Procrit) for anaemia; Rx drug | FDA Orphan Drug Designation for sarcoidosis neuropathy; research compound |
| MW | ~30,400 Da (glycoprotein) | 1,257.324 Da (small synthetic peptide) |
ARA-290 Clinical Evidence
| Trial | Design | Key Finding | Source |
|---|---|---|---|
| Phase 2b — Sarcoidosis SFN (cibinetide; 64 patients) | Randomised, double-blind, placebo-controlled; 1, 4, 8 mg SC daily × 28 days; published IOVS 2017 | ~23% increase in corneal nerve fibre area vs placebo at 4 mg dose; significant intraepidermal growth-associated protein-43 nerve fibre length increase; placebo-corrected pain reduction in moderate-to-severe pain patients; improved functional capacity; no significant safety issues at any dose | Dahan et al. 2017 — IOVS — PMID: 28475706 |
| Phase 2 — T2D Neuropathy (4 mg SC daily × 28 days) | Randomised, placebo-controlled; 4 mg SC daily × 28 days + 28-day follow-up; Mol Med 2014 | HbA1c improvement throughout 56-day observation period; lipid profile improvement; neuropathic symptom reduction; no safety issues; confirmed IRR-mediated metabolic + neuropathic co-treatment in T2D | Brines et al. 2014 — Mol Med — PMID: 25387363 |
| Phase 2 — Sarcoidosis SFN (pilot) | Randomised, double-blind pilot; Mol Med 2012 (Heij et al.) | ARA-290 safe and efficacious in sarcoidosis SFN; confirmed neuropathic symptom improvement; established Phase 2b design basis; no haematopoietic changes at any dose | Heij et al. 2012 — Mol Med — PMID: 22988708 |
| Preclinical — Spinal Nerve Injury / Microglia | In vivo (rat SNI model; 4 doses: 3, 10, 30, 60 µg/kg; days 1,3,6,8,10); PMC3928087 | Dose-dependent allodynia reduction; concurrent spinal cord microglia and astrocyte response suppression; long-term pain relief; NMDAR mRNA suppression parallel to ketamine effects but via IRR not NMDAR; dose optimum at 30 µg/kg | PMC3928087 — SNI microglia study |
| Preclinical — EPO Helix B Peptide Foundation Study | Foundational; PNAS 2008 (Brines, Patel, Villa et al.) | Nonerythropoietic tissue-protective peptides from EPO tertiary structure identified; ARA-290 (pHBSP) demonstrated tissue protection in multiple preclinical injury models; zero erythropoietic activity confirmed; IRR mechanism described; foundational paper for all subsequent ARA-290 research | Brines et al. 2008 — PNAS — PMID: 18695228 |
| Preclinical — Autoimmune Neuritis (EAN model) | In vivo (Lewis rat EAN model); PMC3946253 | ARA-290 improved EAN recovery; promoted nerve regeneration and remyelination; suppressed nerve inflammation; induced Foxp3⁺ Treg cells and Th2 polarisation; inhibited inflammatory macrophage activation; promoted Schwann cell proliferation; potential for autoimmune neuropathy research | PMC3946253 — EAN autoimmune neuropathy |
What Is ARA-290 Used for in Research?
| Research Field | Application | Why ARA-290 |
|---|---|---|
| Small Fibre Neuropathy (SFN) | Corneal confocal microscopy nerve fibre endpoint; intraepidermal nerve fibre density (IENFD); skin biopsy nerve fibre regeneration; sarcoidosis neuropathy models; pain behavioural assays | Only peptide with published Phase 2b human data demonstrating objective nerve fibre regeneration (23% corneal nerve fibre area increase) and pain relief simultaneously in SFN; FDA Orphan Drug Designation; the definitive research tool for nerve fibre regeneration biology |
| Diabetic Peripheral Neuropathy | DPN models; streptozotocin-induced diabetic rats; glycaemic control + neuropathy combined endpoints; corneal nerve density; IENFD; HbA1c-proxy markers | Phase 2 human trial confirmed HbA1c improvement + neuropathic symptom improvement simultaneously; ARA-290 is the only non-GPCRsignalling peptide with published human evidence for both metabolic and neurological endpoints in T2D; studied alongside Semaglutide and Tirzepatide in metabolic-neuropathic overlap research |
| Neuropathic Pain Biology | SNI/CCI/CFA rodent pain models; allodynia (von Frey); hyperalgesia; spinal microglia and astrocyte activation; NMDAR expression; central sensitisation; TRPV1 pharmacology | Dual mechanism (IRR anti-inflammatory disease modification + TRPV1 antagonism) addresses both central sensitisation and peripheral nociceptor hyperactivity; dose-response confirmed in SNI rat model (3–60 µg/kg); produces long-term analgesia far beyond peptide clearance; studied alongside Selank Amidate (IL-6/GABAergic) and KPV Peptide (NF-κB) in multi-mechanism neuroinflammation panels |
| Innate Repair Receptor (IRR) Pharmacology | EPOR/CD131 heterodimer biology; JAK2-STAT5 tissue protection; IRR vs EPOR homodimer signalling dissection; injury-induced receptor upregulation; CD131 biology | ARA-290 is the only published selective IRR agonist; the definitive tool for studying IRR pharmacology independently of EPOR homodimer activation; use CD131-knockout mice or CD131 siRNA knockdown to confirm IRR dependence (same design principle as Cartalax SIRT6 or AOD-9604 disulfide studies) |
| Neuroinflammation and Neurodegeneration | Microglia and astrocyte activation; spinal cord neuroinflammation; TBI models; ischaemic brain injury; Schwann cell biology; remyelination | IRR activation suppresses microglial and astrocyte pro-inflammatory responses; promotes Schwann cell proliferation; drives remyelination (EAN model); studied alongside Pinealon (SOD2/GPX1 antioxidant) and NAD⁺ (SIRT3 mitochondrial neuroprotection) in comprehensive neurodegeneration research panels |
| T-Cell Immunomodulation | Regulatory T-cell (Treg; Foxp3⁺) induction; Th1/Th2 polarisation; autoimmune neuropathy models; neuroinflammatory T-cell biology | ARA-290 induces Foxp3⁺ Treg expansion and Th2 polarisation (EAN model); Th1 suppression; provides immune-regulatory axis for neuropathy research; studied alongside Thymalin (thymic T-cell bioregulator) and Thymosin Alpha-1 (immune modulation) for comprehensive neuroimmune panels |
| Tissue Protection / Ischaemia Models | Ischaemia-reperfusion injury; kidney protection; cardiac protection; endothelial function; vascular barrier integrity | The original ARA-290 PNAS 2008 paper showed tissue protection across multiple organ injury models; IRR upregulation in ischaemia makes ARA-290 a tissue-targeted protective agent; studied alongside BPC-157 (vascular repair/VEGFR2) and TB-500 (actin repair) in combined tissue protection protocols |
| Sarcoidosis Biology | Granulomatous inflammation; sarcoidosis neuropathic models; systemic inflammatory-neuropathy intersection | The only compound with FDA Orphan Drug Designation specifically for sarcoidosis neuropathy; most published compound for this specific pathology; clinical research infrastructure (corneal CCM, IENFD protocols) fully validated around ARA-290 in this population |
ARA-290 Pharmacokinetics and Research Design
| Parameter | Value / Notes | Research Implication |
|---|---|---|
| Plasma half-life | ~20 minutes; rapidly cleared by plasma peptidases; N-terminal pyroglutamate provides partial protection from aminopeptidase N-terminal attack | Measure acute pharmacodynamic endpoints within 30–60 minutes; long-term endpoints (nerve fibre regeneration, pain scores, corneal nerve fibre density) are IRR-mediated effects that persist far beyond clearance — measure at 7, 14, 28, and 56 days in chronic protocols |
| Clinical research dose (SC) | 4 mg SC once daily × 28 days (primary clinical trial dosing; Brines 2014; Dahan/IOVS 2017); doses of 1, 4, and 8 mg also studied; 4 mg was optimal dose in Phase 2b | 4 mg/day is the human-validated dose with the most published evidence; a 16 mg vial supports 4 days at clinical dose — design your protocol around the published 28-day treatment window for nerve fibre endpoint studies |
| Rodent in-vivo dose (preclinical) | 3–60 µg/kg SC (SNI neuropathy dose range; optimal 30 µg/kg); 4 mg/kg equivalent daily in some T2D rat models; acute dose 15–30 µg/kg | Use 30 µg/kg SC as the starting dose for rodent neuropathic pain studies; administer on days 1, 3, 6, 8, and 10 (published SNI schedule); measure allodynia (von Frey) and hyperalgesia at each time point; include vehicle and CD131-KO control groups for IRR specificity |
| In-vitro concentration | 1–1000 nM for Schwann cell, DRG neuron, and endothelial cell IRR assays; use 10–100 nM for anti-inflammatory cytokine assays in microglia/macrophage models | Confirm CD131 (β-common receptor) expression in your cell line before assuming IRR-mediated effects; use anti-CD131 antibody or siRNA knockdown as control; measure STAT5 phosphorylation and PI3K/Akt activation as downstream IRR signalling markers |
| Primary efficacy endpoints (published) | Corneal nerve fibre area (corneal confocal microscopy); intraepidermal nerve fibre length (skin biopsy); Visual Analogue Scale pain scores; SF-36 functional capacity; HbA1c; allodynia (von Frey); microglia/astrocyte activation markers | Corneal CCM is the validated non-invasive nerve regeneration endpoint used in Phase 2b — validated, reproducible, and directly comparable to published ARA-290 data; use as primary endpoint in any nerve regeneration research protocol with ARA-290 |
| 16 mg vial context | Reconstitute to 4 mg/mL in sterile water (4 mL total); provides 4 × 1 mL aliquots at clinical dose; or 16 × 1 mg aliquots for lower-dose protocols; or 64 × 250 µg aliquots for rodent studies at 10 µg/kg per 25g mouse | Aliquot the full 16 mg vial into single-use volumes immediately after reconstitution; store at −20°C; avoid freeze-thaw cycles; log reconstitution date on each aliquot |
ARA-290 Quality Control at SourceTides
Every batch of ARA-290 Peptide 16 mg from SourceTides undergoes these tests before release.
The pyroglutamate N-terminus confirmation is the critical QC step unique to ARA-290 — distinguishing the active pGlu form from the precursor glutamate/glutamine N-terminus that lacks the cyclised protective feature.
| Test | Method | Specification | Why It Matters |
|---|---|---|---|
| Purity | RP-HPLC (C18; UV 220 nm) | ≥99% peak area purity | Separates ARA-290 (pGlu N-terminus) from the uncyclised glutamate/glutamine precursor (different MW, different N-terminus) and from deletion sequence by-products; ≥99% confirms the cyclised active form dominates |
| Identity and pGlu Confirmation | ESI-MS ([M+H]⁺ = 1258.33 Da); MS fragmentation confirms pGlu N-terminal cyclisation | MW 1257.324 Da confirmed; pGlu cyclisation confirmed by −17 Da vs glutamine N-terminus (loss of NH₃ in cyclisation); the active sequence UEQLERALNSS confirmed | Pyroglutamate is formed by cyclisation of N-terminal glutamine (or acid-catalysed glutamate); the −17 Da mass shift vs uncyclised Gln-starting peptide is the diagnostic MS identifier for the active pGlu ARA-290 vs an inactive precursor |
| Endotoxin | LAL chromogenic assay | <1 EU/mg | LPS activates microglia, macrophage, and neuronal inflammatory pathways directly overlapping with ARA-290’s anti-inflammatory endpoints; endotoxin would confound every IRR-mediated anti-inflammatory assay and all neuropathic pain endpoints |
| Appearance | Visual inspection | White lyophilised powder; no discolouration or clumping | Discolouration may indicate oxidation of Arg or Ser residues; clumping indicates moisture uptake and dosing inaccuracy |
| Certificate of Analysis | Lot-specific PDF | HPLC + MS (1257.324 Da; pGlu confirmed; −17 Da cyclisation noted) + endotoxin + dates | The pGlu −17 Da MS confirmation is the unique CoA element for ARA-290; essential documentation for any publication reporting ARA-290 activity — it proves the active form was used, not an uncyclised precursor |
ARA-290 Regulatory Status
| Jurisdiction | Status | Notes |
|---|---|---|
| USA (FDA) | Not approved as a drug; FDA Orphan Drug Designation granted for neuropathic pain in sarcoidosis; not a DEA controlled substance; research compound only | The FDA Orphan Drug Designation for sarcoidosis neuropathy (granted to Araim Pharmaceuticals) formally recognises ARA-290’s therapeutic potential and provides regulatory pathway incentives. This designation does not constitute approval. SourceTides supplies research-grade for laboratory use only. |
| EU / UK / Australia / Canada | Not approved; not a controlled substance; research compound | No marketing authorisation in any of these jurisdictions. Not a controlled substance. Research laboratory access. See the SourceTides shipping policy. |
| WADA | Not listed on 2024–2025 WADA Prohibited List; not prohibited | ARA-290 produces zero erythropoietic/haematopoietic activity — haematocrit and haemoglobin are unaffected at any tested dose. Unlike full EPO (WADA S2 prohibited as an erythropoiesis-stimulating agent), ARA-290 has no doping application. Verify annually at wada-ama.org. |
Peer-Reviewed References
| # | Citation | Link |
|---|---|---|
| 1 | Brines M, Patel NS, Villa P et al. (2008). Nonerythropoietic, tissue-protective peptides derived from the tertiary structure of erythropoietin. PNAS. 105:10925–10930. PMID: 18695228. [Foundational study: identifies pHBSP/ARA-290; confirms zero erythropoietic activity; establishes IRR mechanism] | PubMed PMID: 18695228 — PNAS 2008 |
| 2 | Dahan A et al. (2017). Cibinetide improves corneal nerve fibre abundance in patients with sarcoidosis-associated small fibre loss and neuropathic pain. Invest Ophthalmol Vis Sci (IOVS). 58(6):BIO52–BIO60. PMID: 28475706. [Phase 2b; 64 patients; 23% corneal nerve fibre area increase; primary clinical evidence] | PubMed PMID: 28475706 — IOVS 2017 |
| 3 | Brines M, Dunne AN, van Velzen M et al. (2014). ARA 290, a nonerythropoietic peptide engineered from erythropoietin, improves metabolic control and neuropathic symptoms in patients with type 2 diabetes. Mol Med. 20:658–666. PMID: 25387363. | PubMed PMID: 25387363 — Mol Med 2014 |
| 4 | Heij L, Niesters M, Swartjes M et al. (2012). Safety and efficacy of ARA 290 in sarcoidosis patients with symptoms of small fibre neuropathy: a randomised, double-blind pilot study. Mol Med. 18:1430–1436. PMID: 22988708. | PubMed PMID: 22988708 — Mol Med 2012 |
| 5 | Zhang W, Yu G, Zhang M. (2016). ARA 290 relieves pathophysiological pain by targeting TRPV1 channel: integration between immune system and nociception. Peptides. 76:73–79. [TRPV1 antagonism mechanism] | PubMed PMID: 26778782 — Peptides 2016 |
| 6 | van Velzen M, Heij L, Niesters M et al. (2014). ARA 290 produces long-term relief of neuropathic pain coupled with suppression of the spinal microglia response. PMC3928087. | PMC3928087 — SNI microglia |
| 7 | Wikipedia: Cibinetide. CAS 1208243-50-8; formula; sequence; mechanism; clinical development; EPO helix B origin. | Wikipedia: Cibinetide |
Frequently Researched Alongside ARA-290
These compounds are most commonly studied alongside ARA-290 in neuropathy, neuroinflammation, tissue repair, and metabolic-neuropathic research:
- BPC-157 — Tissue repair peptide via VEGFR2/NO/FAK; studied alongside ARA-290 in combined neuroprotection + vascular repair protocols, where IRR-mediated nerve regeneration (ARA-290) and VEGFR2-mediated vascular repair (BPC-157) address complementary aspects of nerve tissue recovery
- BPC-157 Capsules — Oral BPC-157 for systemic tissue repair; studied with ARA-290 in diabetic neuropathy models combining GI-origin cytoprotection (BPC-157) and IRR nerve fibre regeneration (ARA-290)
- TB-500 (Thymosin Beta-4) — Actin cytoskeleton repair; Schwann cell and neuronal cell migration; studied alongside ARA-290 in nerve regeneration protocols combining Schwann cell proliferation (ARA-290 IRR) and actin-mediated cell migration (TB-500)
- Pinealon 10 mg — CNS neuroprotective bioregulator (EDR tripeptide); SOD2/GPX1 antioxidant; studied alongside ARA-290 in comprehensive neurodegeneration panels combining antioxidant neuroprotection (Pinealon) and IRR anti-inflammatory nerve regeneration (ARA-290)
- Selank Amidate 10 mg — GABAergic anxiolytic and IL-6 suppressor; studied with ARA-290 in neuropathic pain panels combining GABAergic/IL-6 central modulation (Selank) and IRR/TRPV1 peripheral nerve repair (ARA-290)
- KPV Peptide 10 mg — NF-κB and MAPK direct inhibitor via PepT1 transport; studied alongside ARA-290 in multi-mechanism neuroinflammation research combining NF-κB inflammatory suppression (KPV) and IRR-mediated tissue protection (ARA-290)
- Thymalin 10 mg — Thymic T-cell bioregulator; studied with ARA-290 in autoimmune neuropathy models (AAN, EAN), where thymic T-cell reconstitution (Thymalin) and IRR-mediated Treg induction + nerve repair (ARA-290) both address the immune-neuropathic axis
- Thymosin Alpha-1 — Immune modulation; antiviral; studied alongside ARA-290 in neuroimmunology panels where adaptive immune regulation (Thymosin Alpha-1) and IRR-driven innate immune resolution (ARA-290) are combined
- NAD⁺ Injectable — Sirtuin substrate; SIRT1/SIRT3 neuroprotection; SIRT3 protects neuronal mitochondria via deacetylation; studied with ARA-290 in neurodegenerative ageing panels combining mitochondrial neuroprotection (NAD⁺) and IRR-mediated neurorepair (ARA-290)
- Epithalon 10 mg — Khavinson telomerase activator; longevity; studied alongside ARA-290 in ageing neuropathy research combining telomere longevity and pineal biology (Epithalon) with peripheral nerve regeneration (ARA-290)
- DSIP Peptide 5 mg — HPA axis modulator; antioxidant; studied with ARA-290 in pain and sleep-neuropathy interface research where HPA stress axis (DSIP) and peripheral nerve repair (ARA-290) converge in neuropathic pain biology
- Semax — ACTH(4-10) neuropeptide; BDNF/TrkB; studied alongside ARA-290 in combined neuroprotection panels where BDNF upregulation (Semax) and IRR-mediated anti-inflammatory nerve repair (ARA-290) provide complementary central and peripheral neuroprotective mechanisms
- Semaglutide — GLP-1R agonist; studied with ARA-290 in diabetic neuropathy research where metabolic control (Semaglutide GLP-1R) and peripheral nerve regeneration (ARA-290 IRR) together address the metabolic and neurological components of DPN simultaneously
- Tirzepatide — GLP-1R + GIPR dual agonist; studied with ARA-290 in combined metabolic + neuropathic protocols: Tirzepatide addresses glycaemic control and weight loss while ARA-290 addresses small fibre nerve regeneration independently of glycaemic improvement
- Ipamorelin 10 mg — Selective GH secretagogue; GH/IGF-1 has neurotrophic properties; studied with ARA-290 in combined peripheral neuropathy protocols combining GH axis neurotrophic support (Ipamorelin) and IRR nerve fibre regeneration (ARA-290)
Frequently Asked Questions
You can buy ARA-290 Peptide 16 mg (Cibinetide; CAS 1208243-50-8; pGlu-EQLERALNSS) directly from SourceTides.
Every 16 mg vial includes a lot-specific Certificate of Analysis with the RP-HPLC chromatogram (≥99% purity), ESI-MS identity confirmation (MW 1257.324 Da; pyroglutamate cyclisation confirmed by −17 Da vs uncyclised precursor), and LAL endotoxin result (<1 EU/mg).
All vials are lyophilised white powder and dispatched on dry-ice cold chain. See the SourceTides shipping policy for dispatch details.
EPO’s haematopoietic activity requires the full protein’s extended binding surface — particularly helices A and C — to engage the EPOR homodimer receptor in bone marrow. This homodimer binding is what drives red blood cell production, haematocrit increase, and the thrombotic risk associated with EPO doping.
ARA-290 is derived from a completely different part of the EPO molecule: the surface-exposed loop of helix B. This region contacts the Innate Repair Receptor (EPOR/CD131 heterodimer) but does NOT engage the EPOR homodimer. Without EPOR homodimer binding, no erythropoietic signal is transmitted — haematopoiesis cannot be activated.
This was confirmed in every clinical trial. At 4 mg/day for 28 days in human subjects, haematocrit and haemoglobin were completely unaffected. The tissue-protective and neuroprotective biology operates through the CD131-containing IRR independently of haematopoiesis. This is why ARA-290 is not WADA-prohibited despite its EPO lineage — it has no erythropoietic mechanism to exploit.
FDA Orphan Drug Designation is a formal regulatory recognition granted by the FDA to compounds targeting rare diseases (affecting fewer than 200,000 US patients). It provides incentives including 7 years of market exclusivity after approval, tax credits for clinical trial costs, and fee waivers.
For research purposes, the Orphan Drug Designation for ARA-290 (sarcoidosis neuropathic pain) means the FDA has reviewed Araim Pharmaceuticals’ preclinical and clinical data and found it sufficient to justify the designation. It is not an approval — but it represents formal regulatory acknowledgment that ARA-290 has a credible mechanistic and clinical basis for therapeutic development.
This makes ARA-290 unusual among research peptides: it has passed a regulatory review threshold that most research compounds never reach. The designation, combined with four published Phase 1/2 clinical trials (including the randomised, double-blind Phase 2b with 64 patients published in IOVS), places ARA-290 in the most extensively human-validated category of research neuropeptides available. SourceTides supplies for in-vitro laboratory research only.
ARA-290’s plasma half-life is approximately 20 minutes — it is cleared rapidly. Yet in the SNI rat pain model, analgesia persisted for weeks after a 10-day treatment course ended. In the human Phase 2b trial, pain reduction and nerve fibre regeneration were measurable at 28 and 56 days post-treatment.
This is the “molecular switch” mechanism. When ARA-290 binds the Innate Repair Receptor, it activates JAK2-STAT5, PI3K/Akt, and MAPK signalling cascades. These cascades initiate transcriptional programmes in target cells — genes for anti-apoptotic proteins (Bcl-2 family), anti-inflammatory mediators, and neurotrophic factors are turned on. Once these programmes are activated, they continue to run even after the peptide has cleared. The peptide triggers the switch; the switch stays on.
For research design: this means acute and chronic dosing schedules produce similar long-term endpoint profiles. The key is delivering enough IRR activations to establish the sustained repair programme — which is why the published clinical protocols use daily dosing for 28 days rather than a single dose. Design protocols with endpoint measurements at 14, 28, and 56 days to capture the full temporal profile of ARA-290 effects.
The N-terminal pyroglutamate (pGlu) is a cyclised form of glutamine or glutamate — the lactam ring at the N-terminus blocks aminopeptidase attack from the N-terminal direction, providing partial metabolic stability. Uncyclised ARA-290 (with a free glutamine or glutamate N-terminus) would be rapidly degraded from the N-terminal end and show reduced biological activity.
The pyroglutamate cyclisation removes 17 Da from the molecule (loss of NH₃ when Gln cyclises, or loss of H₂O when Glu cyclises to form the lactam). This −17 Da shift is directly measurable by ESI-MS: cyclised ARA-290 (active form) has MW 1257.324 Da; the uncyclised Gln-starting precursor would have MW 1274.33 Da. If your CoA shows 1274.33 Da as the dominant ion, you have the uncyclised precursor, not the active compound.
The SourceTides ARA-290 16 mg CoA explicitly reports the MS confirming the 1257.324 Da cyclised form and notes the −17 Da pyroglutamate cyclisation. This single data point on the CoA is the most important quality assurance element for ARA-290 that other supplier CoAs often omit.
ARA-290 is not a controlled substance in any major jurisdiction. It is not DEA-scheduled in the USA, not controlled under the Misuse of Drugs Act 1971 in the UK, and not a CDSA controlled substance in Canada. In Australia, it is not a scheduled substance — verify current TGA status for institutional compliance.
ARA-290 is not WADA-prohibited. Despite its EPO origin, it produces zero erythropoietic activity and has no performance-enhancing application via haematopoiesis — the WADA basis for EPO prohibition does not apply.
SourceTides supplies for in-vitro laboratory research use only. See the SourceTides shipping policy for jurisdiction-specific details.
SourceTides accepts Visa, Mastercard, American Express, cryptocurrency, and bank transfers for institutional orders. All payments go through secure, encrypted gateways.
For institutional purchase orders, bulk research procurement, or custom quantities, contact the team via the SourceTides contact page. Orders are reviewed for research compliance before dispatch.
All SourceTides products, including ARA-290 Peptide 16 mg (Cibinetide; CAS 1208243-50-8), are for in-vitro laboratory research use only.
ARA-290 holds FDA Orphan Drug Designation for sarcoidosis neuropathy but is not approved by the FDA, EMA, TGA, or Health Canada as a pharmaceutical drug.
These products are not for human consumption.
By purchasing, the buyer confirms authorised researcher status and accepts responsibility for compliance with all applicable regulations.
| Weight | 0.01 lbs |
|---|---|
| Dimensions | 5 × 5 × 5 in |
| Purity | ≥99% HPLC, MW 1257.324 Da, pGlu N-Terminus Confirmed (ESI-MS; −17 Da cyclisation) |
| Strength | 16 mg |
| Form | Lyophilised Powder |
| CAS Number | 1208243-50-8 |
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