ARA-290 is the development code assigned by Araim Pharmaceuticals — the “ARA” prefix reflects the company name, and the number is a compound identifier.

Its assigned generic (INN/USAN) name is cibinetide, adopted in 2015; the “-tide” ending is the standard naming stem for peptide compounds.

In the scientific literature it is also called pyroglutamate helix-B surface peptide (pHBSP) — a name that captures both its origin in erythropoietin and its pyroglutamate N-terminus. In this log the name is treated purely as a reference identifier.

ARA-290 is a short synthetic peptide of 11 amino acids (an 11-mer) with a linear backbone, engineered to reproduce a surface region of the helix-B domain of erythropoietin (EPO).

Its residue sequence is pGlu-Glu-Gln-Leu-Glu-Arg-Ala-Leu-Asn-Ser-Ser (one-letter: pE-EQLERALNSS), where the N-terminal residue is pyroglutamate, a cyclized glutamine. That single-residue ring does not make the whole peptide macrocyclic, so it is described as a linear peptide. Reported molecular formula C51H84N16O21, molecular weight approx 1257 Da.

In the development literature it is described as a selective agonist of the innate repair receptor — proposed to be a heteromeric complex of the EPO receptor (EPOR) and the beta-common receptor (CD131). This receptor model is the accepted framework in the cibinetide literature rather than a fully settled physical structure.

ARA-290 was designed directly from the three-dimensional structure of erythropoietin (EPO). Researchers mapped the exposed, water-facing surface of EPO helix B and built a short peptide reproducing that region.

It grew out of the tissue-protective peptide concept — the idea that EPO’s protective signaling could be captured in a small molecule that does not stimulate red-blood-cell production.

It was developed and advanced clinically by Araim Pharmaceuticals (Tarrytown, New York), with a scientific lineage associated with Michael Brines and Anthony Cerami, recurring authors on the foundational and clinical papers.

Erythropoietin has two broadly separable activities: stimulating red-blood-cell production (erythropoiesis) and protecting and repairing tissue. Using full-length EPO for tissue protection carries risks such as raised red-cell mass and thrombosis.

The rationale for ARA-290 was to isolate the tissue-protective, anti-inflammatory signaling from the erythropoietic effect — giving researchers a tool to probe tissue protection and repair without raising hematocrit.

Consistent with that design goal, the peptide was reported to be non-erythropoietic in cell and animal assays while retaining tissue-protective activity. This log describes that intent only and does not assert that any therapeutic effect was established.

As an 11-residue peptide, ARA-290 is characteristically produced by solid-phase peptide synthesis (SPPS): the chain is assembled residue by residue on a resin, then cleaved, purified by reverse-phase HPLC, and confirmed by mass spectrometry.

Its small size makes it well suited to standard synthetic peptide manufacturing rather than recombinant expression.

Pharmacokinetic characterization in healthy-volunteer studies reported a short terminal elimination half-life (on the order of about 20 minutes subcutaneous and about 2 minutes intravenous). This is a physical PK property of the molecule — not dosing, timing, or administration guidance.

Research-use-only caveat: material offered for laboratory study is a research chemical, not an approved drug product.

Honestly framed: ARA-290 / cibinetide is investigational and has not been approved by the FDA for any use; published development reached Phase 2, and the human evidence is early-stage and mixed.

Clinical studies have investigated it mainly in small-fiber neuropathy — including sarcoidosis-associated small-nerve-fiber loss and neuropathic pain — measuring outcomes such as patient-reported neuropathic symptoms and corneal nerve-fiber density. A Phase 2 study in type 2 diabetes examined neuropathic symptoms alongside metabolic measures.

Other small or exploratory human studies looked at diabetic macular edema (which reported no improvement in mean visual acuity or retinal thickness) and at emotional and cognitive processing in healthy volunteers as a neuropsychological model (where the authors concluded the findings did not clearly support an antidepressant-like profile). Preclinical work has explored mechanisms including suppression of the spinal microglia response and modulation of the TRPV1 channel.

This is research-use-only reference material. No benefit or health claim is made, and no dosing, timing, or protocol is provided. What can be said is limited to what was studied — not what was proven. Consult a physician and the primary literature for specifics.