ARA-290

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Cibinetide (INN) · ARA-290 · ARA 290 · pHBSP (pyroglutamate helix-B surface peptide)

The first residue is pyroglutamate (pGlu / Pyr), a cyclized glutamate rather than a standard amino acid. It is a genuine structural feature of the molecule and not a synthesis artifact — the cyclic lactam confers resistance to aminopeptidase cleavage at the N-terminus.

The eleven residues sum to 1437.44 Da as free amino acids (pGlu 129.11 + Glu 147.13 + Gln 146.14 + Leu 131.17 + Glu 147.13 + Arg 174.20 + Ala 89.09 + Leu 131.17 + Asn 132.12 + Ser 105.09 + Ser 105.09). Removing ten waters for the ten peptide bonds gives 1257.24 Da, matching the reported 1257.32 for C51H84N16O21.

Applies to the compound itself, from any supplier. Vendor-specific batch figures live on each listing’s certificate of analysis.

Appearance

white to off-white lyophilized powder

Storage, lyophilized

−20 °C, protected from light and humidity

Storage, reconstituted

2–8 °C

Handling

avoid repeated freeze-thaw

Erythropoietin has two functionally separable activities, and ARA-290 exists to isolate the second one.

Mediated by the classical EPO receptor homodimer (EPOR)2. This is the activity that raises red cell mass, and the activity responsible for the thrombotic and hypertensive risks that limit therapeutic EPO use.

Mediated by a separate receptor complex — the innate repair receptor — and localized to a different face of the EPO molecule.

The structural insight underlying ARA-290 is that these two activities map to different surfaces of the folded protein. The erythropoietic determinants sit on the surfaces that contact the classical receptor; the tissue-protective determinants sit on the aqueous face of helix B, which is oriented away from the EPOR binding interface.

ARA-290 is an 11-residue linear peptide reproducing that helix-B surface. Because it does not reproduce the EPOR contact surface, it does not engage the classical receptor homodimer and carries no erythropoietic activity. This is why the compound is described as non-erythropoietic or non-hematopoietic — it is a designed separation of function rather than an incidental property.

The innate repair receptor (IRR) is described as a heterodimer of the erythropoietin receptor (EPOR) and the beta-common receptor (βcR, CD131).

Classical EPO receptor

(EPOR)₂ homodimer → erythropoiesis

Innate repair receptor

EPOR + βcR (CD131) → tissue protection

Because the IRR shares the EPOR subunit but pairs it with CD131 rather than a second EPOR, a ligand can be designed to engage one and not the other. ARA-290 is selective for the heterodimer.

The IRR is described as not constitutively expressed but induced in tissues under metabolic stress or injury — which localizes activity to damaged tissue rather than distributing it systemically.

Suppression of pro-inflammatory cytokine production, reduced myeloid cell infiltration, modulation of macrophage and monocyte activation, cytoprotection against apoptosis, and promotion of tissue repair.

Separate work reports direct action on peripheral nociceptors through inhibition of TRPV1 channel activity, alleviating capsaicin-evoked pain responses. This is notable because it is a distinct mechanism from IRR signalling and offers an explanation for analgesic effects that appear faster than tissue repair would account for.

(Zhang, Yu & Zhang, Peptides, 2016)

The most developed clinical line of work. A randomized, double-blind pilot study in sarcoidosis patients with small fiber neuropathy symptoms reported reduced neuropathic pain and improved quality of life. Follow-up work reported increased corneal nerve fiber abundance, positioning the compound as potentially disease-modifying rather than purely symptomatic.

(Heij et al., Molecular Medicine, 2012; van Velzen et al., 2014; Culver et al., 2017)

Reported improvements in metabolic control and neuropathic symptoms, including HbA1c and lipid profiles, alongside increased corneal nerve fiber density.

(Brines et al., Molecular Medicine, 2015)

In Goto-Kakizaki rats, reported improvements in insulin release and glucose tolerance.

(Muller et al., Molecular Medicine, 2015)

A distinct and practically interesting application. Reported inhibition of macrophage activation and prevention of damage to transplanted islets, improved islet allograft function, and protection of isolated human islets under stress conditions — relevant to the pre-engraftment period where islet loss is a limiting factor.

(Watanabe et al., 2016; Yao et al., 2020; Yao et al., 2021)

Long-term relief of neuropathic pain reported following treatment, with effects outlasting the dosing period.

(Swartjes et al., 2014; Dahan et al., Pain Reports, 2016)

Experimental autoimmune encephalomyelitis — reduced disease severity with suppression of Th1 and Th17 responses and promotion of Th2 and regulatory T cells (Chen et al., J Neuroimmunol, 2014).

Experimental autoimmune neuritis — inflammation suppression and nerve regeneration without hematopoiesis (Liu et al., PLoS ONE, 2014). Experimental colitis — dampened innate immune cell function (Nairz et al., Scientific Reports, 2017). Systemic lupus erythematosus model — reduced inflammatory cytokines (Huang et al., J Cell Mol Med, 2018).

Early monocyte modulation reported to decelerate AD-like pathology progression, described as increasing the proportion of patrolling monocytes involved in amyloid-β clearance.

(Al-Onaizi et al., Brain Behav Immun, 2021)

In aged rats over a 15-month course, reported reductions in cardiac inflammation and fibrosis, improved mitochondrial function and autophagy, preserved cardiac function, lowered blood pressure, reduced frailty and prolonged healthspan.

(Winicki et al., Front Cardiovasc Med, 2023)

Reported inhibition of osteoclastogenesis in vitro with increased bone mineral density in mice.

(Awida et al., 2021)

Tissue-protective effects reported in skeletal muscle ischemia models (Yu et al., 2014). In the ischemic retina, reported enhancement of the vasoreparative potential of endothelial colony-forming cells (O'Leary et al., 2019).

A 99mTc-DOTA-ARA-290 conjugate has been synthesized and evaluated as a candidate SPECT tracer for targeting cardiac ischemic regions — an application that exploits IRR upregulation in injured tissue as an imaging target.

(Mohtavinejad et al., 2021)

Cibinetide is an investigational compound developed by Araim Pharmaceuticals. It has not been approved by the FDA or any other regulatory agency for any indication. Clinical work has reached randomized controlled trials in sarcoidosis-associated small fiber neuropathy and type 2 diabetes, and the compound is reported as generally well tolerated in those studies, with adverse events described as mild and including injection-site reactions, fatigue and headache.

Material supplied for laboratory use is a research chemical. It is not a drug, food, cosmetic, or dietary supplement, has not been evaluated by the FDA, and is not intended for human or veterinary use.