Ara-290
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Ara-290 (also designated cyclo LSRR, cibinetide) is a synthetic 11 amino acid cyclic peptide derived from the helix B region of erythropoietin (EPO) that selectively activates the innate repair receptor (IRR) — a heterodimer of EPO receptor (EPOR) and CD131 (beta common receptor, beta-c) — without activating the classical homodimeric EPOR responsible for erythropoiesis. This receptor selectivity allows tissue protection and anti-inflammatory signalling research without the haematopoietic effects (red blood cell production, thrombosis risk) that limit research use of full-length EPO.
Erythropoietin's pleiotropic effects extend far beyond erythropoiesis — EPO receptors are expressed in the nervous system, heart, kidney, and immune cells where they mediate cytoprotective and anti-inflammatory signalling. The discovery that these non-erythropoietic EPO effects are mediated through the heterodimeric IRR (EPOR/CD131) rather than the homodimeric EPOR used for erythropoiesis enabled development of Ara-290 as an IRR-selective research tool.
IRR activation by Ara-290 drives Jak2/STAT5, PI3K/Akt, and MAPK/ERK signalling in non-haematopoietic cells. Published research has characterised Ara-290 in: peripheral neuropathy models (small fibre nerve density restoration, reduced neuropathic pain behaviour); cardiac ischaemia-reperfusion models (cardioprotection through Akt-mediated anti-apoptotic signalling); inflammatory models (macrophage M2 polarisation, TNF-alpha and IL-6 suppression); and diabetic wound healing models (keratinocyte migration, angiogenesis).
Ara-290 has completed Phase 2 clinical trials in sarcoidosis-associated small fibre neuropathy, providing published human pharmacokinetic and pharmacodynamic data for research contextualisation. The clinical dataset includes plasma half-life characterisation, tissue distribution inferences from pharmacodynamic endpoints, and safety profile data.
Ara-290 receptor characterisation research: the IRR (innate repair receptor, EPOR/CD131 heterodimer) can be detected in non-haematopoietic cells by co-immunoprecipitation — immunoprecipitate with anti-EPOR antibody, then Western blot for CD131 to confirm heterodimer co-precipitation. This distinguishes IRR-expressing cells (co-precipitate CD131 with EPOR) from classical EPO-responsive erythroid progenitors (EPOR homodimer without CD131 co-precipitation). Confirming IRR expression in the specific cell model used is an important quality control step before interpreting Ara-290 data.
Ara-290 in diabetic neuropathy research models: streptozotocin (STZ)-induced diabetic rats develop reproducible small fibre peripheral neuropathy over 8-12 weeks, characterised by reduced intraepidermal nerve fibre density (IENFD) in skin punch biopsies (measured by PGP9.5 immunofluorescence), mechanical allodynia (von Frey filament testing), and thermal hypoalgesia (Hargreaves plantar test). Published research has characterised Ara-290 effects on IENFD restoration and sensory function in this model. For in vitro modelling, culturing DRG neurons in high-glucose medium (25-30mM versus 5mM control) for 72-96 hours produces glucose-induced neurite retraction and oxidative stress mimicking diabetic neuropathy. Ara-290 treatment (1-100nM) in this high-glucose paradigm allows mechanistic research into IRR-mediated neuroprotection under diabetic conditions. Comparing Ara-290 with full-length EPO (1 IU/mL) at matched STAT3 phosphorylation-inducing concentrations, then measuring erythropoiesis-stimulating activity in bone marrow colony-forming unit assays, directly quantifies the separation between neuroprotective and erythropoietic signalling that defines Ara-290's pharmacological advantage over EPO itself. MW: approximately 1200 Da. CAS: 895158-95-9. Reconstitute in bacteriostatic water at 1mg/mL. Store lyophilised at -20°C. For laboratory and analytical research purposes only.
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