Ara-290 10mg

Full-length EPO at doses required for tissue protection stimulates the classical EPO receptor (EPOR homodimer) and drives red blood cell production. This hematopoietic stimulation raises hematocrit and increases blood viscosity, which at high EPO doses causes thrombosis and hypertension in models -- the serious effects associated with high-dose EPO exposure. By engineering a peptide that selectively activates the tissue-protective receptor pathway (EPOR/beta common receptor heterodimer, the innate repair receptor) without engaging the erythropoietic homodimer, Ara-290 provides a tool for studying neuroprotective and anti-inflammatory signaling without the cardiovascular sequelae of EPO-driven polycythemia.

Small fiber neuropathy (SFN) is a condition affecting the unmyelinated C-fibers and thinly myelinated A-delta fibers that carry pain and autonomic signals. It is characterised by burning pain, sensory changes, and autonomic dysfunction. SFN-associated nerve fiber loss can be quantified by corneal confocal microscopy (measuring corneal nerve fiber density). Preclinical and in-vitro research on Ara-290 in SFN models has examined corneal nerve fiber density (as a marker of nerve regeneration) and neuropathic-pain readouts relative to controls -- a notable model system for studying pharmacological peripheral nerve regeneration.

The innate repair receptor (EPOR/beta common receptor heterodimer) is expressed in many non-hematopoietic tissues including endothelium, neurons, astrocytes, and immune cells. Its activation promotes cell survival under stress, reduces inflammatory cytokine production, and supports tissue repair. In models of myocardial ischemia, EPO derivatives protecting through this receptor reduce infarct size in animal models. For inflammation, activation shifts macrophage phenotype toward anti-inflammatory M2-like states. Ara-290's selectivity for this receptor makes it a research tool for dissecting the IRR-mediated versus erythropoietic arms of EPO biology.