ARA-290
Repairs nerves and reduces chronic pain
- Small Fiber Neuropathy
- Tissue Repair
- Pain Modulation
Limited long-term safety data available - clinical trials were relatively short duration Not FDA approved - investigational compound with limited human exposure data Safety profile established only in specific patient populations (sarcoidosis, type 2 diabetes)
Mechanism of Action
ARA-290 is an 11-amino acid peptide derived from the tertiary structure of erythropoietin that selectively activates the innate repair receptor (IRR), a heteromeric complex consisting of the erythropoietin receptor (EPOR) and beta-common receptor (CD131). Unlike erythropoietin itself, ARA-290 does not bind to or activate the classical EPOR homodimer, meaning it produces tissue-protective and anti-inflammatory effects without stimulating red blood cell production (erythropoiesis). Key Pathways: Innate Repair Receptor (EPOR/CD131 heteromer) activation, TRPV1 ion channel antagonism for pain modulation, Suppression of spinal microglia and astrocyte inflammatory activation, Inhibition of pro-inflammatory macrophage cytokine secretion, Modulation of helper T cell differentiation toward regulatory T cells and Th2 cells By activating the innate repair receptor, ARA-290 triggers sustained tissue-protective signaling that reduces inflammation and promotes nerve regeneration, which translates clinically to improved neuropathic pain symptoms and measurable increases in corneal nerve fiber density. The compound's antagonism of TRPV1 channels provides an additional mechanism for pain relief, while its suppression of microglial activation in the spinal cord may explain the long-lasting analgesic effects observed weeks after treatment cessation.
Common Dose Reference Ranges
Educational reference ranges only — discuss actual dosing with a qualified healthcare provider.
Full ARA-290 protocols — frequency, timing, cycle length, reconstitution & research
- Injection site reactions
- No significant adverse events reported