| Lot ID | Purity | Net Content | Endotoxin | Sterility |
|---|---|---|---|---|
| ARA0100314261 | 99.6 % | 9 mg (90.3 %) | 10.9 EU/vial | Pass |
ARA-290
ARA-290 is a synthetic erythropoietin-derived peptide investigated for selective activation of innate repair receptor signaling pathways involved in inflammatory modulation and tissue protection.
Original price was: $40.00.$36.00Current price is: $36.00.
In stock
What is ARA-290?
ARA-290, also known as cibinetide, is a synthetic peptide derived from the structure of erythropoietin (EPO). Unlike erythropoietin, ARA-290 does not stimulate red blood cell production but is designed to selectively activate the innate repair receptor (IRR), a signaling complex associated with cellular protection and inflammatory regulation. The peptide has been investigated in both preclinical and human research models examining tissue-protective signaling mechanisms.
Research Interest
ARA-290 is studied for biological processes related to inflammatory modulation, cellular stress responses, and tissue protection. Research areas include neuropathic signaling pathways, metabolic inflammation, vascular function, and recovery responses following cellular injury. Investigators examine how selective activation of innate repair signaling pathways influences coordinated biological adaptation without hematopoietic effects.
Mechanisms Under Investigation
Research suggests ARA-290 activates the innate repair receptor complex, triggering downstream pathways involved in anti-inflammatory signaling, mitochondrial protection, and cellular survival responses. Studies have explored its effects on cytokine regulation, neural signaling pathways, and microvascular function associated with tissue stress and recovery models.
Current State of Research
ARA-290 has been evaluated in multiple preclinical investigations and early-phase human clinical studies examining inflammatory and neurological signaling outcomes. Ongoing research continues to explore its pharmacology, receptor selectivity, and broader implications for tissue-protective signaling mechanisms.

