ARA-290

Peptides such as BPC-157, TB-500, and ARA-290 may affect pathways implicated in peripheral nerve repair, including inflammation regulation, cytoprotection, angiogenic signaling, extracellular matrix remodeling, Schwann cell biology, and axonal regeneration.; This biological evidence derives mainly from preclinical models and has not been directly established in patients with IAN injury.; Three illustrative cases treated with a multimodal peptide-containing approach showed neurosensory recovery, but uncontrolled design precludes causal inference.; Peptide-based interventions remain investigational, with unresolved questions on safety, delivery, dosing, and long-term outcomes; controlled trials with standardized outcome measures are needed.

Db/db mice exhibited delayed task engagement and longer response latencies but maintained intact associative learning accuracy.; Reversal learning revealed pronounced impairments in cognitive flexibility, characterized by increased perseveration and reduced adaptation to changed reward contingencies.; ARA 290 treatment improved insulin sensitivity and altered circulating monocyte proportions but did not rescue executive cognitive flexibility deficits.; Hippocampal RNA-seq showed enrichment of immune pathways consistent with chronic low-grade inflammation, providing molecular context for the behavioral phenotype.

ARA290 reduced cisplatin-induced DNA damage parameters in comet assay and micronuclei frequency.; ARA290 improved oxidative stress by reducing MDA/ROS levels and enhancing antioxidant enzyme levels.; ARA290 mitigated cisplatin-induced renal inflammation by reducing pro-inflammatory cytokines.; ARA290 ameliorated cisplatin-induced cell injury by antagonizing apoptosis, with decreased Caspase-3 and Bax and increased Bcl2.

ARA 290 early treatment decelerated Aβ pathology and improved cognitive functions in young APP/PS1 mice.; ARA 290 increased total monocytes by stimulating generation of Ly6C Low patrolling subset, reducing brain Aβ burden.; ARA 290 was ineffective in aged APP/PS1 mice with advanced pathology and in chimeric mice with depleted patrolling monocytes.; The study suggests ARA 290 prevents AD-like progression via monocyte modulation, specifically increasing patrolling monocytes.

Radiolabeling purity exceeded 96% with in vitro stability of 85% up to 6 hours.; Binding of 99mTc-ARA-290 to hypoxic cells was 3 times higher than to normoxic cells at 1 hour.; SPECT imaging in cardiac ischemic rats showed a cardiac ischemic-to-lung ratio of 3.65 ID/g% at 0.5 hours.; The radiopeptide is a promising candidate for early diagnosis of cardiac ischemia.

ARA290 significantly reduced doxorubicin-induced DNA damage, as measured by decreased percentage of DNA in tail and micronuclei frequency.; ARA290 markedly attenuated doxorubicin-induced oxidative stress by preserving antioxidant defense enzyme activities.; ARA290 protected against doxorubicin-induced inflammation and apoptotic cell death in the tested cell lines.; The protective effects of ARA290 suggest it may also extend to cardiac cells, potentially reducing doxorubicin cardiotoxicity.

ARA-290 undergoes extensive exopeptidase-driven metabolism, producing a main metabolite PyrEQLERALN.; GHRP-3 and Peforelin exhibit considerable metabolic stability with a low tendency for deamidation.; The study presents two principle strategies for simulating peptide metabolism in vitro using blood specimens and recombinant amidase.

Eight studies met inclusion criteria, evaluating infliximab, adalimumab, ARA 290, methylphenidate, armodafinil, and exercise programs.; Anti-TNF therapies (adalimumab, infliximab) and neurostimulants (methylphenidate, armodafinil) showed some evidence of treatment effect.; Five studies had high risk of bias in most domains; the remaining three had small sample sizes and short duration.; Trial evidence for treating sarcoidosis-associated fatigue is limited and requires further investigation.

What is ARA-290?

**Mechanism of Action** ARA-290 (cibinetide) is an 11-amino-acid peptide derived from the helix B domain of erythropoietin (EPO). It selectively binds the heterodimeric innate repair receptor (IRR), composed of the erythropoietin receptor (EPOR) and the β common receptor (CD131). This interaction activates tissue-prote

How does ARA-290 work?

Erythropoietin-derived 11-aa peptide targeting the innate repair receptor (EPOR/CD131) for tissue protection without erythropoiesis.

What is the research status of ARA-290?

ARA-290 is currently classified as clinical trials, with 25 research references on record. This is for research purposes only and is not medical advice.

What is the molecular weight of ARA-290?

ARA-290 has a molecular weight of approximately 1257.3 g/mol (formula C51H84N16O21).