Product Name:ARA-290
Cas No:1208243-50-8
Molar Mass:1257.00
Chemical Formula:C51H84N16O21
Synonyms:Cibinetide, PHBSP
Storage:Store at -20°C
Sequence: XEQLERALNSS
Target Indicators:EPO recepter
Purity:98%
Application:ARA-290 is a synthetic peptide designed to mimic the effects of erythropoietin (EPO) without stimulating red blood cell production. It acts as a tissue-protective agent by targeting the innate repair receptor (IRR), which plays a crucial role in tissue repair and regeneration processes. ARA-290 demonstrates potential therapeutic benefits in treating various conditions associated with tissue damage and inflammation, including diabetic neuropathy, chronic kidney disease, and ischemic heart disease. In pharmaceutical chemistry, ARA-290 is studied for its ability to promote tissue repair and alleviate symptoms of neuropathic pain, making it a promising candidate for developing novel treatments in regenerative medicine. Additionally, its mechanism of action in modulating inflammatory responses and promoting tissue healing highlights its potential applications in fields such as neurology, nephrology, and cardiology.
Current Research:ARA-290, an 11-amino acid linear nonhematopoietic peptide derived from the three-dimensional structure of helix B of erythropoietin (EPO), exhibits selective interaction with the innate repair receptor (IRR), mediating tissue protection. This study aimed to investigate ARA290’s protective effects against cisplatin-induced nephrotoxicity. HEK-293 and ACHN cells were pretreated with ARA290 (50–400 nM) and cisplatin (2.5 μM). Evaluation encompassed cytotoxicity, genotoxicity, oxidative stress parameters (ROS, GPx, SOD, MDA), and inflammatory markers (TNFα, IL6, IL1β). Apoptotic cell death was assessed via caspase-3 activity and tunnel assay. Molecular mechanisms were elucidated by evaluating gene and protein expressions of TNFα, IL1β, IL6, Caspase-3, Bax, and Bcl2 using real-time PCR and western blot assay. ARA290 significantly mitigated DNA damage, oxidative stress, and inflammation induced by cisplatin, while antagonizing apoptosis. Molecular analysis revealed downregulation of pro-inflammatory cytokines and apoptotic markers and upregulation of anti-apoptotic markers in the ARA290 plus cisplatin group compared to cisplatin alone. These findings highlight ARA290’s potential as a chemo-preventive agent against cisplatin-induced nephrotoxicity, suggesting its therapeutic promise for acute kidney injury.
Cisplatin (CDDP) is widely used in cancer treatment, but its severe side effects, including nephrotoxicity, pose significant challenges. CDDP induces lipid membrane peroxidation, enhances free oxygen radicals, and diminishes antioxidant generation, leading to extensive tissue damage. Oxidative stress, apoptosis, and inflammation are implicated in CDDP-induced nephrotoxicity. Recent studies emphasize the role of reactive oxygen species (ROS) in initiating renal injury by CDDP. ARA290, a nonhematopoietic derivative of EPO, interacts with IRR, activating anti-inflammatory and anti-apoptotic pathways. ARA290 enhances endothelial nitric oxide synthase activity, improving renal function. The current research evaluated ARA290’s protective effects against CDDP-induced nephrotoxicity in renal cell lines. ARA290 significantly reduced oxidative stress, inflammation, and apoptosis induced by CDDP, as evidenced by reduced ROS levels, increased antioxidant enzyme activity, and decreased pro-inflammatory cytokine expression. Moreover, ARA290 attenuated genotoxicity, suggesting its potential as a geno-/chemoprotective agent. These findings underscore ARA290’s therapeutic potential in mitigating CDDP-induced nephrotoxicity and suggest further investigation into its clinical applications.
