ABR-238901 是一种口服有效的 S100A8/A9 阻滞剂，可抑制 S100A8/A9 与其受体 RAGE (晚期糖基化终产物受体) 和 TLR4(toll 样受体 4）的相互作用。ABR-238901 具有用于心肌梗塞 (MI) 研究的潜力。
货号:ajcx35644
CAS:1638200-22-2
分子式:C11H9BrClN3O4S
分子量：394.63
溶解度:DMSO : 33.33 mg/mL (84.46 mM; ultrasonic and warming and heat to 60°C)
纯度：98%
存储：Store at -20°C
库存：现货

Background:

ABR-238901 is an orally active and potent S100A8/A9 blocker and inhibits S100A8/A9 interaction with its receptors RAGE (receptor for advanced glycation endproducts) and TLR4 (toll-like receptor 4). ABR-238901 has the potential for myocardial infarction (MI) research[1][2][3].

ABR-238901 (30 mg/kg/day; gavage; for 3 weeks) causes less angiogenesis and less IL6 and IL10 in MDSCs[1]. ABR-238901 (30 mg/kg/day; gavage) in combination with Bortezomib (0.6 mg/kg; sc; 2 times/week) reduces tumor load compared with treatments of either agent alone[1]. ABR-238901 (30 mg/kg; IP for the first 3 d and thereafter continuously p.o.; daily; for 21 days) leads to gradual deterioration of cardiac function and accelerated left ventricular remodeling in C57BL/6NRJ mice with myocardial ischemia induced by permanent coronary artery ligation. Treatment with ABR-238901 during the first 3 days post-myocardial infarction (MI) restricts the inflammatory damage and promotes a reparatory environment[2].

[1]. Kim De Veirman, et al. Extracellular S100A9 Protein in Bone Marrow Supports Multiple Myeloma Survival by Stimulating Angiogenesis and Cytokine Secretion. Cancer Immunol Res. 2017 Oct;5(10):839-846.
[2]. Goran Marinkovi?, et al. S100A9 Links Inflammation and Repair in Myocardial Infarction. Circ Res. 2020 Aug 14;127(5):664-676.
[3]. A. Schiopu, et al. Short-term blockade of the S100A8/A9 alarmin in the immediate post-myocardial infarction period inhibits acute myocardial inflammation and preserves myocardial repair. European Heart Journal, Volume 38, Issue suppl_1, August 2017, ehx504.