ABR-238901

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].

Signaling Pathways >> Others >> Others

Research Areas >> Inflammation/Immunology

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]. Animal Model: C57BL/KaLwRij mice with 5T33MMvv cells[1] Dosage: 30 mg/kg Administration: Gavage; daily; for 3 weeks Result: Caused less angiogenesis.Caused less IL6 and IL10 in myeloid-derived suppressor cells (MDSCs).

[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 Marinković, 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.