| Identification | Back Directory | [Name]
3-Pyridinesulfonamide, 5-bromo-N-(5-chloro-4-hydroxy-3-pyridinyl)-6-methoxy- | [CAS]
1638200-22-2 | [Synonyms]
ABR-238901
3-Pyridinesulfonamide, 5-bromo-N-(5-chloro-4-hydroxy-3-pyridinyl)-6-methoxy- | [Molecular Formula]
C11H9BrClN3O4S | [MOL File]
1638200-22-2.mol | [Molecular Weight]
394.63 |
| Chemical Properties | Back Directory | [Boiling point ]
576.7±60.0 °C(Predicted) | [density ]
1.830±0.06 g/cm3(Predicted) | [storage temp. ]
Store at -20°C | [solubility ]
DMSO : 33.33 mg/mL (84.46 mM; ultrasonic and warming and heat to 60°C) | [form ]
Solid | [pka]
2.17±0.50(Predicted) | [color ]
Light brown to khaki |
| Hazard Information | Back Directory | [Uses]
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]. | [Biological Activity]
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]. | [in vivo]
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).
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| [storage]
Store at -20°C | [References]
[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. |
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