产品
编 号：F199809
分子式：C16H17ClN2O4S
分子量：368.84
分子式：C16H17ClN2O4S
分子量：368.84
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
询价
询价
50mg
360
In-stock
100mg
480
In-stock
结构图
CAS No: 16673-34-0
产品详情
生物活性：
NLRP3-IN-2, an intermediate substrate in the synthesis of glyburide, inhibits the formation of the NLRP3 inflammasome in cardiomyocytes and limits the infarct size following myocardial ischemia/reperfusion in the mouse, without affecting glucose metabolism.
体内研究：
NLRP3-IN-2 is well tolerated with no effects on the glucose levels in vivo.NLRP3-IN-2 (100 mg/kg) treatment in a model of AMI due to ischemia+reperfusion significantly inhibits the activity of inflammasome (caspase-1) in the heart by 90% (P40%, P70%, P90% reduction in caspase-1 activity (reflective of the formation of an active inflammasome) in the heart tissue measured 24 hours after ischemia. Led to a significant reduction in the infarct size measured with TTC (>40% reduction) or troponin I levels (>70% reduction) when compared with vehicle alone.
NLRP3-IN-2, an intermediate substrate in the synthesis of glyburide, inhibits the formation of the NLRP3 inflammasome in cardiomyocytes and limits the infarct size following myocardial ischemia/reperfusion in the mouse, without affecting glucose metabolism.
体内研究：
NLRP3-IN-2 is well tolerated with no effects on the glucose levels in vivo.NLRP3-IN-2 (100 mg/kg) treatment in a model of AMI due to ischemia+reperfusion significantly inhibits the activity of inflammasome (caspase-1) in the heart by 90% (P40%, P70%, P90% reduction in caspase-1 activity (reflective of the formation of an active inflammasome) in the heart tissue measured 24 hours after ischemia. Led to a significant reduction in the infarct size measured with TTC (>40% reduction) or troponin I levels (>70% reduction) when compared with vehicle alone.
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