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.In Vivo: 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% (P<0.01) and reduced infarct size, measured at pathology (by >40%, P<0.01) and with troponin I levels (by >70%, P<0.01) .