| Bioactivity | 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[1]. | ||||||||||||
| In Vivo | NLRP3-IN-2 is well tolerated with no effects on the glucose levels in vivo[1].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%, P<0.01) [1]. Animal Model: | ||||||||||||
| Name | NLRP3-IN-2 | ||||||||||||
| CAS | 16673-34-0 | ||||||||||||
| Formula | C16H17ClN2O4S | ||||||||||||
| Molar Mass | 368.84 | ||||||||||||
| Appearance | Solid | ||||||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | ||||||||||||
| Storage |
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| Reference | [1]. Carlo Marchetti, et al. A novel pharmacologic inhibitor of the NLRP3 inflammasome limits myocardial injury after ischemia-reperfusion in the mouse. J Cardiovasc Pharmacol. 2014 Apr;63(4):316-322. |
NLRP3-IN-2
CAS: 16673-34-0 F: C16H17ClN2O4S W: 368.84
NLRP3-IN-2, an intermediate substrate in the synthesis of glyburide, inhibits the formation of the NLRP3 inflammasome in
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