Biological Activity
Necrostatin-1 is a potent, selective and cell-permeable necroptosis inhibitor with an EC50 of 490 nM in Jurkat cells. It acts by inhibiting the death domain kinase RIP (RIP1) in the necroptosis pathway.
In Vitro
Necrostatin-1 (Nec-1) is a specific and potent small-molecule inhibitor of cell death caused by death-domain receptor (DR) stimulation in the presence of caspase inhibition in multiple cell types. Necrostatin-1 efficiently inhibits the TNFα-induced necrotic death of L929 cells, which does not require exogenous caspase inhibitors[1]. Necrostatin-1 (Nec-1) prevents radiocontrast media (RCM)-induced dilation of peritubular capillaries, suggesting a novel role unrelated to cell death for the RIP1 kinase domain in the regulation of microvascular hemodynamics and pathophysiology of contrast-induced AKI (CIAKI)[2]. The decreased viability of C6 glioma cells caused by 3.0 µM and 6.0 µM shikonin is improved by pretreatment with Necrostatin-1 (Nec-1) to 92.3% and 82.9% at 1.5 h and 84.4% and 78.6% at 3.0 h, respectively. Similarly, the viability of U87 glioma cells is elevated by Necrostatin-1 to 91.6% and 81.5% at 1.5 h, and 81.8% and 71.2% at 3.0 h, respectively[3]. Necrostatin-1 (Nec-1) (30 µM) increases the survival of cardiomyocyte progenitor cell (CMPCs) by inhibiting necrotic cell death[4].
In Vivo
Necrostatin-1 (Nec-1) induces tubular bilation and affects the kinetics of the dilation of peritubular capillaries after RCM application. Upon a single intraperitoneal application of a single dose of Necrostatin-1 (1.65 mg/kg body weight, i.p.) 15 minutes before RCM, the return to baseline levels is prevented within the observation period[2].
References & source
Published experimental findings depend on the model and assay conditions. They do not guarantee equivalent performance in every application. For laboratory research use only.