| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
Preparation Method | Cells were lysed, Immunoprecipitation was carried out for 16 h at 4 ℃ using anti-FLAG M2 agarose beads, Beads were incubated in 15 ul of the reaction buffer for 15 min at 23-25 ℃ in the presence of different concentrations of necrostatins (including Necrostatin-1). Kinase reaction was initiated by addition of 10 μM cold ATP and 1 μCi of [y-32P]ATP, and reactions were carried out for 30 min at 30℃. |
Reaction Conditions | RIP1 kinase assay（ Necrostatin-1） was performed at 30℃ for 30 min |
Applications | Necrostatin-1 is a RIP1 kinase inhibitor, RIP1 is the primary cellular target responsible for the antinecroptosis activity of necrostatin-1. |
Cell lines | Cardiomyocyte progenitor cells (CMPCs) |
Preparation Method | CMPCs were pretreated with vehicle or Necrostatin-1 for 30 min prior to the addition of tert-Butyl hydroperoxide in serum-free M199 medium. |
Reaction Conditions | 30 μM Necrostatin-1 for 30 min |
Applications | Under oxidative stress conditions, CMPC mainly displayed a necrotic phenotype and by pretreatment with Necrostatin-1, we observed a 37 ± 8% reduction in necrotic cell death in CMPCs compared with vehicle. Not find differences in apoptotic-mediated cell death. Therefore, Necrostatin-1 increased the survival of CMPCs by inhibiting necrotic cell death. |
Animal models | Eight-week-old male C57Bl/6 mice |
Preparation Method | Mice undergo sham surgery or bilateral renal pedicle clamping 24 hours before intraperitoneal injection of either PBS, the highly specific RIP1 kinase inhibitor Necrostatin-1, or the inactive derivate of necrostatin-1 (Necrostatin-1i) in the presence or absence of RCM. |
Dosage form | Necrostatin-1 (1.65 mg/kg body weight) was applied intraperitoneally 15 min before RCM-injection. |
Applications | CIAKI Is Attenuated by Necrostatin-1, an Inhibitor of the Kinase Domain of Receptor-Interacting Protein Kinase-1. |
| 产品描述 | Necrostatin-1 mainly acts on RIP1 in cells[5], Necrostatin-1 is a RIP1 kinase inhibitor with an IC50 value of 0.32 mM[1]. Necrostatin-1 can effectively inhibit RIP1 autophosphorylation, Necrostatin-1 effectively blocks RIP1-RIP3-MLKL signaling by inhibiting RIP1 phosphorylation[7]. Necrostatin-1 is also an IDO inhibitor[2]. Under oxidative stress conditions, CMPC mainly displayed a necrotic phenotype and by pretreatment with Necrostatin-1, we observed a 37 ± 8% reduction in necrotic cell death in CMPCs compared with vehicle. Not find differences in apoptotic-mediated cell death. Therefore, Necrostatin-1 increased the survival of CMPCs by inhibiting necrotic cell death[4]. The ratios of apoptotic and necrotic C2C12 cells were increased following CoCl2 treatment, typical necroptotic morphological characteristics were able to observe by TEM, whereas Necrostatin-1 exhibited a protective effect against CoCl2 induced oxidative stress. Treatment with Necrostatin-1 significantly decreased the levels of RIP1, p ERK1/2, HIF 1α, BNIP3 and ROS induced by CoCl2, and promoted C2C12 differentiation. Necrostatin-1 reversed the CoCl2 induced decrease in mitochondrial membrane potential[6]. In mice,Necrostatin-1 (Nec-1), a specific inhibitor of the receptor-interacting protein 1 (RIP1) kinase domain, prevented osmotic nephrosis and CIAKI, whereas an inactive Necrostatin-1 derivate (Nec-1i) or the pan-caspase inhibitor zVAD did not. Necrostatin-1 prevented 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 CIAKI[3]. References: |
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