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1、Hotline: 400-820-3792Inhibitors Agonists Screening Librarieswww.MedChemENecrostatin-1Cat. No.: HY-15760CAS No.: 4311-88-0Synonyms: Nec-1分式: CHNOS分量: 259.33作靶點(diǎn): RIP kinase; Autophagy; Indoleamine 2,3-Dioxygenase (IDO)作通路: Apoptosis; Autophagy; Metabolic Enzyme/Protease儲(chǔ)存式: Powder -20C 3 years4C 2 yea
2、rsIn solvent -80C 6 months-20C 1 month溶解性數(shù)據(jù)體外實(shí)驗(yàn) DMSO : 46 mg/mL (177.38 mM)* means soluble, but saturation unknown.Mass Solvent1 mg 5 mg 10 mg Concentration制備儲(chǔ)備液1 mM 3.8561 mL 19.2805 mL 38.5609 mL5 mM 0.7712 mL 3.8561 mL 7.7122 mL10 mM 0.3856 mL 1.9280 mL 3.8561 mL請(qǐng)根據(jù)產(chǎn)品在不同溶劑中的溶解度,選擇合適的溶劑配制儲(chǔ)備液,并請(qǐng)注意儲(chǔ)
3、備液的保存式和期限。體內(nèi)實(shí)驗(yàn) Necrostatin-1 (Nec-1) is dissolved in DMSO (50 mg/mL) as stock. It is diluted in PBS before injection5.BIOLOGICAL ACTIVITY物活性 Necrostatin-1 (Nec-1)種有效,選擇性和可滲透細(xì)胞的壞死性凋亡 (necroptosis) 抑制劑,在Jurkat細(xì)胞中的 EC50 為490 nM。Necrostatin-1 (Nec-1) 通過(guò)抑制壞死性凋亡途徑中 (RIP1) 激酶域起作。1/3 Master of Small Molecul
4、es 您邊的抑制劑師www.MedChemEIC50 & Target RIP1 kinase 1體外研究 Necrostatin-1 (Nec-1) is a specific and potent small-molecule inhibitor of cell death caused by death-domainreceptor (DR) stimulation in the presence of caspase inhibition in multiple cell types. Necrostatin-1 efficientlyinhibits the TNF-induced
5、necrotic death of L929 cells, which does not require exogenous caspase inhibitors1. 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 microvascularhemody
6、namics and pathophysiology of contrast-induced AKI (CIAKI) 2. The decreased viability of C6glioma cells caused by 3.0 M and 6.0 M shikonin is improved by pretreatment with Necrostatin-1 (Nec-1) to92.3% and 82.9% at 1.5 h and 84.4% and 78.6% at 3.0 h, respectively. Similarly, the viability of U87 gli
7、omacells 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, respectively3. Necrostatin-1 (Nec-1) (30 M) increases the survival of cardiomyocyte progenitor cell (CMPCs) byinhibiting necrotic cell death 4.體內(nèi)研究 Necrostatin-1 (Nec-1) induces tubular bilation and affe
8、cts the kinetics of the dilation of peritubular capillariesafter RCM application. Upon a single intraperitoneal application of a single dose of Necrostatin-1 (1.65 mg/kgbody weight, i.p.) 15 minutes before RCM, the return to baseline levels is prevented within the observationperiod 2.PROTOCOLCell As
9、say 3 C6 (3105 cells/well) and U87 (1.5105 cells/well) glioma cells are seeded onto 96-well microplate andcultured 24 h. PBS is added into the control group and Shikonin is added into experimental group to reachthe final concentration. Cellular viability is assessed using an MTT assay after Shikonin
10、 treatment atindicated time point. The absorbance value (A) at 570 nm is read using an automatic multi-wellspectrophotometer. Two groups of glioma cells from the same cell line are treated with Shikonin at lower orhigher concentration, respectively; other two groups of glioma cells are treated 1 h w
11、ith 100 M Necrostatin-1or 40 M z-VAD-fmk prior to co-incubation with Shikonin at indicated concentration. Additionally, another twogroups of glioma cells are treated only with 100 M Necrostatin-1 or 40 M Z-VAD-fmk at corresponding timepoint 3.MCE has not independently confirmed the accuracy of these
12、 methods. They are for reference only.Animal Mice 2Administration 8-10 week old male C57BL/6 mice (average weight approx.23 g) are used. Mice receive intravenousapplication of 200 L PBS or radiocontrast media (RCM) via the tail vein. A single dose of Z-VAD-fmk (10mg/kg body weight) or Necrostatin-1
13、(1.65 mg/kg body weight) is applied intraperitoneally 15 min. beforeRCM-injection. Mice are harvested another 24 hours after RCM-application (48 hours after reperfusion).Blood samples are obtained from retroorbital bleeding and serum levels of urea and creatinine aredetermined.MCE has not independen
14、tly confirmed the accuracy of these methods. They are for reference only.戶使本產(chǎn)品發(fā)表的科研獻(xiàn)2/3 Master of Small Molecules 您邊的抑制劑師www.MedChemE Autophagy. 2019 Mar 20:1-12. ACS Appl Mater Interfaces. 2019 Apr 10;11(14):13123-13133. Cancer Lett. 2016 Aug 28;379(1):134-142. Cell Death and Disease (2019) 10:487
15、Cell Death Dis. 2019 Apr 15;10(5):331.See more customer validations on HYPERLINK / www.MedChemEREFERENCES1. Degterev A, et al. Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury. Nat Chem Biol. 2005Jul;1(2):112-9.2. Linkermann A, et al. The RIP1-kinase
16、 inhibitor necrostatin-1 prevents osmotic nephrosis and contrast-induced AKI in mice. J Am SocNephrol. 2013 Oct;24(10):1545-57.3. Huang C, et al. Shikonin kills glioma cells through necroptosis mediated by RIP-1. PLoS One. 2013 Jun 28;8(6):e66326.4. Feyen D, et al. Increasing short-term cardiomyocyte progenitor cell (CMPC) survival by necrostatin-1 did not further preserve cardiacfunction. Cardiovasc Res. 2013 Jul 1;99(1):83-91.5. Zhou K, et al. RIP1-RIP3-DRP1 pathway regulates NLRP3 inflammasome activation following subar
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