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产品编号 T1847   CAS 4311-88-0
别名: Nec-1, Necrostatin 1

Necrostatin-1 是一种坏死性凋亡抑制剂,在 Jurkat 细胞中的 EC50为 490 nM。它抑制 RIP1激酶,可抑制 TNF-α 诱导的坏死性凋亡,EC50为182 nM。

Necrostatin-1, CAS 4311-88-0
产品目录号及名称: Necrostatin-1 (T1847)
纯度: 99.81%
纯度: 99.74%
纯度: 99.25%
存储 & 溶解度
产品描述 Necrostatin-1 is a specific RIP1 inhibitor and inhibits TNF-α-induced necroptosis (EC50: 490 nM in Jurkat cells).
靶点活性 RIP1:490 nM(EC50, Jurkat cells)
体外活性 Necrostatin-1 efficiently inhibited kinase activity of overexpressed protein in a dose-dependent manner. Similar to the results with overexpressed protein, Necrostatin-1 efficiently suppressed endogenous RIP1 kinase activity [1]. The cell death in C6 and U87 glioma cells could be inhibited by necroptosis inhibitor necrotatin-1. The increased ROS level caused by shikonin was attenuated by necrostatin-1 and blocking ROS by anti-oxidant NAC rescued shikonin-induced cell death in both C6 and U87 glioma cells [2].
体内活性 Necrostatin-1 (Nec-1) prevented osmotic nephrosis and contrast-induced AKI (CIAKI), whereas an inactive Nec-1 derivate (Nec-1i) or the pan-caspase inhibitor zVAD did not. In addition, Nec-1 prevented RCM-induced dilation of peritubular capillaries [3].
激酶实验 The assay was performed essentially as described. 293T cells were transfected with pcDNA3-FLAG-RIP1 vector, vectors encoding RIP1 mutant proteins or pcDNA3-RIP2-Myc and pcDNA3-FLAG-RIP3 vectors using standard Ca3(PO4)2 precipitation procedure. Culture medium was replaced 6 h after the transfection and cells were lysed 48 h later in the TL buffer consisting of 1% Triton X-100, 150 mM NaCI, 20 mM HEPES, pH 7.3, 5 mM EDTA, 5 mM NaF, 0.2 mM NaVO3 and complete protease inhibitor cocktail. Immunoprecipitation was carried out for 16 h at 4 °C using anti-FLAG M2 agarose beads, followed by three washes with TL buffer and two washes with 20 mM HEPES, pH 7.3. Beads were incubated in 15 μl of the reaction buffer containing 20 mM HEPES, pH 7.3, 10 mM MnCl2 and 10 mM MgCl2 for 15 min at 23–25 °C in the presence of different concentrations of necrostatins. For these assays, compound stocks (in DMSO) were diluted to appropriate concentrations in DMSO before the addition to the reactions to maintain final concentration of DMSO for all samples at 3%. Kinase reaction was initiated by addition of 10 μM cold ATP and 1 mCi of [γ-32P] ATP, and reactions were carried out for 30 min at 30 °C. Reactions were stopped by boiling in SDS-PAGE sample buffer and subjected to 8% SDS-PAGE. RIP1 band was visualized by analysis in a Storm 8200 Phosphorimager. Similar protocol was used for endogenous RIP1 kinase reactions, except mouse monoclonal RIP1 antibody and protein magnetic beads or rabbit RIP1 antibody-coupled agarose beads were used. For recombinant baculovirally expressed RIP1, protein was expressed in Sf9 cells according to manufacturer's instructions and purified using glutathione-sepharose beads. Protein was eluted in 50 mM Tris-HCl, pH 8.0 supplemented with 10 mM reduced glutathione, and eluted protein was used in the kinase reactions, supplemented with 5 × kinase reaction buffer (100 mM HEPES, pH 7.3, 50 mM MnCl2, 50 mM MgCl2, 50 μM cold ATP and 5 μCi of [γ-32P]ATP) [1].
细胞实验 Determination of EC50 was performed in FADD-deficient Jurkat cells treated with human TNFα as previously described. Briefly, cells were seeded into 96-well plates and treated with a range of necrostatin concentrations (30 nM to 100 μM, 11 dose points) in the presence and absence of 10 ng ml–1 human TNFα for 24 h. For these and all other cellular assays, compound stocks (in DMSO) were diluted to appropriate concentrations in DMSO before addition to the cells to maintain final concentration of DMSO for all samples at 0.5%. Cell viability was determined using CellTiter-Glo luminescent cell viability assay. Ratio of luminescence in compound and TNF-treated wells to compound-treated, TNF-untreated wells was calculated (viability, %) [1].
动物实验 24 hours after reperfusion, mice received intravenous application of 200 μl PBS or RCM via the tail vein. A single dose of zVAD (10 mg/kg body weight) or Nec-1 (1.65 mg/kg body weight) was applied intraperitoneally 15 min. before RCM-injection. To test the activity of zVAD, we applied zVAD from the same byculture to anti-Fas-treated Jurkat cells to assure its quality before mice were treated with this compound. Mice were harvested another 24 hours after RCM-application (48 hours after reperfusion). Blood samples were obtained from retroorbital bleeding and serum levels of urea and creatinine 5 were determined according to clinical standards in the central laboratory of the University Hospital Schleswig-Holstein, Campus Kiel, Germany, employing an enzymatic ultraviolettest for urea and an enzymatic peroxidase-dependent test for creatinine according to the manufacturer's instructions. Kidneys were conserved for histology. In addition to the demonstrated experiments, we compared the PBS group to mice that only received IRI without 200 μl of PBS and detected no changes in serum concentrations of urea and creatinine or histologically [3].
别名 Nec-1, Necrostatin 1


Crystal structure of RIP1 kinase in complex with necrostatin-1 analog

分子量 259.33
分子式 C13H13N3OS
CAS No. 4311-88-0


Powder: -20°C for 3 years | In solvent: -80°C for 2 years


DMSO: 40 mg/mL (154.24 mM)

( < 1 mg/mL refers to the product slightly soluble or insoluble )


1. Degterev A, et al. Identification of RIP1 kinase as a specific cellular target of necrostatins. Nat Chem Biol. 2008 May;4(5):313-21. 2. Huang C, et al. Shikonin kills glioma cells through necroptosis mediated by RIP-1. PLoS One. 2013 Jun 28;8(6):e66326. 3. Linkermann A, et al. The RIP1-kinase inhibitor necrostatin-1 prevents osmotic nephrosis and contrast-induced AKI in mice. J Am Soc Nephrol. 2013 Oct;24(10):1545-57. 4. Zhang Y, Fan B Y, Pang Y L, et al. Neuroprotective effect of deferoxamine on erastin-induced ferroptosis in primary cortical neurons[J]. Neural regeneration research. 2020, 15(8): 1539. 5. Wu H, Cheng X, Huang F, et al. Aprepitant Sensitizes Acute Myeloid Leukemia Cells to the Cytotoxic Effects of Cytosine Arabinoside in vitro and in vivo[J]. Drug Design. Development and Therapy. 2020, 14: 2413. 6. hang C, Liu Z, Zhang Y, et al. Z“Iron free” zinc oxide nanoparticles with ion-leaking properties disrupt intracellular ROS and iron homeostasis to induce ferroptosis[J]. Cell Death & Disease. 2020, 11(3): 1-15. 7. Yao X, Ma S, Peng S, et al. Zwitterionic Polymer Coating of Sulfur Dioxide‐Releasing Nanosystem Augments Tumor Accumulation and Treatment Efficacy[J]. Advanced Healthcare Materials. 2020, 9(5): 1901582. 9. Wang S, Li F, Qiao R, et al. Arginine-Rich Manganese Silicate Nanobubbles as a Ferroptosis-Inducing Agent for Tumor-Targeted Theranostics[J]. ACS nano. 2018 Dec 26;12(12):12380-12392. 10. Yan B, Ai Y, Sun Q, et al. Membrane Damage during Ferroptosis Is Caused by Oxidation of Phospholipids Catalyzed by the Oxidoreductases POR and CYB5R1[J]. Molecular Cell. 2020


1. Hu G, Cui Z, Chen X, et al.Suppressing Mesenchymal Stromal Cell Ferroptosis Via Targeting a Metabolism‐Epigenetics Axis Corrects their Poor Retention and Insufficient Healing Benefits in the Injured Liver Milieu.Advanced Science.2023: 2206439. 2. Li Y, Yang W, Zheng Y, et al.Targeting fatty acid synthase modulates sensitivity of hepatocellular carcinoma to sorafenib via ferroptosis.Journal of Experimental & Clinical Cancer Research.2023, 42(1): 1-19. 3. Wang X, Ji Y, Qi J, et al.Mitochondrial carrier 1 (MTCH1) governs ferroptosis by triggering the FoxO1-GPX4 axis-mediated retrograde signaling in cervical cancer cells.Cell Death & Disease.2023, 14(8): 1-13. 4. Lei S, Chen C, Han F, et al.AMER1 deficiency promotes the distant metastasis of colorectal cancer by inhibiting SLC7A11-and FTL-mediated ferroptosis.Cell Reports.2023, 42(9). 5. Zhou R, You Y, Zha Z, et al.Biotin decorated celastrol-loaded ZIF-8 nano-drug delivery system targeted epithelial ovarian cancer therapy.Biomedicine & Pharmacotherapy.2023, 167: 115573. 6. Zhu X, Huang N, Ji Y, et al.Brusatol induces ferroptosis in oesophageal squamous cell carcinoma by repressing GSH synthesis and increasing the labile iron pool via inhibition of the NRF2 pathway.Biomedicine & Pharmacotherapy.2023, 167: 115567. 7. Li H, Guan J, Chen J, et al.Necroptosis signaling and NLRP3 inflammasome cross-talking in epithelium facilitate Pseudomonas aeruginosa mediated lung injury.Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease.2022: 166613. 8. Wu Z, Lin C, Zhang F, et al.TIGD1 Function as a Potential Cuproptosis Regulator Following a Novel Cuproptosis-Related Gene Risk Signature in Colorectal Cancer.Cancers.2023, 15(8): 2286. 9. Huang F, Liang J, Lin Y, et al.Repurposing of Ibrutinib and Quizartinib as potent inhibitors of necroptosis.Communications Biology.2023, 6(1): 972. 10. Cai H, Qin D, Liu Y, et al.Remodeling of Gut Microbiota by Probiotics Alleviated Heat Stroke‐Induced Necroptosis in Male Germ Cells.Molecular Nutrition & Food Research.2023: 2300291.
FINO2 Gallic acid Simvastatin Acetylcysteine D-glutamine Artesunate CIL56 Lapatinib


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