480065
Necrostatin-1
≥95% (HPLC), crystalline solid, necroptosis inhibitor, Calbiochem
别名:
Necrostatin-1
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选择尺寸
关于此项目
经验公式（希尔记法）:
C13H13N3OS
化学文摘社编号:
分子量:
259.33
UNSPSC Code:
12352200
NACRES:
NA.77
MDL number:
产品名称
Necrostatin-1, Necrostatin-1, CAS 4311-88-0, is a cell-permeable, potent, and selective blocker of necroptosis (EC50 = 494 nM in FADD-deficient Jurkat cells treated with TNF-α).
SMILES string
S=C1NC(C(=O)N1C)Cc2c3c([nH]c2)cccc3
InChI
1S/C13H13N3OS/c1-16-12(17)11(15-13(16)18)6-8-7-14-10-5-3-2-4-9(8)10/h2-5,7,11,14H,6H2,1H3,(H,15,18)
InChI key
TXUWMXQFNYDOEZ-UHFFFAOYSA-N
assay
≥95% (HPLC)
form
crystalline solid
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze, protect from light
color
yellow
solubility
DMSO: 10 mg/mL, methanol: 5 mg/mL
shipped in
ambient
Quality Level
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General description
Biochem/physiol Actions
主要靶标
坏死性凋亡的阻滞剂
坏死性凋亡的阻滞剂
产物与ATP竞争。
可逆：否
在阻断用TNF-处理的FADD缺陷型Jurkat细胞的坏死中EC50=494 nMα
细胞可渗透性：具有
Packaging
用惰性气体包装
Preparation Note
复溶后，等分并冷冻保存（-20°C）。贮备液在-20°C下可稳定保存至多3个月。
Other Notes
Degterev, A., et al. 2013.Nat. Chem. Biol.9, 192.
Degterev, A., et al. 2012.Cell Death Differ.20, 366.
Christofferson, D.E., et al. 2012.Cell Death Dis.3, e320.
Takahashi, N., et al. 2012.Cell Death Dis.3, e437.
Degterev, A., et al. 2008.Nat. Chem. Biol.4, 313.
Degterev, A., et al. 2005.Nat. Chem. Biol.1, 112.
Muller, A.J., et al. 2005.Nat. Med.11, 312.
Teng, X., et al. 2005.Bioorg.Med. Chem. Lett.15, 5039.
Degterev, A., et al. 2012.Cell Death Differ.20, 366.
Christofferson, D.E., et al. 2012.Cell Death Dis.3, e320.
Takahashi, N., et al. 2012.Cell Death Dis.3, e437.
Degterev, A., et al. 2008.Nat. Chem. Biol.4, 313.
Degterev, A., et al. 2005.Nat. Chem. Biol.1, 112.
Muller, A.J., et al. 2005.Nat. Med.11, 312.
Teng, X., et al. 2005.Bioorg.Med. Chem. Lett.15, 5039.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
毒性：标准处理（A）
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Roberto Fernández-Acosta et al.
Molecules (Basel, Switzerland), 27(13) (2022-07-10)
The use of nanomaterials rationally engineered to treat cancer is a burgeoning field that has reported great medical achievements. Iron-based polymeric nano-formulations with precisely tuned physicochemical properties are an expanding and versatile therapeutic strategy for tumor treatment. Recently, a peculiar
Bolin Hou et al.
Cell death discovery, 8(1), 319-319 (2022-07-14)
The underlying mechanism by which growth factor receptor-bound protein 2 (Grb2) regulates necroptosis remains unexplored. In the present study, we found that rasfonin, a fungal natural product and an activator of necroptosis, enhanced Grb2 binding to receptor-interacting serine/threonine kinase 1
Sasker Grootjans et al.
Nature protocols, 11(8), 1444-1454 (2016-07-16)
Several cell death assays have been developed based on a single biochemical parameter such as caspase activation or plasma membrane permeabilization. Our fluorescent apoptosis/necrosis (FAN) assay directly measures cell death and distinguishes between caspase-dependent apoptosis and caspase-independent necrosis of cells
Peng He et al.
Cell death discovery, 10(1), 255-255 (2024-05-25)
Caspase-8 (Casp8) serves as an initiator of apoptosis or a suppressor of necroptosis in context-dependent manner. Members of the p90 RSK family can phosphorylate caspase-8 at threonine-265 (T265), which can inactivate caspase-8 for bypassing caspase-8-mediated blockade of necroptosis and can
Chi G Weindel et al.
Cell, 185(17), 3214-3231 (2022-07-31)
Although mutations in mitochondrial-associated genes are linked to inflammation and susceptibility to infection, their mechanistic contributions to immune outcomes remain ill-defined. We discovered that the disease-associated gain-of-function allele Lrrk2G2019S (leucine-rich repeat kinase 2) perturbs mitochondrial homeostasis and reprograms cell death
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