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Necroptosis inhibitor. Blocks mixed lineage kinase domain-like protein (MLKL), a critical substrate of receptor-interacting serine-threonine kinase 3 (RIP3) during necrosis. Prevents MLKL-RIP1-RIP3 necrosome complex from interacting with downstream necrosis effectors. Binds and inhibits gasdermin D. Inhibits pyroptosis.
|Storage||Store at +4°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 461.47. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|0.2 mM||10.83 mL||54.17 mL||108.35 mL|
|1 mM||2.17 mL||10.83 mL||21.67 mL|
|2 mM||1.08 mL||5.42 mL||10.83 mL|
|10 mM||0.22 mL||1.08 mL||2.17 mL|
References are publications that support the biological activity of the product.
Zhou et al (2012) New components of the necroptotic pathway. Protein Cell 3 811 PMID: 23073834
Sun et al (2012) Mixed lineage kinase domain-like protein mediates necrosis signaling downstream of RIP3 kinase. Cell 148 213 PMID: 22265413
Kreuzaler et al (2012) Killing a cancer: what are the alternatives? Nat.Rev.Cancer. 12 411 PMID: 22576162
Pandeya et al (2019) Gasdermin D (GSDMD) as a new target for the treatment of infection. Medchemcomm 10 660 PMID: 31191857
If you know of a relevant reference for Necrosulfonamide, please let us know.
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Keywords: Necrosulfonamide, Necrosulfonamide supplier, non-apoptotic, cell, death, necroptosis, necrosis, necrosome, mixed, lineage, kinase, domain-like, protein, MLKL, receptor, interacting, serine, threonine, kinases, 3, RIP3, Gasdermin, D, GSDMD, pyroptosis, inhibitors, inhibits, Necroptosis, Inflammasomes, 5025, Tocris Bioscience
8 Citations for Necrosulfonamide
Citations are publications that use Tocris products. Selected citations for Necrosulfonamide include:
Heulot et al (2016) The TAT-RasGAP317-326 anti-cancer peptide can kill in a caspase-, apoptosis-, and necroptosis-independent manner. Oncotarget 7 64342 PMID: 27602963
Bittner et al (2016) Death receptor 3 mediates necroptotic cell death. Cellular and Molecular Life Sciences PMID: 27592300
Chefetz et al (2019) A Pan-ALDH1A Inhibitor Induces Necroptosis in Ovarian Cancer Stem-like Cells. Cell Rep 26 3061 PMID: 30865894
Bagnjuk et al (2019) Necroptosis in primate luteolysis: a role for ceramide. Cell Death Discov 5 67 PMID: 30774995
Gonzalez-Juarbe et al (2015) Pore-Forming Toxins Induce Macrophage Necroptosis during Acute Bacterial Pneumonia. Channels (Austin) 11 e1005337 PMID: 26659062
Greer et al (2018) ONC201 kills breast cancer cells in vitro by targeting mitochondria. Oncotarget 9 18454 PMID: 29719618
Gonzalez-Juarbe et al (2017) Pore-forming toxin-mediated ion dysregulation leads to death receptor-independent necroptosis of lung epithelial cells during bacterial pneumonia. Cell Death Differ 24 917 PMID: 28387756
Xie et al (2017) The Tumor Suppressor p53 Limits Ferroptosis by Blocking DPP4 Activity. Cell Rep 20 1692 PMID: 28813679
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Reviews for Necrosulfonamide
Average Rating: 5 (Based on 1 Review.)
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We used Necrosulfonamide as a positive control to inhibit the induction of pyroptosis by staphylococcal cytolysin. Differentiated THP-1 cells were pretreated with 25uM Necrosulfonamide (NSA) for 1 h before treating with or without 1 ug/ml Staphylococcal pore-forming toxin for 4 h. The LDH release in culture supernatants of treated cells was measured. Our data indicated that Necrosulfonamide treatment can significantly inhibit staphylococcal cytolysin induced pyroptosis.
Literature in this Area
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Programmed Cell Death Poster
There are two currently recognized forms of programmed cell death: apoptosis and necroptosis. This poster summarizes the signaling pathways involved in apoptosis, necroptosis and cell survival following death receptor activation, and highlights the influence of the molecular switch, cFLIP, on cell fate.