Necrostatin-1 - CAS 4311-88-0
Catalog number:
4311-88-0
Category:
Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
C13H13N3OS
Molecular Weight:
259.33
COA:
Inquire
Targets:
TNF-alpha
Description:
Necrostatin-1 is a specific RIP1 inhibitor and inhibits TNF-α-induced necroptosis with EC50 of 490 nM.
Publictions citing BOC Sciences Products
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Purity:
>98%
MSDS:
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1.Activation of innate antiviral immune response via double-stranded RNA-dependent RLR receptor-mediated necroptosis.
Wang W1, Wang WH1, Azadzoi KM2, Su N3,4, Dai P1, Sun J1, Wang Q1, Liang P1, Zhang W1, Lei X1, Yan Z1, Yang JH2,4. Sci Rep. 2016 Mar 3;6:22550. doi: 10.1038/srep22550.
Viruses induce double-stranded RNA (dsRNA) in the host cells. The mammalian system has developed dsRNA-dependent recognition receptors such as RLRs that recognize the long stretches of dsRNA as PAMPs to activate interferon-mediated antiviral pathways and apoptosis in severe infection. Here we report an efficient antiviral immune response through dsRNA-dependent RLR receptor-mediated necroptosis against infections from different classes of viruses. We demonstrated that virus-infected A549 cells were efficiently killed in the presence of a chimeric RLR receptor, dsCARE. It measurably suppressed the interferon antiviral pathway but promoted IL-1β production. Canonical cell death analysis by morphologic assessment, phosphatidylserine exposure, caspase cleavage and chemical inhibition excluded the involvement of apoptosis and consistently suggested RLR receptor-mediated necroptosis as the underlying mechanism of infected cell death. The necroptotic pathway was augmented by the formation of RIP1-RIP3 necrosome, recruitment of MLKL protein and the activation of cathepsin D.
2.Necroptosis in Niemann-Pick disease, type C1: a potential therapeutic target.
Cougnoux A1, Cluzeau C1, Mitra S2, Li R3, Williams I1, Burkert K1, Xu X3, Wassif CA1, Zheng W3, Porter FD1. Cell Death Dis. 2016 Mar 17;7:e2147. doi: 10.1038/cddis.2016.16.
Niemann-Pick disease, type C1 (NPC1) is a neurodegenerative, lysosomal storage disorder due to mutation of the NPC1 gene. The NPC1 phenotype is characterized by progressive neuronal dysfunction, including cerebellar ataxia and dementia. There is histological evidence of neuroinflammation and progressive neuronal loss, with cerebellar Purkinje cells particularly vulnerable to loss of NPC1 function. Necroptosis was evaluated as a mechanism of neuronal loss. Receptor-interacting protein kinase 1 (RIP1) and RIP3 are key components of the necrosomal complex that regulates necroptotic cell death. We report increased expression of RIP1 and RIP3 in NPC1 fibroblasts, NPC1 iPS cell-derived neuronal precursors, and in cerebellar tissue from both NPC1 mice and patients. Our data suggest a positive correlation between NPC1 neurological disease severity and assembly of the necrosome complex. Furthermore, we demonstrate that pharmacological inhibition of RIP1 decreases cell death both in vitro and in vivo.
3.Necrostatin-1 rescues mice from lethal irradiation.
Huang Z1, Epperly M2, Watkins SC3, Greenberger JS2, Kagan VE1, Bayır H4. Biochim Biophys Acta. 2016 Apr;1862(4):850-6. doi: 10.1016/j.bbadis.2016.01.014. Epub 2016 Jan 20.
There is an emerging need in new medical products that can mitigate and/or treat the short- and long-term consequences of radiation exposure after a radiological or nuclear terroristic event. The direct effects of ionizing radiation are realized primarily via apoptotic death pathways in rapidly proliferating cells within the initial 1-2days after the exposure. However later in the course of the radiation disease necrotic cell death may ensue via direct and indirect pathways from increased generation of pro-inflammatory cytokines. Here we evaluated radiomitigative potential of necrostatin-1 after total body irradiation (TBI) and the contribution of necroptosis to cell death induced by radiation. Circulating TNFα levels were increased starting on d1 after TBI and associated with increased plasmalemma permeability in ileum of irradiated mice. Necrostatin-1 given iv. 48h after 9.5Gy TBI attenuated radiation-induced receptor interacting protein kinase 3 (RIPK3) serine phosphorylation in ileum and improved survival vs.
4.Necrostatin-1 enhances the resolution of inflammation by specifically inducing neutrophil apoptosis.
Jie H1,2, He Y1,2, Huang X1,2, Zhou Q1,2, Han Y1,2,3, Li X1,2, Bai Y1,2, Sun E1,2. Oncotarget. 2016 Mar 24. doi: 10.18632/oncotarget.8346. [Epub ahead of print]
Neutrophils play a central role in innate immunity and are rapidly recruited to sites of infection and injury. Neutrophil apoptosis is essential for the successful resolution of inflammation. Necrostatin-1 (Nec-1,methyl-thiohydantoin-tryptophan (MTH-Trp)), is a potent and specific inhibitor of necroptosis[1] (a newly identified type of cell death representing a form of programmed necrosis or regulated non apoptotic cell death) by inhibiting the receptor interacting protein 1(RIP1) kinase. Here we report that Nec-1 specifically induces caspase-dependent neutrophils apoptosis and overrides powerful anti-apoptosis signaling from survival factors such as GM-CSF and LPS. We showed that Nec-1 markedly enhanced the resolution of established neutrophil-dependent inflammation in LPS-induced acute lung injury in mice. We also provided evidence that Nec-1 promoted apoptosis by reducing the expression of the anti-apoptotic protein Mcl-1 and increasing the expression of pro-apoptotic protein Bax.
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CAS 4311-88-0 Necrostatin-1

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