size : | Price | Quantity | |
---|---|---|---|
10 mg | $55.00 | ||
50 mg | $165.00 |
Necrostatin-1 (4311-88-0) is an inhibitor of necroptosis (non-apoptotic cell death pathway; EC50 = 494 nM).1 It is an ATP-competitive death domain receptor-associated adaptor kinase (RIP1) inhibitor (EC50 = 182 nM).2 Necrostatin-1 displays a protective effect in a mouse model of ischemic brain injury1, inhibits myocardial cell death and reduces infarct size in various mouse heart models3 and inhibits glutamate-induced oxytosis in HT-22 cells4.
References/Citations:
1) Degterev, et al. (2005), Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury‘ Nature Chem. Biol., 1 112
2) Degterev et al. (2008) Identification of RIP1 kinase as a specific cellular target of necrostatins; Nature Chem. Biol., 4 313
3) Smith et.al. (2007), Necrostatin: a potentially novel cardioprotective agent?; Cardiovasc. Drugs Ther., 21 227
4) Xu et.al. (2007), Necrostatin-1 protects against glutamate-induced glutathione depletion and caspase-independent cell death in HT-22 cells; J. Neurochem., 103 2004
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Necrostatin-1 (4311-88-0) is an inhibitor of necroptosis (non-apoptotic cell death pathway; EC50 = 494 nM).1 It is an ATP-competitive death domain receptor-associated adaptor kinase (RIP1) inhibitor (EC50 = 182 nM).2 Necrostatin-1 displays a protective effect in a mouse model of ischemic brain injury1, inhibits myocardial cell death and reduces infarct size in various mouse heart models3 and inhibits glutamate-induced oxytosis in HT-22 cells4.
References/Citations:
1) Degterev, et al. (2005), Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury‘ Nature Chem. Biol., 1 112
2) Degterev et al. (2008) Identification of RIP1 kinase as a specific cellular target of necrostatins; Nature Chem. Biol., 4 313
3) Smith et.al. (2007), Necrostatin: a potentially novel cardioprotective agent?; Cardiovasc. Drugs Ther., 21 227
4) Xu et.al. (2007), Necrostatin-1 protects against glutamate-induced glutathione depletion and caspase-independent cell death in HT-22 cells; J. Neurochem., 103 2004
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