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经验公式(希尔记法):
C12H11N3OS
化学文摘社编号:
分子量:
245.30
MDL number:
UNSPSC Code:
12352200
NACRES:
NA.77
InChI
1S/C12H11N3OS/c16-11-10(14-12(17)15-11)5-7-6-13-9-4-2-1-3-8(7)9/h1-4,6,10,13H,5H2,(H2,14,15,16,17)
InChI key
MPLRRPKKFHUEEL-UHFFFAOYSA-N
assay
≥95% (HPLC)
form
crystalline solid
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze, protect from light
color
light yellow
solubility
DMSO: 10 mg/mL, methanol: 5 mg/mL
shipped in
ambient
Quality Level
General description
A cell-permeable N-demethylated thiohydantoin analog of Nec-1 (Cat. No. 480065) that is devoid of anti-necroptotic properties and serves as a suitable inactive control.
Note: This inactive inhibitor of necrosis should not be used in high concentration.
Note: This inactive inhibitor of necrosis should not be used in high concentration.
Biochem/physiol Actions
Cell permeable: yes
Primary Target
Inactive control for Nec-1 (Cat. No. 480065)
Inactive control for Nec-1 (Cat. No. 480065)
Product does not compete with ATP.
Reversible: no
Packaging
Packaged under inert gas
Preparation Note
Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.
Other Notes
Takahashi et al. 2012. Cell Death and Disease3, e437.
Degterev, A., et al. 2005. Nat. Chem. Biol.1, 112.
Degterev, A., et al. 2005. Nat. Chem. Biol.1, 112.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
Toxicity: Standard Handling (A)
存储类别
11 - Combustible Solids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
N Takahashi et al.
Cell death & disease, 3, e437-e437 (2012-11-30)
Necrostatin-1 (Nec-1) is widely used in disease models to examine the contribution of receptor-interacting protein kinase (RIPK) 1 in cell death and inflammation. We studied three Nec-1 analogs: Nec-1, the active inhibitor of RIPK1, Nec-1 inactive (Nec-1i), its inactive variant
Alexei Degterev et al.
Nature chemical biology, 1(2), 112-119 (2006-01-13)
The mechanism of apoptosis has been extensively characterized over the past decade, but little is known about alternative forms of regulated cell death. Although stimulation of the Fas/TNFR receptor family triggers a canonical 'extrinsic' apoptosis pathway, we demonstrated that in
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