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Biological Activity for MSC 2032964A
MSC 2032964A is a potent and selective ASK1 inhibitor (IC50 = 93 nM). Selective for ASK1 over a panel of 210 kinases. Blocks LPS-induced ASK1 and p38 phosphorylation in cultured mouse astrocytes. Suppresses neuroinflammation in a mouse EAE model. Orally bioavailable and brain penetrant.
Compound Libraries for MSC 2032964A
Technical Data for MSC 2032964A
|Storage||Store at -20°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.
Solubility Data for MSC 2032964A
|Solvent||Max Conc. mg/mL||Max Conc. mM|
|ethanol||3.62||10 with gentle warming|
Preparing Stock Solutions for MSC 2032964A
The following data is based on the product molecular weight 362.31. 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||13.8 mL||69 mL||138 mL|
|1 mM||2.76 mL||13.8 mL||27.6 mL|
|2 mM||1.38 mL||6.9 mL||13.8 mL|
|10 mM||0.28 mL||1.38 mL||2.76 mL|
References for MSC 2032964A
References are publications that support the biological activity of the product.
Guo et al (2010) Regulation of the severity of neuroinflammation and demyelination by TLR-ASK1-p38 pathway. EMBO Mol.Med. 2 504 PMID: 21064192
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Keywords: MSC 2032964A, MSC 2032964A supplier, MSC2032964A, apoptosis, signal, regulating, kinase, 1, ASK1, inhibits, inhibitors, potent, selective, orally, bioavailable, neuroinflammation, EAE, experimental, autoimmune, encephalomyelitis, 5641, Tocris Bioscience
Citations for MSC 2032964A
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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.