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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.
MSC 2032964A is also offered as part of the Tocriscreen 2.0 Max and Tocriscreen Antiviral Library. Find out more about compound libraries available from Tocris.
|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.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
|ethanol||3.62||10 with gentle warming|
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 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
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This product guide provides a review of the cell cycle and DNA damage research area and lists over 170 products, including research tools for:
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.