Selective inhibitor of apoptosis signal-regulating kinase 1 (ASK1, MAP3K5) (IC50 = 3 μM, Ki = 500 nM).
|Storage||Store at +4°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 319.31. Batch specific molecular weights may vary from batch to batch due to solvent of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||3.13 mL||15.66 mL||31.32 mL|
|5 mM||0.63 mL||3.13 mL||6.26 mL|
|10 mM||0.31 mL||1.57 mL||3.13 mL|
|50 mM||0.06 mL||0.31 mL||0.63 mL|
References are publications that support the products' biological activity.
Bu et al (2001) Synthesis and cytotoxic activity of 7-oxo-7H-dibenz[f,ij]isoquinoline and 7-oxo-7H-benzo[e]perimidine derivatives. J.Med.Chem. 44 2004 PMID: 11384245
Volynets et al (2011) Identification of 3H-naphtho[1,2,3-de]quinoline-2,7-diones as inhibitors of apoptosis signal-regulating kinase 1 (ASK1). J.Med.Chem. 54 2680 PMID: 21449566
If you know of a relevant reference for NQDI 1, please let us know.
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Keywords: NQDI 1, supplier, NQDI1, Apoptosis, signal-regulating, kinase, ASK1, inhibitors, inhibits, MAP3K5, ASK1, ASK1, Tocris Bioscience
1 Citation for NQDI 1
Citations are publications that use Tocris products. Selected citations for NQDI 1 include:
Song and Lee (2015) ASK1 modulates the expression of microRNA Let7A in microglia under high glucose in vitro condition. Psychopharmacology (Berl) 9 198 PMID: 26041997
Do you know of a great paper that uses NQDI 1 from Tocris? If so please let us know.
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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.