Potent inhibitor of Aβ oligomer and fibril formation (IC50 = 50 nM for formation of fibrils from Aβ1-42). Reduces cytotoxicity of Aβ oligomers and increases cell viability in neuronal cells. Significantly extends lifespan of Drosophila expressing human Aβ1-42.
|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|
Preparing Stock Solutions
The following data is based on the product molecular weight 360.36. 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||2.78 mL||13.88 mL||27.75 mL|
|5 mM||0.56 mL||2.78 mL||5.55 mL|
|10 mM||0.28 mL||1.39 mL||2.78 mL|
|50 mM||0.06 mL||0.28 mL||0.56 mL|
References are publications that support the biological activity of the product.
Zhang et al (2013) Atomic and dynamic insights into the beneficial effect of the 1,4-naphthoquinon-2-yl-L-tryptophan inhibitor on Alzheimer's Aβ1-42 dimer in terms of aggregation and toxicity. ACS Chem.Neurosci. 5 148 PMID: 24246047
Scherzer-Attali et al (2010) Complete phenotypic recovery of an Alzheimer's disease model by a quinone-tryptophan hybrid aggregation inhibitor. PLoS ONE 5 e11101 PMID: 20559435
If you know of a relevant reference for NQTrp, please let us know.
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Keywords: NQTrp, NQTrp supplier, amyloid, Abeta, AB, Aβ, inhibits, inhibitors, fibrils, oligomers, Alzheimer's, disease, Amyloid, Beta, Peptides, 5398, Tocris Bioscience
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* or download your copy today!
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Alzheimer's disease (AD) is a degenerative brain disease and the most common cause of dementia, affecting approximately 47 million people worldwide. Updated in 2015, this poster summarizes the structural and functional changes observed in the progression of this neurodegenerative disease, as well as classic AD drug targets.