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Discontinued Product
NQTrp (Cat. No. 5398) has been withdrawn from sale for commercial reasons.
Description: Potent inhibitor of Aβ oligomer and fibril formation
Chemical Name: N-(1,4-Dihydro-1,4-dioxo-2-naphthalenyl)-L-tryptophan
Purity: ≥98% (HPLC)
Biological Activity for NQTrp
NQTrp is a 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.
Technical Data for NQTrp
| M. Wt | 360.36 |
| Formula | C21H16N2O4 |
| Storage | Store at -20°C |
| Purity | ≥98% (HPLC) |
| CAS Number | 185351-19-3 |
| PubChem ID | 56605052 |
| InChI Key | DZZUYZXINNHEGM-SFHVURJKSA-N |
| Smiles | O=C1C4=C(C=CC=C4)C(C(N[C@H]([C@@](O)=O)CC3=CNC2=CC=CC=C23)=C1)=O |
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.
Product Datasheets for NQTrp
References for NQTrp
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
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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
Citations for NQTrp
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Currently there are no citations for NQTrp.
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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* your copy today!
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Alzheimer's Poster
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.