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Discontinued Product
5398 has been discontinued.
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
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Alzheimer's Disease Poster
Alzheimer's disease (AD) is a debilitating and progressive neurodegenerative disease and the most common cause of dementia, affecting approximately 30% of individuals aged over 85 years. This poster summarizes the cellular and molecular mechanisms of AD.