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About This Item
Empirical Formula (Hill Notation):
C16H11BrN2O2
CAS Number:
Molecular Weight:
343.17
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77
SMILES string
BrC1=CC(C2=CC(C3=CC(OCO4)=C4C=C3)=NN2)=CC=C1
InChI
1S/C16H11BrN2O2/c17-12-3-1-2-10(6-12)13-8-14(19-18-13)11-4-5-15-16(7-11)21-9-20-15/h1-8H,9H2,(H,18,19)
InChI key
RCQIIBJSUWYYFU-UHFFFAOYSA-N
assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 20 mg/mL, clear
storage temp.
2-8°C
Quality Level
Related Categories
Biochem/physiol Actions
Anle138b is a fluorescent inhibitor of α-synuclein and prion-protein (PrPSc) aggregation that reduces the progression of prion and Parkinson′s disease in animal models. Anle138b extends the survival of mice infected with prions. Anle138b strongly inhibits BSE-derived and human prions. The fluorescence strongly increases upon binding with α-synuclein fibrils. Apparently, Anie138b binds to hydrophobic pockets in the fibrils.
Anle138b is a fluorescent inhibitor of α-synuclein and prion-protein (PrPSc) aggregation.
Anle138b, an oligomer modulator, inhibits neuronal degeneration. It rescues neurons from the aggregation effects of α-synuclein.
signalword
Warning
hcodes
Hazard Classifications
Eye Irrit. 2 - Skin Irrit. 2 - STOT SE 3
target_organs
Respiratory system
Storage Class
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Regulatory Information
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Jens Wagner et al.
Acta neuropathologica, 125(6), 795-813 (2013-04-23)
In neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD) and prion diseases, deposits of aggregated disease-specific proteins are found. Oligomeric aggregates are presumed to be the key neurotoxic agent. Here we describe the novel oligomer modulator anle138b [3-(1,3-benzodioxol-5-yl)-5-(3-bromophenyl)-1H-pyrazole]
Elisa Turriani et al.
Proceedings of the National Academy of Sciences of the United States of America, 114(25), E4971-E4977 (2017-06-07)
Recent epidemiological and clinical studies have reported a significantly increased risk for melanoma in people with Parkinson's disease. Because no evidence could be obtained that genetic factors are the reason for the association between these two diseases, we hypothesized that
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