D8942
Dichlorophenyl-ABA
≥98% (HPLC), solid
Synonym(s):
2-[(3,5-Dichlorophenyl)amino]benzoic acid
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About This Item
Empirical Formula (Hill Notation):
C13H9Cl2NO2
CAS Number:
Molecular Weight:
282.12
UNSPSC Code:
12352200
PubChem Substance ID:
MDL number:
assay
≥98% (HPLC)
form
solid
color
white
solubility
DMSO: ~18 mg/mL at ~60 °C
storage temp.
2-8°C
SMILES string
OC(=O)c1ccccc1Nc2cc(Cl)cc(Cl)c2
InChI
1S/C13H9Cl2NO2/c14-8-5-9(15)7-10(6-8)16-12-4-2-1-3-11(12)13(17)18/h1-7,16H,(H,17,18)
InChI key
FNGSQOJHNAYHAT-UHFFFAOYSA-N
Gene Information
human ... TTR(7276)
Biochem/physiol Actions
Inhibitor of transthyretin amyloid fibril formation in vitro.
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
ppe
dust mask type N95 (US), Eyeshields, Gloves
Regulatory Information
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Natàlia Reixach et al.
Proceedings of the National Academy of Sciences of the United States of America, 101(9), 2817-2822 (2004-02-26)
The transthyretin (TTR) amyloidoses are human diseases in which the misfolded TTR protein aggregates in tissues with subsequent visceral, peripheral, and autonomic nerve dysfunction. Recent reports have stressed the importance of oligomeric intermediates as major cytotoxic species in various forms
Christopher A Ross et al.
Nature medicine, 10 Suppl, S10-S17 (2004-07-24)
Neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), amyotrophic lateral sclerosis (ALS) and prion diseases are increasingly being realized to have common cellular and molecular mechanisms including protein aggregation and inclusion body formation. The aggregates
Per Hammarström et al.
Science (New York, N.Y.), 299(5607), 713-716 (2003-02-01)
Genetic evidence suggests that inhibition of amyloid fibril formation by small molecules should be effective against amyloid diseases. Known amyloid inhibitors appear to function by shifting the aggregation equilibrium away from the amyloid state. Here, we describe a series of