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Merck
CN

D8942

Dichlorophenyl-ABA

≥98% (HPLC), solid

别名:

2-[(3,5-Dichlorophenyl)amino]benzoic acid

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关于此项目

经验公式(希尔记法):
C13H9Cl2NO2
化学文摘社编号:
分子量:
282.12
UNSPSC Code:
12352200
PubChem Substance ID:
MDL number:
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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.


pictograms

Exclamation mark

signalword

Warning

Hazard Classifications

Eye Irrit. 2 - Skin Irrit. 2 - STOT SE 3

target_organs

Respiratory system

存储类别

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

dust mask type N95 (US), Eyeshields, Gloves

法规信息

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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