D8942
Dichlorophenyl-ABA
≥98% (HPLC), solid
Sinónimos:
2-[(3,5-Dichlorophenyl)amino]benzoic acid
Iniciar sesión para ver los precios por organización y contrato.
Seleccione un Tamaño
Cambiar Vistas
Acerca de este artículo
Fórmula empírica (notación de Hill):
C13H9Cl2NO2
Número CAS:
Peso molecular:
282.12
UNSPSC Code:
12352200
PubChem Substance ID:
MDL number:
Servicio técnico
¿Necesita ayuda? Nuestro equipo de científicos experimentados está aquí para ayudarle.
Permítanos ayudarleassay
≥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
Clase de almacenamiento
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
dust mask type N95 (US), Eyeshields, Gloves
Elija entre una de las versiones más recientes:
¿Ya tiene este producto?
Encuentre la documentación para los productos que ha comprado recientemente en la Biblioteca de documentos.
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
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
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