1028299-41-3

Basic information

• Product Name: N-(5-bromo-2-nitro-4-(trifluoromethyl)phenyl)acetamide
• Synonyms: N-(5-bromo-2-nitro-4-(trifluoromethyl)phenyl)acetamide
• CAS NO: 1028299-41-3
• Molecular Weight: 327.057
• Mol File: 1028299-41-3.mol

Chemical Properties

• CAS DataBase Reference: N-(5-bromo-2-nitro-4-(trifluoromethyl)phenyl)acetamide(CAS DataBase Reference)
• NIST Chemistry Reference: N-(5-bromo-2-nitro-4-(trifluoromethyl)phenyl)acetamide(1028299-41-3)
• EPA Substance Registry System: N-(5-bromo-2-nitro-4-(trifluoromethyl)phenyl)acetamide(1028299-41-3)

Safety Data

• Hazardous Substances Data: 1028299-41-3(Hazardous Substances Data)

Upstream product

• 172215-91-7 3-bromo-4-(trifluoromethyl)aniline 
• 1025812-78-5 N-(3-bromo-4-(trifluoromethyl)phenyl)acetamide 

Downstream Products

• 1193384-47-2 5-(methylthio)-2-nitro-4-(trifluoromethyl)benzenamine 
• 157590-60-8 4-bromo-5-(trifluoromethyl)benzene-1,2-diamine 
• 1026267-58-2 5-Bromo-2-nitro-4-trifluoromethyl-phenylamine 

Relevant articles and documents

METHODS USING HDAC11 INHIBITORS

The present invention provides methods and uses of inhibitors of histone deacetylase 11 (HDAC11) in the treatment of diseases and/or disorders, such as, for example, cell proliferative diseases.

Synthesis and structure-activity relationships of substituted 1,4- dihydroquinoxaline-2,3-diones: Antagonists of N-methyl-D-aspartate (NMDA) receptor glycine sites and non-NMDA glutamate receptors

A series of mono-, di-, tri-, and tetrasubstituted 1,4- dihydroquinoxaline-2,3-diones (QXs) were synthesized and evaluated as antagonists at N-methyl-D-aspartate (NMDA)/glycine sites and α-amino-3- hydroxy-5-methylisoxazole-4-propionic acid-preferring non-NMDA receptors. Antagonist potencies were measured by electrical assays in Xenopus oocytes expressing rat whole brain poly(A)+ RNA. Trisubstituted QXs 17a (ACEA 1021), 17b (ACEA 1031), 24a, and 27, containing a nitro group in the 5 position and halogen in the 6 and 7 positions, displayed high potency (K(b) ~ 6-8 nM) at the glycine site, moderate potency at non-NMDA receptors (K(b) = 0.9-1.5 μM), and the highest (120-250-fold) selectivity in favor of glycine site antagonism over non-NMDA receptors. Tetrasubstituted QXs 17d,e were more than 100-fold weaker glycine site antagonists than the corresponding trisubstituted QXs with F being better tolerated than Cl as a substituent at the 8 position. Di- and monosubstituted QXs showed progressively weaker antagonism compared to trisubstituted analogues. For example, removal of the 5-nitro group of 17a results in a ~100-fold decrease in potency (10a,b,z), while removal of both halogens from 17a results in a ~3000-fold decrease in potency (10v). In terms of steady-state inhibition, most QX substitution patterns favor antagonism at NMDA/glycine sites over antagonism at non-NMDA receptors. Among the QXs tested, only 17i was slightly selective for non- NMDA receptors.