172215-95-1

Basic information

• Product Name: 2-ACETAMINO-5-CHLORO-3-NITRO BENZOTRIFLUORIDE
• Synonyms: 2-ACETAMINO-5-CHLORO-3-NITRO BENZOTRIFLUORIDE;N-(4-Chloro-2-nitro-6-(trifluoroMethyl)phenyl)acetaMide
• CAS NO: 172215-95-1
• Molecular Formula: C₉H₆ClF₃N₂O₃
• Molecular Weight: 282.6
• Mol File: 172215-95-1.mol

Chemical Properties

• Appearance: /
• CAS DataBase Reference: 2-ACETAMINO-5-CHLORO-3-NITRO BENZOTRIFLUORIDE(CAS DataBase Reference)
• NIST Chemistry Reference: 2-ACETAMINO-5-CHLORO-3-NITRO BENZOTRIFLUORIDE(172215-95-1)
• EPA Substance Registry System: 2-ACETAMINO-5-CHLORO-3-NITRO BENZOTRIFLUORIDE(172215-95-1)

Safety Data

• Hazardous Substances Data: 172215-95-1(Hazardous Substances Data)

Usage

Uses

Used in Pharmaceutical Industry:
2-Acetamino-5-chloro-3-nitro benzotrifluoride is used as an intermediate in the synthesis of various drugs for its wide range of pharmacological activities.
Used in Agrochemical Industry:
2-ACETAMINO-5-CHLORO-3-NITRO BENZOTRIFLUORIDE is also used as an intermediate in the production of agrochemicals, contributing to the development of effective agricultural products.
Used in Organic Chemistry:
2-Acetamino-5-chloro-3-nitro benzotrifluoride serves as a building block in the development of new chemicals, playing a crucial role in advancing the field of organic chemistry.

Upstream product

• 445-03-4 4-chloro-2-(trifluoromethyl)aniline 
• 344-53-6 N-<4-chloro-2-(trifluoromethyl)phenyl>acetamide 

Downstream Products

• 156425-10-4 5-chloro-3-trifluoromethyl-1,2-phenylenediamine 
• 62924-50-9 4-chloro-6-(trifluoromethyl)-2-nitroaniline 

Relevant articles and documents

Glycine receptor antagonists and the use thereof

Methods of treating or preventing neuronal loss associated with stroke, ischemia, CNS trauma, hypoglycemia and surgery, as well as treating neurodegenerative diseases including Alzheimer's disease, amyotrophic lateral sclerosis, Huntington's disease and Down's syndrome, treating or preventing the adverse consequences of the hyperactivity of the excitatory amino acids, as well as treating anxiety, chronic pain, convulsions, inducing anesthesia and treating psychosis are disclosed by administering to an animal in need of such treatment a compound having high affinity for the glycine binding site, lacking PCP side effects and which crosses the blood brain barrier of the animal. Also disclosed are novel 1,4-dihydroquinoxaline-2,3-diones, and pharmaceutical compositions thereof. Also disclosed are highly soluble ammonium salts of 1,4-dihydroquinoxaline-2,3-diones.

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.