50408-94-1

Basic information

• Product Name: 3-Chloro-2,4-difluoro-6-nitroaniline
• Synonyms: 3-Chloro-2,4-difluoro-6-nitroaniline
• CAS NO: 50408-94-1
• Molecular Formula: C₆H₃ClF₂N₂O₂
• Molecular Weight: 208.5500264
• Mol File: 50408-94-1.mol
• Article Data: 3

Chemical Properties

• Melting Point: 96-97 °C
• Boiling Point: 317.1±37.0 °C(Predicted)
• Appearance: /
• Density: 1.682±0.06 g/cm3(Predicted)
• PKA: -2.85±0.25(Predicted)
• CAS DataBase Reference: 3-Chloro-2,4-difluoro-6-nitroaniline(CAS DataBase Reference)
• NIST Chemistry Reference: 3-Chloro-2,4-difluoro-6-nitroaniline(50408-94-1)
• EPA Substance Registry System: 3-Chloro-2,4-difluoro-6-nitroaniline(50408-94-1)

Safety Data

• Hazard Codes: Xi
• Hazardous Substances Data: 50408-94-1(Hazardous Substances Data)

Usage

General Description

3-Chloro-2,4-difluoro-6-nitroaniline is a chemical compound characterized by its specific structure, which includes chlorine, fluorine and nitro functional groups attached to an aniline segment. It is an aromatic amine derivative and falls under the category of organofluorines. Organofluorines are organic compounds that contain one or more carbon–fluorine bonds. Akin to all chemicals, it possesses particular physical and chemical properties, such as molecular weight, solubility, boiling and melting points etc., which determine its reactions and interactions with other substances. Potential applications of 3-Chloro-2,4-difluoro-6-nitroaniline could include pharmaceuticals, agrochemicals, and dyes, although specific uses would depend on further chemical transformations and research into its properties.

Upstream product

• 2613-34-5 2,4-difluoro-3-chloro-aniline 
• 170098-82-5 3-Chloro-2,4-difluoro-(trifluoroacetamido)benzene 
• 170098-83-6 3-chloro-2,4-difluoro-1-(trifluoroacetamido)-6-nitrobenzene 

Downstream Products

• 3828-41-9 2-chloro-1,3-difluoro-5-nitrobenzene 
• 170098-84-7 1,2-diamino-4-chloro-3,5-difluorobenzene 
• 774-19-6 3.5-Difluor-2.4-dichlor-1-nitro-benzol 

Relevant articles and documents

Alkyl, azido, alkoxy, and fluoro-substituted and fused quinoxalinediones

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, and inducing anesthesia are disclosed by administering to an animal in need of such treatment an alkyl or azido-substituted 1,4-dihydroquinoxaline-2,3-dione or pharmaceutically acceptable salts thereof, which have high binding to the glycine receptor.

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.