50408-94-1

Usage

Uses

Used in Pharmaceutical Industry:
3-Chloro-2,4-difluoro-6-nitroaniline is used as an intermediate compound for the synthesis of various pharmaceutical products. Its unique structure allows for further chemical transformations that can lead to the development of new drugs with potential therapeutic applications.
Used in Agrochemical Industry:
In the agrochemical sector, 3-Chloro-2,4-difluoro-6-nitroaniline is utilized as a precursor in the production of agrochemicals. Its properties can be harnessed to create compounds that serve as pesticides, herbicides, or other agricultural chemicals, contributing to crop protection and yield enhancement.
Used in Dye Industry:
3-Chloro-2,4-difluoro-6-nitroaniline is employed as a key component in the formulation of dyes. Its chemical structure contributes to the color properties of the dyes, making it a valuable resource in the development of new dye products for various applications, such as textiles, plastics, and printing inks.

Upstream product

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

Downstream Products

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

Relevant academic research and scientific papers

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.

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.