367-65-7

Usage

Uses

It is applied as an active pharmaceutical intermediate.

InChI:InChI=1/C8H6F6N2/c9-7(10,11)3-1-4(8(12,13)14)6(16)5(15)2-3/h1-2H,15-16H2

Upstream product

• 320-21-8 2-nitro-4,6-bis-trifluoromethyl-aniline 
• 654-55-7 2-chloro-1-nitro-3,5-bis-trifluoromethyl-benzene 
• 7732-18-5 water 
• 16143-84-3 (3,5-bis(trifluoromethyl)methyl)acetanilide 
• 328-74-5 3,5-Bis-(trifluoromethyl)aniline 
• 367-71-5 2,4-bis(trifluoromethyl)aniline 

Downstream Products

• 1355991-91-1 (1R,2R)-N₁-(5,7-bis(trifluoromethyl)-1H-benzo[d]imidazol-2-yl)cyclohexane-1,2-diamine 
• 1355991-56-8 (1R,2R)-N₁,N₂-bis(5,7-bis(trifluoromethyl)-1H-benzo[d]imidazol-2-yl)cyclohexane-1,2-diamine 
• 1396396-53-4 tert-butyl (2-((2-amino-3,5-bis(trifluoromethyl)phenyl)amino)-2-oxoethyl)carbamate 
• 1396396-59-0 N-(2-amino-3,5-bis(trifluoromethyl)phenyl)-2-(methylthio)acetamide 
• 1396396-61-4 C₁₈H₂₁F₆N₃O₃ 
• 1396396-62-5 C₁₈H₂₁F₆N₃O₃ 
• 1396396-66-9 tert-butyl 3-(2-((2-amino-3,5-bis(trifluoromethyl)phenyl)amino)-2-oxoethyl)azetidine-1-carboxylate 
• 1396396-64-7 tert-butyl 4-(2-((2-amino-3,5-bis(trifluoromethyl)phenyl)amino)-2-oxoethyl)-3-oxopiperazine-1-carboxylate 
• 1396396-70-5 tert-butyl 4-(3-((2-amino-3,5-bis(trifluoromethyl)phenyl)amino)-3-oxopropyl)-3-oxopiperazine-1-carboxylate 
• 1396396-72-7 tert-butyl 4-(3-((2-amino-3,5-bis(trifluoromethyl)phenyl)amino)-3-oxopropanoyl)piperazine-1-carboxylate 

Relevant academic research and scientific papers

Chiral 2-aminobenzimidazole bifunctional organocatalysts: Effect of di-CF3 and TFA on catalytic mechanisms

(S,S)-trans-Cyclohexanediamine-5,7-di-CF3-benzimidazole (3b) was developed as a new chiral bifunctional organocatalyst and successfully applied to Michael addition of diethyl malonate to nitroolefins (up to 99%, 98% ee) under neutral condition.

Novel cinchona-aminobenzimidazole bifunctional organocatalysts

Efficient Cinchona-derived chiral 2-aminobenzimidazole catalysts were prepared by the coupling of 5,7-bis(trifluoromethyl)-2-chlorobenzimidazole with C(9S)-aminodihydroquinine or C(9R)-aminodihydroquinidine and successively applied to the Michael addition

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.