2894-61-3

Basic information

• Product Name: 7-bromo-5-phenyl-1,2-dihydro-2H-1,4-benzodiazepin-2-one
• Synonyms: 7-bromo-5-phenyl-1,2-dihydro-2H-1,4-benzodiazepin-2-one;5-Phenyl-7-bromo-1,3-dihydro-2H-1,4-benzodiazepine-2-one;7-Bromo-5-(phenyl)-1H-1,4-benzodiazepin-2(3H)-one;7-Bromo-5-phenyl-1H-1,4-benzodiazepine-2(3H)-one;7-bromo-5-phenyl-1,3-dihydro-1,4-benzodiazepin-2-one;7-bromo-5-phenyl-1H-benzo[e][1,4]diazepin-2(3H)-one;7-Bromo-5-phenyl-1,3-dihydro-benzo[e][1,4]diazepin-2-one;7-Bromo-5-phenyl-1,3-dihydro-2H-benzo[e][1,4]diazepin-2-one
• CAS NO: 2894-61-3
• Molecular Formula: C₁₅H₁₁BrN₂O
• Molecular Weight: 315.18
• Mol File: 2894-61-3.mol

Chemical Properties

• Melting Point: 220-221 °C(Solv: ethyl ether (60-29-7))
• Boiling Point: 464.8°Cat760mmHg
• Flash Point: 234.9°C
• Appearance: /
• Density: 1.51g/cm³
• Vapor Pressure: 8.13E-09mmHg at 25°C
• Refractive Index: 1.68
• PKA: 11.72±0.70(Predicted)
• CAS DataBase Reference: 7-bromo-5-phenyl-1,2-dihydro-2H-1,4-benzodiazepin-2-one(CAS DataBase Reference)
• NIST Chemistry Reference: 7-bromo-5-phenyl-1,2-dihydro-2H-1,4-benzodiazepin-2-one(2894-61-3)
• EPA Substance Registry System: 7-bromo-5-phenyl-1,2-dihydro-2H-1,4-benzodiazepin-2-one(2894-61-3)

Safety Data

• Hazardous Substances Data: 2894-61-3(Hazardous Substances Data)

Usage

Uses

7-Bromo-5-phenyl-2,3-dihydro-1H-1,4-benzodiazepin-2-one inhibits HIV-1 reverse transcription.

Application

Desalkylgidazepam is an analytical reference standard categorized as a benzodiazepine metabolite.Desalkylgidazepam is a metabolite of gidazepam. This product is intended for research and forensic applications.

InChI:InChI=1/C15H11BrN2O/c16-11-6-7-13-12(8-11)15(17-9-14(19)18-13)10-4-2-1-3-5-10/h1-8H,9H2,(H,18,19)

Upstream product

• 2898-08-0 2,3-dihydro-5-phenyl-1H-1,4-benzodiazepin-2-one 
• 17972-71-3 N-(2-benzoyl-4-bromophenyl)-2-bromoacetamide 
• 106-40-1 4-bromo-aniline 
• 98-88-4 benzoyl chloride 
• 5680-79-5 glycine ethyl ester hydrochloride 
• 39859-36-4 2-amino-5-bromobenzophenone 
• 56-40-6 glycine 
• 34099-70-2 7-bromo-1,3-dihydro-5-phenyl-2H-1,4-benzodiazepine-2-thione 
• 2835-77-0 (2-aminophenyl)(phenyl)methanone 
• 14439-71-5 2'-benzoyl-2-bromo-acetanilide 
• 79-04-9 chloroacetyl chloride 
• 70890-58-3 5-Bromo-2-(chloroacetamido)benzophenone 
• 100-97-0 hexamethylenetetramine 

Downstream Products

• 1072906-66-1 C₂₄H₁₇BrF₂N₂O₃ 
• 1072906-54-7 C₂₂H₁₄Br₂N₂O 
• 1072906-64-9 C₂₂H₁₄BrN₃O₃ 
• 62642-82-4 3-benzylidene-7-bromo-5-phenyl-1,2-dihydro-3H-1,4-benzodiazepin-2-one 
• 1072906-52-5 cis-7-bromo-3-(4'-methoxybenzylidene)-5-phenyl-1,2-dihydro-3H-1,4-benzodiazepin-2-one 
• 1072906-55-8 C₂₂H₁₄Br₂N₂O 
• 1072906-53-6 C₂₂H₁₄Br₂N₂O 
• 17972-72-4 7-bromo-5-phenyl-1,3,4,5-tetrahydro-2H-benzo[e][1,4]-diazepin-2-one 
• 313683-81-7 7-bromo-5-phenyl-4-propionyl-1,3,4,5-tetrahydro-2H-benzo[e][1,4]diazepin-2-one 

Relevant articles and documents

Facile and efficient one-pot protocol for synthesis of 5-phenyl-1,4- benzodiazepine-2-one derivatives

Several new derivatives of 5-pheny-1,4-benzodiazepine-2-ones were synthesized from 2-aminobenzophenone derivatives containing electron-withdrawing substituents in one pot with mild conditions using THF as a solvent with ammonium hydroxide solution and K2C

Structure-Activity Relationship Studies of Retro-1 Analogues against Shiga Toxin

High-throughput screening has shown that Retro-1 inhibits ricin and Shiga toxins by diminishing their intracellular trafficking via the retrograde route, from early endosomes to the Golgi apparatus. To improve the activity of Retro-1, a structure-activity relationship (SAR) study was undertaken and yielded an analogue with a roughly 70-fold better half-maximal effective concentration (EC50) against Shiga toxin cytotoxicity measured in a cell protein synthesis assay.

Retro-1-oligonucleotide conjugates. Synthesis and biological evaluation

Addition of small molecule Retro-1 has been described to enhance antisense and splice switching oligonucleotides. With the aim of assessing the effect of covalently linking Retro-1 to the biologically active oligonucleotide, three different derivatives of Retro-1 were prepared that incorporated a phosphoramidite group, a thiol or a 1,3-diene, respectively. Retro-1–oligonucleotide conjugates were assembled both on-resin (coupling of the phosphoramidite) and from reactions in solution (Michael-type thiol-maleimide reaction and Diels-Alder cycloaddition). Splice switching assays with the resulting conjugates showed that they were active but that they provided little advantage over the unconjugated oligonucleotide in the well-known HeLa Luc705 reporter system.

COMPOUNDS WHICH HAVE A PROTECTIVE ACTIVITY WITH RESPECT TO THE ACTION OF TOXINS AND OF VIRUSES WITH AN INTRACELLULAR MODE OF ACTION

The subject matter of the present invention is novel families of compounds which are aromatic amine, imine, aminoadamantane and benzodiazepine derivatives, medicaments comprising same and the use thereof as inhibitors of the toxic effects of toxins with intracellular activity, such as, for example, ricin, and of viruses that use the internalization pathway for infecting cells.

Synthesis, Chiral Separation, Absolute Configuration Assignment, and Biological Activity of Enantiomers of Retro-1 as Potent Inhibitors of Shiga Toxin

The Shiga toxin (Stx) family is composed of related protein toxins produced by the bacteria Shigella dysenteriae and certain pathogenic strains of E.coli. No effective therapies for Stx intoxication have been developed yet. However, inhibitors that act on the intracellular trafficking of these toxins may provide new options for the development of therapeutic strategies. This study reports the synthesis, chromatographic separation, and pharmacological evaluation of the two enantiomers of Retro-1, a compound active against Stx and other such protein toxins. Retro-1 works by inhibiting retrograde transport of these toxins inside cells. In vitro experiments proved that the configuration of the stereocenter at position 5 is not crucial for the activity of this compound. X-ray diffraction data revealed (S)-Retro-1 to be slightly more active than (R)-Retro-1.

INHIBITORS OF THE SHIGA TOXINS TRAFFICKING THROUGH THE RETROGRADE PATHWAY

The present invention relates to the use of compounds of general formula (I) and (II) for the preparation of a drug for preventing and/or treating disorders caused by Shiga toxins and related toxins.

Stereospecific anxiolytic and anticonvulsant agents with reduced muscle-relaxant, sedative-hypnotic and ataxic effects

The present invention provides compositions and methods of using stereospecific benzodiazepine derivatives, their salts and prodrugs for the treatment of anxiolytic or convulsant disorders having the side effects of reduced alcohol craving in human alcoholics and a concomitant reduced sedative, hypnotic, muscle relaxant and ataxic side-effects. The invention further provides pharmaceutical compositions for treatment of anxiolytic and convulsant disorders in subjects in need thereof, comprising a compound, prodrug or a salt having a chemical structure represented by any one of Formula I-XXI and a pharmaceutically-acceptable carrier.

GABAERGIC AGENTS TO TREAT MEMORY DEFICITS

The present invention provides molecules and methods for the prevention and/or treatment of memory deficit related conditions and/or enhancement of cognizance. In a preferred embodiment, the invention includes compounds, salts and prodrugs thereof for the prevention and/or treatment of these conditions.

Studies in the search for α5 subtype selective agonists for GABA(A)/BzR sites

In the search for α5 selective ligands, several series of diazepam analogs with individual and/or simultaneous modifications at positions-2, -5 and -7 were prepared and their in vitro affinities determined on recombinant receptors. These ligands were deliberately designed to test the effects of interaction at H1, H2, L2 and L3 of the pharmacophore/receptor model on ligand binding affinities and selectivities at different GABA(A)/BzR subtypes. In agreement with previous reports, none of these 1,4- benzodiazepines bound to the α4β3γ2 and α6β3γ2 receptor isoforms, two diazepam-insensitive(DI) GABA(A) receptor subtypes which appear to be devoid of lipophilic pocket L3. The presence of a 2'-fluorophenyl or 2'-nitrophenyl group at the C(5) position enhanced ligand affinity for the receptors but favored α1β3γ2 subtypes over α5β3γ2 subtypes. Replacement of the 2'- fluorophenyl or 2'-nitrophenyl group with a phenyl, 2'-thienyl or 2'-furyl moiety at the same position resulted in lower affinities of the ligands at all GABA(A) subtypes. Most importantly, when the carbonyl groups at position- 2 were replaced by methylene moieties (21 and 23), the affinities for all subtypes diminished. These results strongly suggest that the hydrogen bonding interaction of the ligand at H1 (as well as H2) with the receptor protein is important for high affinity at all DS sites. This implies that H1 is very similar in all receptor isoforms and may not be a descriptor which will readily lend itself to pharmacological receptor subtype selectivity.