2191-60-8

Upstream product

• 2658-24-4 2,2-dimethylaziridine 
• 108-98-5 thiophenol 
• 26654-39-7 4,4-dimethyl-1,3-oxazolidin-2-one 
• 927-82-2 2-amino-2-methylpropyl hydrogensulfate 
• 546-68-9 titanium(IV) isopropylate 
• 775-12-2 diphenylsilane 
• 115011-46-6 2-acetamido-2-methyl-1-(phenylthio)-propane 

Downstream Products

• 141363-00-0 N-(1,1-Dimethyl-2-phenylthioethyl)trimethylacetamide 
• 141362-87-0 1,1-Dimethyl-2-phenylsulfanyl-ethylamine; compound with benzoic acid 
• 1155-29-9 N-(1,1-Dimethyl-2-phenylthioethyl)benzamide 
• 406234-40-0 4-(2-methyl-1-(phenylthio)propan-2-ylamino)-3-nitrobenzenesulfonamide 
• 141362-99-4 N-(1,1-Dimethyl-2-phenylthioethyl)-4-bromobenzamide 
• 141363-17-9 N-(1,1-Dimethyl-2-phenylthioethyl)toluene-4-sulfonamide 

Relevant academic research and scientific papers

N-sulfonylcarboximidamide apoptosis promoters

Compounds having the formula are apoptosis promoters. Also disclosed are methods of making the compounds, compositions containing the compounds, and methods of treatment using the compounds.

Process for production of thioalkylamine derivatives

The present invention relates to a thioalkylamine derivative represented by general formula (I); and a process for production thereof: wherein each of R1and R2is H, (C1-C4)alkyl, (C3-C8)cyc

N-acylsulfonamide apoptosis promoters

N-Benzoyl arylsulfonamides having the formula are BCL-Xl inhibitors and are useful for promoting apoptosis. Also disclosed are BCL-Xl inhibiting compositions and methods of promoting apoptosis in a mammal.

N-Acylsulfonamide apoptosis promoters

N-Benzoyl arylsulfonamides having the formula Are BCL-X1 inhibitors and are useful for promoting apoptosis. Also disclosed are BCL-X1 inhibiting compositions and methods of promoting apoptosis in a mammal.

Oxamide IMPDH inhibitors

Disclosed are compounds of the general formula which are oxamide derivatives and inhibitors of the enzyme inosine monophosphate dehydrogenase (IMPDH).

The Use of 2-Oxazolidinones as Latent Aziridine Equivalents. 2. Aminoethylation of Aromatic Amines, Phenols, and Thiophenols

The utility of 2-oxazolidinones 1 as latent, carboxylated aziridine functionalities was examined.Reaction of 2-oxazolidinone (1a), 3-methyl2-oxazolidinone (1b), 3-(phenylmethyl)-2-oxazolidinone (1c), 3-phenyl-2-oxazolidinone (1d) 4,4-dimethyl-2-oxazolidinone (1e), and 5-ethyl-2-oxazolidinone (1f) with aromatic amine salts, phenol, or thiophenols at elevated temperatures (> 130 deg C) afforded aminoethylated adducts.The aminoethylation occurred with concomitant loss of carbon dioxide to furnish variously substituted N-aryl-1,2-ethanediamines 4, 1-(2-phenoxyethyl)-2-imidazolidinone (8), or 2-(arylthio)ethanamines 9 on reactions of 1 with aromatic amine salts, phenol, and thiophenols, respectively.Imidazolidinone 8 is believed to be a secondary reaction product resulting from the condensation of the initially formed 2-phenoxyethanamine with starting oxazolidinone 1a.The aminoethylation reaction did not proceed with aliphatic amine hydrochlorides or alkyl mercaptans.Preliminary mechanistic pathways for these ring openings were also investigated employing a specific, C-5 deuterium-labeled oxazolidinone 1b-d2.Ring-opening experiments of 1b-d2 with N-methylaniline hydrochloride suggest reaction can occur through either a dioxazolinium 5 and/or 5 intermediate.In contrast, reaction of 1b-d2 with thiophenol suggests ring-opening to proceed only via the dioxazolinium pathway.

Acylated 2,2-dimethylaziridines: Regioselectivity of ring opening by sodium thiophenolate; borderline S(N)2 due to planarization of nitrogen pyramid

2,2-Dimethylaziridines 1 carrying a COR group on nitrogen are opened by PhS(Θ) with a regioselectivity RS = abnormal:normal ≥ 20 in MeOH and 5-16 in THF. Practically no influence of COR on RS was found except for the poorest oxidant 1g (R = tBu) that gave the highest RS (95, MeOH). This rules out an SET mechanism for the abnormal opening. Absence of homolytic ring opening is directly shown by the failure to detect products resulting from cyclization of a homolytically formed radical when COR is cinnamoyl (1f). Direct nucleophilic attack is indicated by suppression of any reaction with PhS(Θ) when the steric hindrance is increased (N-benzoylaziridine 13). The observed S(N)2 borderline behaviour with 1 is explained by reaction in a flattened nitrogen conformation of the otherwise poorly reactive 1. Carboxamide resonance in this (nearly) planar conformation generates a substantial positive charge on N which will shift the mechanism closer to S(N)1 by partial heterolysis of the N-CMe2 bond prior to attack by PhS(Θ).