40473-30-1

Upstream product

• 7693-46-1 4-Nitrophenyl chloroformate 

Downstream Products

• 951743-34-3 4-(4,5-bis(4-methoxyphenyl)oxazol-2-yl)-1-(N-hydroxycarbamoyl)piperidine 
• 1398411-02-3 methyl 2-N-methyl-(3-hydroxy)ureayl-2-deoxy-3,4,6-tri-O-benzyl-β-D-glucopyranoside 
• 54711-44-3 1-morpholin-3-hydroxy-urea 
• 100-02-7 4-nitro-phenol 
• 25653-44-5 hydroxyiminoketone 

Relevant academic research and scientific papers

Zinc(II)-mediated inhibition of a ribonuclease by an N-hydroxyurea nucleotide

The inhibition of ribonuclease Bi by 3′-N-hydroxyurea-3′-deoxythymidine 5′-phosphate is enhanced by 30-fold in the presence of Zn2+. Thus, an N-hydroxyurea nucleotide can recruit Zn2+ to inhibit the enzymatic activity of a ribonuclease. This result engenders a general strategy for the inhibition of non-metalloenzymes by metal complexes.

Access to functionalized imidazolidin-2-one derivatives by Iron-catalyzed oxyamination of alkenes

Functionalized imidazolidin-2-one were prepared by using an iron-catalyzed alkene oxyamination reaction. Hy-droxylamine derivatives were used in this atom-economical process, and the addition of an external oxidant was not required. The conditions developed were shown to be efficient for mono-, di-, and trisubstituted double bonds, and a large scope of diamino alcohol precursors were delivered in good yields with good diastereoselectivities. The mechanistic pathway was studied and appears to involve both a fused aziridine and a carbocationic species.

UREIDE DERIVATIVE AND USE THEREOF FOR MEDICAL PURPOSES

This invention relates to a pharmaceutical comprising, as an active ingredient, a ureide derivative represented by formula: or a pharmaceutically acceptable salt thereof. The ureide derivative or a pharmaceutically acceptable salt thereof according to the present invention is useful for relieving pain and treating or preventing neuropathic pain.

Kinetics and mechanism of base-catalysed degradations of substituted aryl-N-hydroxycarbamates, their N-methyl and N-phenyl analogues

The kinetics and mechanism of the degradation reactions of substituted phenyl N-hydroxycarbamates and their N-methyl and N-phenyl analogues have been studied at pseudo-first-order reaction conditions in aqueous buffers and sodium hydroxide solutions at 20°C and 60°C and at I = 1 mol·1 -1. The dependence of log kobs on pH for phenyl N-hydroxycarbamates at pH 13 is linear with the unit slope; at pH 10-12 log kobs is pH independent. The Bronsted coefficient βlg is about -1 (pH 7-13) and -1.53 (pH > 13) indicating that the degradation reaction of phenyl N-hydroxycarbamates follows an ElcB mechanism giving the corresponding phenol/phenolate and HO-N=C=O. The latter species undergoes further decomposition to give carbonate, nitrogen and ammonia as final products. In contrast to the phenyl N-hydroxycarbamates the N-methyl derivatives at pH 7-9 undergo degradation to the corresponding phenol/phenolate, carbonate and methylamine via a concerted mechanism (βlg is about - 0.75). The only exception is 4-nitrophenyl N-hydroxy-N-methylcarbamate in which the predominant break down pathway proceeds via the Smiles rearrangement to give sodium N-methyl-(4-nitrophenoxy)carbamate. At pH > 9 the reaction of N-hydroxy-N-methylcarbamates is kinetically complex: the dependence of absorbance on time is not exponential and it proceeds as a consecutive two-step reaction. N-Hydroxy-N-phenylcarbamate under the same conditions undergoes degradation to phenol, carbonate, aniline and azoxybenzene.