1293993-63-1

Upstream product

• 31767-14-3 ethyl 2-(hydroxyimino)acetate 
• 824-94-2 p-methoxybenzyl chloride 

Downstream Products

• 1293993-64-2 2-(4-methoxybenzyloxyimino)-N-propylacetamide 
• 1293993-66-4 2-(4-methoxybenzyloxyimino)-N-propylethanethioamide 
• 1293993-67-5 N-butyl-2-(4-methoxybenzyloxyimino)ethanethioamide 
• 1293993-65-3 N-butyl-2-(4-methoxybenzyloxyimino)acetamide 
• 1353880-22-4 N-isopentyl-2-(4-methoxybenzyloxyimino)acetamide 
• 1353880-29-1 2-(4-methoxybenzyloxyimino)-N-pentylethanethioamide 
• 1353880-30-4 N-isopentyl-2-(4-methoxybenzyloxyimino)ethanethioamide 
• 1353880-31-5 2-(4-methoxybenzyloxyimino)-N-(2-methoxyethyl)-ethanethioamide 
• 1353880-32-6 2-(4-methoxybenzyloxyimino)-N-(3-methoxypropyl)-ethanethioamide 
• 1353880-33-7 N-cyclopropyl-2-(4-methoxybenzyloxyimino)ethanethioamide 
• 1353880-34-8 N-cyclobutyl-2-(4-methoxybenzyloxyimino)ethanethioamide 
• 1353880-35-9 N-benzyl-2-(4-methoxybenzyloxyimino)ethanethioamide 
• 1353880-37-1 2-(4-methoxybenzyloxyimino)-N-phenylethanethioamide 

Relevant academic research and scientific papers

BLOOD BRAIN BARRIER-PENETRATING OXIMES FOR CHOLISTENERASES REACTIVATION

The invention describes pharmaceutical agents capable of crossing the blood brain barrier to protect against organophosphate pesticides and nerve agents or other electrophiles by reactivating inhibited cholinesterase (i.e., acetylcholinesterase and butyrylcholinesterase) and other proteins in the peripheral and central nervous system.

Amidine-Oximes: Reactivators for organophosphate exposure

Figure Presented. Figure presented. A new class of amidine-oxime reactivators of organophosphate (OP)-inhibited cholinesterases (ChE) were designed, synthesized, and tested. These compounds represent a novel group of oximes with enhanced capabilities of crossing the blood-brain barrier. Lack of brain penetration is a major limitation for currently used oximes as antidotes of OP poisoning. The concept described herein relies on a combination of an amidine residue and oxime functionality whereby the amidine increases the binding affinity to the ChE and the oxime is responsible for reactivation. Amidine-oximes were tested in vitro and reactivation rates for OP-BuChE were greater than pralidoxime (2-PAM) or monoisonitrosoacetone (MINA). Amidine-oxime reactivation rates for OP-AChE were lower compared to 2-PAM but greater compared with MINA. After pretreatment for 30 min with oximes 15c and 15d (145 μmol/kg, ip) mice were challenged with a soman model compound. In addition, 15d was tested in a post-treatment experiment (145 μmol/kg, ip, administration 5 min after sarin model compound exposure). In both cases, amidine-oximes afforded 100% 24 h survival in an animal model of OP exposure.