Kinetic analysis of the protection afforded by reversible inhibitors against irreversible inhibition of acetylcholinesterase by highly toxic organophosphorus compounds

Design and synthesis of N-substituted-2-hydroxyiminoacetamides and interactions with cholinesterases

“…3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 11 It can be concluded from molecular docking studies that the predicted binding modes of 2-4 in Knowledge of the degree of AChE/BChE selectivity of oxime compounds is may be important for more successful treatment in cases of OP nerve agent poisoning. The most notable pretreatment strategies include protection of the AChE catalytic serine from phosphylating agent by ligands that bind reversibly to AChE [61][62][63][64][65] and the use of bioscavengers, i.e. BChE, prone to inhibition by a phosphylating agent [66,67].…”

In vivo experimental approach to treatment against tabun poisoning

“…Pyridostigmine, an AChE carbamylating compound that has been used as prophylaxis, calls for a replacement that will provide better protection 21,27 . In addition to carbamylation, the AChE catalytic site can also be protected by ligands that reversibly bind to AChE, such as huperzine A, SAD, and decamethonium, due to direct competition between the ligand and the phosphorylating agent [28][29][30][31] . A new approach to reduce the in vivo toxicity of chemical warfare nerve agents is the use of bioscavengers-enzymes that react with a nerve agent before it inhibits AChE at physiologically important target sites (i.e.…”

Competitive binding between 4,4′-diphenylmethane-bis(methyl) carbamate and RAGE ligand MG-H1 on human umbilical vein endothelial cell by cell membrane chromatography

“…was selected as a ligand for competition binding based on the following reasons: on one hand, HMGB-1 and S100B were chosen as ligand for competition binding owing to its endogenous characteristic. HMGB-1 was released passively from monocytes and endothelial cells whereas S100B was secreted from astrocytes in response to endotoxin [21,22]. In our previous experiment, HUVEC damage was induced by exogenous AGEs.…”