PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
20385200-2	2010	To alleviate peripheral respiratory failure oximes, e.g. obidoxime and pralidoxime, are used to reactivate inhibited acetylcholinesterase (AChE) with the intention to restore the disturbed neuromuscular function.	Obidoxime Chloride	57-66	acetylcholinesterase	Mus musculus	117-137	
20385200-2	2010	To alleviate peripheral respiratory failure oximes, e.g. obidoxime and pralidoxime, are used to reactivate inhibited acetylcholinesterase (AChE) with the intention to restore the disturbed neuromuscular function.	Obidoxime Chloride	57-66	acetylcholinesterase	Mus musculus	139-143	
16040183-9	2005	Only with obidoxime a significant increase in AChE activity was found.	Obidoxime Chloride	10-19	acetylcholinesterase	Mus musculus	46-50	
16876764-3	2006	Crystal structures of the oximes HI-6, Ortho-7 and obidoxime in complex with Mus musculus acetylcholinesterase (mAChE) reveal different roles of the peripheral anionic site (PAS) in the binding of the oximes.	Obidoxime Chloride	51-60	acetylcholinesterase	Mus musculus	90-110	
16876764-8	2006	The structural data clearly show analogous coordination of Ortho-7 and obidoxime within the active-site gorge of AChE.	Obidoxime Chloride	71-80	acetylcholinesterase	Mus musculus	113-117	
16876764-9	2006	Different ability to reactivate AChE inhibited by tabun is shown in end-point reactivation experiments where HI-6, Ortho-7 and obidoxime showed an efficiency of 1, 45 and 38%, respectively.	Obidoxime Chloride	127-136	acetylcholinesterase	Mus musculus	32-36	
16876764-10	2006	The low efficiency of HI-6 and the significantly higher efficiency of Ortho-7 and obidoxime may be explained by the differential binding of the oximes in the PAS and active-site gorge of AChE.	Obidoxime Chloride	82-91	acetylcholinesterase	Mus musculus	187-191	
15446360-4	2004	The therapeutic efficacy of antidotal treatment of tabun-induced acute poisoning depends on the time of its administration when obidoxime or the oxime HI-6 was used as an acetylcholinesterase reactivator.	Obidoxime Chloride	128-137	acetylcholinesterase	Mus musculus	171-191	
6327447-4	1984	AChE from electric eel as well as from mouse erythrocytes inhibited with C(+)P(-)-soman is much more effectively reactivated with the oximes HI-6, HGG-42, and obidoxime than these enzymes inhibited with C(-)P(-)-soman.	Obidoxime Chloride	159-168	acetylcholinesterase	Mus musculus	0-4	
15065394-8	2004	Obidoxime, which is the most widely used reactivator of acetylcholinesterase in the therapy of poisonings by nerve agents at present, is, like in the case of soman poisonings, a relatively least suitable oxime ensuring the survival in lethal tabun poisonings.	Obidoxime Chloride	0-9	acetylcholinesterase	Mus musculus	56-76	
33096123-3	2021	Herein, we developed transferrin receptor (TfR) aptamer-functionalized liposomes (Apt-LP) that could deliver AChE reactivator (obidoxime) across the BBB to act against paraoxon (POX) poisoning.	Obidoxime Chloride	127-136	acetylcholinesterase	Mus musculus	109-113	
6710485-5	1984	The enzyme inhibited with C(+)P(-)-soman is much more effectively reactivated with the oximes HI-6, HGG-42, and obidoxime than AChE inhibited with C(-)P(-)-soman.	Obidoxime Chloride	112-121	acetylcholinesterase	Mus musculus	127-131	
20406208-7	2010	The results show that obidoxime, trimedoxime, K074 and K075 present higher reactivating effects on malaoxon-inhibited AChE under in vitro conditions when compared with pralidoxime.	Obidoxime Chloride	22-31	acetylcholinesterase	Mus musculus	118-122	
20406208-8	2010	Taking into account the unsatisfactory effects of pralidoxime as antidotal treatment in malathion poisonings, the present results suggest that obidoxime, trimedoxime, K074 and K075 might be interesting therapeutic strategies to reactivate malaoxon-inhibited AChE in malathion poisonings.	Obidoxime Chloride	143-152	acetylcholinesterase	Mus musculus	258-262