Most of the literature describe that Obidoxime is better compared to that of Pralidoxme for treatment of organophophate poisoning, however, many countries use Pralidoxime.
Oximes (pralidoxime or obidoxime) are used in a complementary role to atropine to treat features associated with stimulation of the nicotinic receptors including muscle fasciculations, progressive muscle weakness (features of OP poisoning).
The differences in the oxime effectiveness are mainly due to the variation in aging rates.
Bisquaternary oximes, designated "H-oximes" i.e. HI-6 is most effective re-activator of AChE.
its the choice of the physician or clinical toxicologist that which antidote has to be used. broad availability and traditional uses of pralidoxime may be the factors that pralidoxime is more preferred.
The probable reason is that there are many research publications on Pralidoxime . The role of this drug has become controversial , with some studies suggesting that it has no role , while other studies have found it useful . There is also a controversy about the role of high dose Pralidoxime . I Agree that HI-6 is valuable in rapid acting OP Poisoning , such as nerve gas . Our experience has revealed that Pralidoxime is a valuable drug .
Oxime reactivators are specific antidotes for the treatment of organophosphorus pesticides (OP) poisoning. These agents reactivate OP-inhibited acetylcholinesterase (AChE), allowing normal metabolism of acetylcholine (ACh) by AChE. These antidotes were primarily developed in the second half of the 20th century to diminish the intoxications of highly toxic nerve agents.
Among five commercially available AChE reactivators (pralidoxime, methoxime, trimedoxime, obidoxime, asoxime), the pralidoxime was the first clinically available oxime reactivator for the treatment of OP intoxication. Since 1950's, this drug was introduced globally and it remains in the standard treatment of OP poisoning in many countries. Therefore, it is rational more studies have been performed concerning pralidoxime rather than other oximes. However, after many years of its utilization, the role of pralidoxime in the treatment of OP poisoning is still controversial.
In the other hand, obidoxime, a bispyridinium oxime, was developed with the aim to improve reactivation ability of pralidoxime. It is more potent than pralidoxime, so a lower dose of obidoxime has the same effect at reactivating AChE than a higher dose of pralidoxime. Furthermore, obidoxime antagonize nicotinic ACh receptors, so this may be an alternative potentially beneficial mechanism of action. These may contribute to the positive experiences with obidoxime-based observational studies, compared to the uncertainty in pralidoxime-based studies. However, obidoxime showed to be a relatively toxic compound in some animal studies. Its less clinical use may be related to its toxicity.
Thanks, In my view, the line "obidoxime showed to be a relatively toxic compound in some animal studies. Its less clinical use may be related to its toxicity" is more convincing. I will come back soon.
I found that hepatotoxicity of obidoxime, especially with high doses, is higher than that of pralidoxime (2-PAM) and HI-6; however, the latter is less available. Human data are only about 2-PAM and obidoxime in pesticide-poisoned patients.
Also, different countries have chosen different oximes as standard therapy, for example methanesulfonate salt of 2-PAM in the United Kingdom, TMB4 and obidoxime in European countries, Pralidoxime iodide in Japan, 2-PAM in the United States, and HI-6 in Canada.
Another important reason is obidoxime is itself acts as both acetylcholinesterase reactivator and also as acetylcholinesterase inhibitor (at high doses). Another important reason is pralidoxime potentiate the effects of atropine whilst absence with obidoxime.
I wrote this with my standard of knowledge. if any updates or corrections are most welcome.