| Stereochemistry | ACHIRAL |
| Molecular Formula | C7H9N2O.CH3O3S |
| Molecular Weight | 232.257 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 1 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
CS([O-])(=O)=O.C[N+]1=CC=CC=C1\C=N/O
InChI
InChIKey=WWZYJJGFUIAWNW-UHFFFAOYSA-N
InChI=1S/C7H8N2O.CH4O3S/c1-9-5-3-2-4-7(9)6-8-10;1-5(2,3)4/h2-6H,1H3;1H3,(H,2,3,4)
| Molecular Formula | C7H8N2O |
| Molecular Weight | 136.1512 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 1 |
| Optical Activity | NONE |
| Molecular Formula | CH4O3S |
| Molecular Weight | 96.106 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
Pralidoxime is a cholinesterase reactivator used as the antidote to organophosphate pesticides or acetylcholinesterase inhibitors (nerve agents) in conjunction with atropine and diazepam. Organophosphates bind to the esteratic site of acetylcholinesterase, which results initially in reversible inactivation of the enzyme. Acetylcholinesterase inhibition causes acetylcholine to accumulate in synapses, producing continuous stimulation of cholinergic fibers throughout the nervous systems. If given within 24 hours after organophosphate exposure, pralidoxime reactivates the acetylcholinesterase by cleaving the phosphate-ester bond formed between the organophosphate and acetylcholinesterase. Pralidoxime is indicated as an adjunct in the treatment of moderate and severe poisoning caused by organophosphate pesticides that have anticholinesterase activity or by chemicals with anticholinesterase activity such as some chemicals used as nerve agents during chemical warfare. Pralidoxime is also indicated as an adjunct in the management of the overdose of cholinesterase inhibitors, such as ambenonium, neostigmine, and pyridostigmine, used in the treatment of myasthenia gravis. Pralidoxime, used in conjunction with atropine, reverses nicotinic effects, such as muscle weakness and fasciculation, respiratory depression, and central nervous system (CNS) effects, associated with toxic exposure to organophosphate anticholinesterase pesticides and chemicals and with cholinesterase inhibitor overdose. Atropine, by antagonizing the action of cholinesterase inhibitors at muscarinic receptor sites, reverses muscarinic effects, such as tracheobronchial and salivary secretion, bronchoconstriction, bradycardia, and, to a moderate extent, CNS effects.
CNS Activity
Approval Year
Doses
AEs
Sourcing
PubMed
Patents
Sample Use Guides
1-2 g IV infusion (10-20 mg/mL) over 15-30 min, repeat in 1 hr if necessary and repeat q12hr thereafter PRN; if not practical or if pulmonary edema present or fluid restriction necessary administer as 50 mg/mL over 5 min; a second bolus of 1-2 g may be indicated after about 1 hr if muscle weakness has not been relieved; may repeat q10-12hr prn
Alternatively, administer 30 mg/kg IV (IM, SC if no IV access) over 20 min; follow by 4-8 mg/kg/hr maintenance IV infusion
Use with atropine, which affects muscarinic receptors; pralidoxime's actions most striking at nicotonic sites (increase muscle strength 10-40 min)
IM: 600 mg IM x3 doses; administer each dose 15 minutes apart for mild symptoms, or in rapid succession for severe symptoms; not to exceed 1800 mg total dose initially; if symptoms persist may repeat series of three injections 1 hr after last injection
Route of Administration:
Other
The stock solutions of the nerve agents, sarin and VX were prepared freshly in 2-propanol and stored under refrigeration. Appropriate quantity of the individual NA (sarin and VX) was added to the suspension of enzyme hAChE in phosphate buffer at 37 C and incubated for ten minutes to achieve 95–98% inhibition of the control activity. The oxime (Pralidoxime) solution of particular concentration (1.0–0.01 mkM) was added to the nerve agent inhibited hAChE and the reactivation profile was monitored over the time period of sixty minutes at different time intervals. Spontaneous reactivation of the inhibited hAChE was determined using the same protocol (reaction mixture containing enzyme and OP but no oxime), but the spontaneous reactivation was found to be insignificant. All the values were corrected for their oxime induced hydrolysis of ATChI.
