101-26-8

Pyridostigmine is an inhibitor of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE; IC₅₀s = 0.35 and 1 μM, respectively, for the human enzymes). Pyridostigmine (10 μM) reduces decreases in AChE activity induced by the organophosphate pesticides diisopropyl fluorophosphate, chlorpyrifos-oxon, diazinon-oxon, paraoxon, and malaoxon in isolated bovine red blood cells. It also reduces soman-induced membrane depolarization and decreases in AChE activity in isolated human muscle bundles in a concentration-dependent manner. Pyridostigmine (3 mg/kg per day for four weeks) prevents tachycardia and increases in sympathetic tone in mice following myocardial infarction induced by left coronary artery ligation. Formulations containing pyridostigmine have been used in the treatment of myasthenia gravis and as neuromuscular protective agents against organophosphate poisoning.

White Solid

Cholinergic, used in the treatment of myasthenia gravis, and is a pre-exposure antidote to chemical warfare agents.

ChEBI: Pyridostigmine bromide is a pyridinium salt.

Mestinon (Valeant); Regonol (Sandoz).

Pyridostigmine bromide,3-hydroxy-1-methylpyridinium bromide dimethylcarbamateor pyridostigmine bromide (Mestinon), occurs as a white, hygroscopic,crystalline powder with an agreeable, characteristicodor. It is freely soluble in water, alcohol, and chloroform.
Pyridostigmine bromide is about one fifth as toxic asneostigmine. It appears to function in a manner similar tothat of neostigmine and is the most widely used anticholinesteraseagent for treating myasthenia gravis. Theliver enzymes and plasma cholinesterase metabolize thedrug. The principal metabolite is 3-hydroxy-N-methylpyridinium.Orally administered pyridostigmine has a half-lifeof 90 minutes and a duration of action of between 3 and6 hours.

Acetylcholinesterase inhibitor.

Myasthenia gravis

Potentially hazardous interactions with other drugs
Aminoglycosides, clindamycin and polymyxins antagonise effects of pyridostigmine.

Pyridostigmine undergoes hydrolysis by cholinesterases and is also metabolised in the liver. It appears that 75% of the plasma clearance of pyridostigmine depends on renal function. 3-Hydroxy-N-methylpyridinium has been identified as one of the 3 metabolites isolated from the urine. Pyridostigmine is excreted mainly in the urine as unchanged drug and metabolites.

[1] ALEXEY D. STRELNIK . Novel potent pyridoxine-based inhibitors of AChE and BChE, structural analogs of pyridostigmine, with improved in vivo safety profile[J]. Bioorganic & Medicinal Chemistry Letters, 2016, 26 16: Pages 4092-4094. DOI: 10.1016/j.bmcl.2016.06.070
[2] JOHN D. HENDERSON. Pyridostigmine bromide protection against acetylcholinesterase inhibition by pesticides[J]. Journal of Biochemical and Molecular Toxicology, 2011, 26 1: 31-34. DOI: 10.1002/jbt.20410
[3] RICARDO A MASELLI. Protection of human muscle acetylcholinesterase from soman by pyridostigmine bromide.[J]. Muscle & Nerve, 2011, 43 4: 591-595. DOI: 10.1002/mus.21922
[4] MARINA T DURAND. Pyridostigmine restores cardiac autonomic balance after small myocardial infarction in mice.[J]. PLoS ONE, 2014: e104476. DOI: 10.1371/journal.pone.0104476