Pyridostigmine Bromide

Therapy for MG, which is caused by decreased postsynaptic ACh receptors.

Antagonism of nondepolarizing NMBDs.

Therapy for glaucoma.

Therapy for atony of GI and urinary tracts.

Muscarinic effects on GI, respiratory, and CV systems.

Prolonged response to succinylcholine if administered shortly afterward by inhibition of pseudocholinesterase and increased postsynaptic depolarization.

Paralysis may be prolonged by excessive doses, which can produce a depolarizing NMB

Oxydiaphoretic (acid-transferring) inhibitor of AChE.

Transfers a carbamate group to AChE and forms a covalent bond at the esteratic site.

Quaternary ammonium ion, which is poorly lipid soluble; does not effectively penetrate GI tract or blood-brain barrier (no CNS side effects).

Onset is within 10–15 min (vs. 5–10 min for neostigmine); duration is 4 h (similar to neostigmine).

20% as potent as neostigmine.

Renal excretion accounts for approximately 75% of elimination.

Very large volume of distribution with extensive tissue storage.

Oral bioavailability is 7.6 ± 2.4%.