Trade name Prostigmin
Bioavailability probably less than 5%.
Metabolism occurs by slow hydrolysis by acetylcholinesterase and also by plasma esterases.
Has a half-life of 50–90 minutes.
Up to 70% excreted unchanged and an alcoholic metabolite of 30% is excreted in the urine.
A parasympathomimetic that acts as a reversible acetylcholinesterase inhibitor.
By interfering with the breakdown of acetylcholine, neostigmine indirectly stimulates both nicotinic and muscarinic receptors.
Neostigmine does not enter the CNS, unlike physostigmine, and it has a greater effect on skeletal muscle than that of physostigmine.
Duration of action is usually two to four hours.
The drug binds to the anionic and esteric site of cholinesterase.
The drug blocks the active site of acetylcholinesterase, so it can no longer break down the acetylcholine molecules before they reach the postsynaptic membrane receptors.
Neostigmine is used in myasthenia gravis where there are too few acetylcholine receptors so with the acetylcholinesterase blockage acetylcholine can bind to the few receptors and trigger a muscular contraction.
Neostigmine is used to improve muscle tone in people with myasthenia gravis and routinely in anesthesia to reverse the effects of non-depolarizing muscle relaxants such as rocuronium and vecuronium.
Dose is usually 25 to 50 μg per kilogram.
Utilized for urinary retention resulting from general anesthesia and to treat curariform drug toxicity.
Indicated for use is the Ogilvie syndrome.
Intravenous neostigmine may delay the effects of envenomation through snakebite.
Associated with brow pain, blurred vision, phacodonesis, pericorneal injection, congestive iritis, various allergic reactions, retinal detachment, and headache.
Because it causes bradycardia, it is given along with a parasympatholytic drug such as atropine or glycopyrrolate.
Gastrointestial symptoms include anorexia, nausea, vomiting, abdominal cramps, and diarrhea.