|Systematic (IUPAC) name|
|Bioavailability||Unclear, probably less than 5%|
|Metabolism||Slow hydrolysis by acetylcholinesterase and also by plasma esterases|
|Excretion||Unchanged drug (up to 70%) and alcoholic metabolite (30%) are excreted in the urine|
|ATC code||N07 S01 QA03|
|Mol. mass||223.294 g/mol|
| (what is this?)
Neostigmine was first synthesized by Aeschlimann and Reinert in 1931.
Neostigmine is made by first reacting 3-dimethylaminophenol with N-dimethylcarbamoyl chloride, which forms a dimethylcarbamate. Next, that product is alkylated using dimethylsulfate, which forms neostigmine.
By interfering with the breakdown of acetylcholine, neostigmine indirectly stimulates both nicotinic and muscarinic receptors. Unlike physostigmine, neostigmine has a quaternary nitrogen; hence, it is more polar and does not enter the CNS. Its effect on skeletal muscle is greater than that of physostigmine. Neostigmine has moderate duration of action, usually two to four hours. Neostigmine binds to the anionic and esteric site of cholinesterase. The drug blocks the active site of acetylcholinesterase so the enzyme can no longer break down the acetylcholine molecules before they reach the postsynaptic membrane receptors. This allows for the threshold to be reached so a new impulse can be triggered in the next neuron. In myasthenia gravis there are too few acetylcholine receptors so with the acetylcholinesterase blocked, acetylcholine can bind to the few receptors and trigger a muscular contraction.
Clinical uses 
It 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 at the end of an operation, usually in a dose of 25 to 50 mcg per kilogram.
Another indication for use is the Ogilvie syndrome which is a pseudoobstruction of the colon in critically ill patients.
Historically, it has been used as a test for early pregnancy. In a non-pregnant female whose menstrual period is delayed, administration of neostigmine can provoke menstrual bleeding. Modern tests which rely on detecting hCG in urine have rendered this application obsolete.
Though one of only two treatments available for myasthenia gravis, this drug is no longer available to anyone using the Medicare Part D program.
Side effects 
Neostigmine can induce generic ocular side effects including: headache, brow pain, blurred vision, phacodonesis, pericorneal injection, congestive iritis, various allergic reactions, and rarely, retinal detachment.
Gastrointestial symptoms occur earliest after ingestion and include anorexia, nausea, vomiting, abdominal cramps, and diarrhea.
Spectral data 
Neostigmine shows notable UV/VIS absorption at 261nm, 267nm, and 225nm.
Neostigmine's 1H NMR Spectroscopy reveals shifts at: 7.8, 7.7, 7.4, 7.4, 3.8, and 3.1 parts per million. The higher shifts are due to the aromatic hydrogens. The lower shifts at 3.8ppm and 3.1ppm are due to the electronic withdrawing nature of the tertiary and quarterary nitrogen, respectively.
Neostigmine, N,N,N-trimethyl-meta-(dimethylcarbomoyloxy)-phenylammonium methylsulfonate, which can be viewed as a simplified analog of physostigmine, is made by reacting 3-dimethylaminophenol with N-dimethylcarbamoyl chloride, which forms the dimethylcarbamate, and its subsequent alkylation using dimethylsulfate forming the desired compound.
- 43. J.A. Aeschlimann, U.S. Patent 1,905,990 (1933).
See also 
- David M. Whitacre (2007). Reviews of Environmental Contamination and Toxicology. Springer. p. 57. ISBN 978-0-387-73162-9.
- Gilman, A.G..; Goodman L.S.; Gilman A. Goodman and Guildman's The Pharmacological Basis of Therapeutics; 6th ed. Macmillan Publishing Co., Inc., 1980; pp 103
- Howland, R. D., Mycek, M. J., Harvey, R. A., Champe, P. C., & Mycek, M. J. Pharmacology 3rd edition, Lippincott's Illustrated Reviews, 2008, pg. 51.
- [Gilman, A. G., L. S. Goodman, and A. Gilman. (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 6th ed. New York: Macmillan Publishing Co., Inc. 1980.,p.114]
- [Gilman, A. G., L. S. Goodman, and A. Gilman. (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 6th ed. New York: Macmillan Publishing Co., Inc. 1980., p.109]
- Porst, Hella; Kny, L. Pharmazie, 1985 , vol. 40, # 5 p. 325 - 328
- Ferdous, Abu J.; Waigh, Roger D. Journal of Pharmacy and Pharmacology, 1993 , vol. 45, # 6 p. 559 - 562