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{{User sandbox}}
<!-- EDIT BELOW THIS LINE -->
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| image = Physostigmine structure.png

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'''Physostigmine''' (also known as '''eserine''' from ''éséré'', the West African name for the [[Calabar bean]]) is a [[parasympathomimetic]] [[alkaloid]], specifically, a reversible [[cholinesterase inhibitor]]. It occurs naturally in the Calabar bean.

The chemical was synthesized for the first time in 1935 by [[Percy Lavon Julian]] and Josef Pikl.  It is available in the U.S. under the trade names Antilirium and  Isopto Eserine, and as eserine salicylate and eserine sulfate. Today, physostigmine is most commonly used for its medicinal value but before it's discovery by western medicine in 1846 it was much more prevalent as a poison. Physostigmine has an [[LD50]] of 3&nbsp;mg/kg in mice.

== Pharmacology ==
Physostigmine acts by interfering with the metabolism of [[acetylcholine]]. It is a covalent (reversible - bond hydrolyzed and released) inhibitor of [[acetylcholinesterase]], the enzyme responsible for the breakdown of acetylcholine in the synaptic cleft of the neuromuscular junction.<ref>{{cite book | last = Katzung | first = B. G. | coauthors = Masters, S.; Trever, A. | title = Basic and Clinical Pharmacology | publisher = [[McGraw Hill]] | year = 2009 | isbn = 978-0-07-160405-5 | page = 110 }}</ref> It indirectly [[agonist|stimulates]] both [[nicotinic acetylcholine receptor|nicotinic]] and [[muscarinic acetylcholine receptor|muscarinic]] acetylcholine receptors.a

== Synthesis ==
[[File:Julian synthesis.gif|left|thumb|Julian's synthesis of physostigmine]]
Physostigmine has two chiral carbon atoms. Therefore, attention needs to be paid to the synthesis of the correct [[diastereomers]]. The 71 syntheses of physostigmine yield 33 racemic mixtures and 38 products of a single enantiomer. The first total synthesis of physostigmine was achieved by Julian and Piki in 1935.<ref>{{ cite journal | author = Julian, P. L.; Pikl, J. | title = Studies in the Indole Series. III. On the Synthesis of Physostigmine | journal = Journal of the American Chemical Society | year = 1935 | volume = 57 | issue = 3 | pages = 539–544 | doi = 10.1021/ja01306a046 }}</ref> The main goal of Julian’s physostigmine synthesis was to get the intermediate key compound, l-eseroline (compound 10 in the diagram to the left). Then, this compound would be easily converted to physostigmine. In one of his earlier works<ref>{{ cite journal | author = Julian, P. L.; Pikl, J.; Boggess, D. | title = Studies in the Indole Series. II. Alkylation of 1-Methyl-3-Formyloxindole and a Synthesis of the Basic Ring Structure of Physostigmine | journal = Journal of the American Chemical Society | year = 1934 | volume = 56 | issue = 8 | pages = 1797–1801 | doi = 10.1021/ja01323a046 }}</ref> Julian synthesized the ring of physostigmine from starting material 1-methyl-3-formyl oxindole, which was discovered by Friedlander.  However, he faced the problems that the starting material was expensive, and the reduction of a nitrile to an amine (similar to the reaction of compound 6 to given compound 7 in the diagram) with sodium and alcohol did not result in good yield. In his second work “Studies in the Indole Series III,” he had improved the yield of amine from nitrile significantly by using palladium and hydrogen. Although he succeeded in the synthesis of the target chemical, the route had several drawbacks.  First, the chemical resolution of compound 8 is unreliable, and the chemical resolution of d,l-eserethole gives optically pure enantiomers after eight recrystallizations of its tartrate salt.  Second, the reaction of compound 8 to give compound 9 requires a large amount of Na. In the years since this initial work, many other groups have used a variety of approaches to overcome these problems.

== Biosynthesis ==
{{unreferenced section|date=April 2014}}
Physostigmine biosynthesis is proposed from [[tryptamine]] methylation and post-heterocyclization catalyzed by an unknown enzyme:

[[File:Physostigmine proposed biosynthesis.png|center|750px|Physostigmine proposed biosynthesis]]

== Clinical uses ==

Physostigmine is used to treat [[glaucoma]], [[Alzheimer's disease]], and [[delayed gastric emptying]]. It has been shown to improve short term memory.<ref>Krus  et al. 1968</ref> Recently, it has begun to be used in the treatment of [[orthostatic hypotension]].

Because it is a tertiary [[amine]], it can cross the [[blood–brain barrier]], and physostigmine salicylate is used to treat the [[central nervous system]] effects of [[atropine]], [[scopolamine]], and other anticholinergic drug overdoses.

Physostigmine is the [[antidote]] of choice for ''[[Datura stramonium]]'' poisoning.  It is also an antidote for ''[[Atropa belladonna]]'' poisoning, the same as for [[atropine]].<ref>{{cite book | last = Potter | first = S. O. L. | title = A Handbook of Materia Medica, Pharmacy and Therapeutics | publisher = P. Blakiston's | year = 1893 | location = London | page = 53 | url = https://books.google.com/books?id=q2ku1dbnaLYC&pg=PA53 }}</ref> It has been also used as an antidote for poisoning with [[gamma-Hydroxybutyrate|GHB]],<ref>{{Cite journal| pmid = 12475191| year = 2002| last1 = Traub   | first1 = S. J.| last2 = Nelson  | first2 = L. S.| last3 = Hoffman | first3 = R. S.| title = Physostigmine as a treatment for gamma-hydroxybutyrate toxicity: a review| volume = 40| issue = 6| pages = 781–787| journal = Journal of Toxicology. Clinical Toxicology| doi = 10.1081/CLT-120015839| s2cid = 11134665}}</ref> but is poorly effective and often causes additional toxicity, so is not a recommended treatment.<ref>{{Cite journal   | last1 = Zvosec    | first1 = D. L.| last2 = Smith     | first2 = S. W.| last3 = Litonjua  | first3 = R.| last4 = Westfal   | first4 = R. E.| title = Physostigmine for gamma-hydroxybutyrate coma: inefficacy, adverse events, and review| journal = Clinical Toxicology| volume = 45| issue = 3| pages = 261–265| year = 2007| pmid = 17453877 | doi = 10.1080/15563650601072159| s2cid = 39337739}}</ref>

== Bioactivity ==
{{unreferenced section|date=April 2014}}
Physostigmine functions as an acetylcholinesterase inhibitor. Its mechanism is to prevent the hydrolysis of acetylcholine by acetylcholinesterase at the transmitted sites of acetylcholine. This inhibition enhances the effect of acetylcholine, making it useful for the treatment of cholinergic disorders and myasthenia gravis. More recently, physostigmine has been used to improve the memory of Alzheimer’s patients due to its potent anticholinesterase activity.{{medcn|date=April 2014}} However, its drug form, physostigmine salicylate, has poor bioavailability.

Physostigmine also has a miotic function, causing pupillary constriction. It is useful in treating [[mydriasis]]. Physostigmine also increases outflow of the aqueous humor in the eye, making it useful in the treatment of glaucoma.

Recently, physostigmine has been proposed as antidote for intoxication with [[gamma hydroxybutyrate]] (GHB, a potent sedative-hypnotic agent that can cause loss of consciousness, loss of muscle control, and death). Physostigmine may treat GHB by producing a nonspecific state of arousal. However, not enough scientific evidence shows physostigmine properly treats GHB toxicity. Furthermore, lower doses of GHB produce a stronger action at the [[GHB receptor]] than the [[GABAB receptor|GABA<sub>B</sub>-receptor]], resulting in a stimulating effect which would act synergistically with physostigmine and producing hyperstimulation when the GHB blood levels begin to drop.

Physostigmine also has other proposed uses: it could reverse undesired side effects of [[benzodiazepines]] such as [[diazepam]], alleviating anxiety and tension. Another proposed use of physostigmine is to reverse the effects of [[barbiturates]] (any of a group of [[barbituric acid]]s derived for use as sedatives or [[hypnotics]]).

== History ==
=== The Calabar Bean ===
The [[Efik people]], of what is now modern day Nigeria, were the first to come in contact with physostigmine, the active ingredient in the [[Calabar bean]].<ref>{{cite book | last = Roberts | first = M. F. | coauthor = Wink, M. | title = Alkaloids: Biochemistry, Ecology, and Medicinal Applications | publisher = Plenum Press | year = 1998 | isbn = 978-1-4419-3263-1 | page = 38}}</ref> The Calabar bean, or chopping nut, was very prevalent in Efik culture as an [[ordeal poison]]. Individuals accused of witchcraft would drink the white, milky extract of the bean, made by crushing the bean in a mortar and soaking the remains in water. If the accused died, it was considered proof of their use of witchcraft. If they lived, usually due to vomiting up the poison, then they were declared innocent and sent free.<ref>{{cite journal | author = Scheindlin, S. | title = Episodes in the Story of Physostigmine | journal = Molecular Interventions | year = 2010 | volume = 10 | issue = 1 | pages = 4–5 | doi = 10.1124/mi.10.1.1| pmid = 20124558 }}</ref>

=== Western Medicine's Discovery ===
In 1846, European missionaries arrived in what was referred to as Old Calabar, now part of Nigeria. These missionaries wrote about the use of the calabar bean as a test for witchcraft. These beans eventually made there way back to Scotland, the home of these particular missionaries, where in 1855 [[Robert Christison]], a toxicologist, tested the toxicity of the poison on himself by eating one. He survived to document the experience. The bean was studied throughout the 1860’s by a few different Edinburgh scientists; including [[Douglas Argyll Robertson]] who wrote a paper on the use of calabar bean extract on the eye and was the first to use it medicinally, and [[Thomas Richard Fraser]] who researched how to best extract the active principle, which was later determined to be physostigmine. Fraser also studied the antagonism between physostigmine and atropine incredibly rigorously, at a time when the concept of antagonism had little if any experimental support. Fraser's research is still the basis of today's knowledge about the interactions between atropine and physostigmine at many different and specific doses.<ref>{{cite journal | author = Proudfoot, A. | title = The early toxicology of physostigmine: a tale of beans, great men and egos | journal = Toxicology Review | year = 2006 | volume = 25 | issue = 2 | pages = 99–138| doi = 10.2165/00139709-200625020-00004 | pmid = 16958557 | s2cid = 28243177 }}</ref> Physostigmine's first use as a treatment for [[glaucoma]] was by [[Ludwig Laqueur]] in 1876. Laqueur himself suffered from glaucoma so, like Christison, he experimented on himself, although Laqueur was much more scientific and methodical in his self-treatment.

In the 1920's, [[Otto Loewi]] determined the biomechanical mechanism for the effects of physostigmine on the body. Loewi was studying how actions that we now consider to be controlled by the parasympathetic nervous system, were directed by chemicals. During his studies, Loewi discovered acetylcholine and that physostigmine acted by preventing acetylcholine inhibition. In 1936, Loewi was awarded the Nobel Prize for his work on discovering acetylcholine and biological chemical transmitters. More important discoveries surrounding physostigmine were made at Edinburgh University in 1925. Edgar Stedman and George Barger determined the structure of physostigmine using a method called chemical degradation. Percy Levon Julian was later the first to synthesize physostigmine in 1935. English scientist Sir Robert Robinson was also working on the synthesis of physostigmine, but surprisingly Julian, a relatively unknown scientist at the time, was the successful one.<ref>{{cite journal | author = Scheindlin, S. | title = Episodes in the Story of Physostigmine | journal = Molecular Interventions | year = 2010 | volume = 10 | issue = 1 | pages = 5–10 | doi = 10.1124/mi.10.1.1| pmid = 20124558 }}</ref>

== Side effects ==

An overdose can cause [[SLUD|cholinergic syndrome]].  Other side effects may include [[nausea]], [[vomiting]], [[diarrhea]], [[Anorexia (symptom)|anorexia]], dizziness, headache, stomach pain, sweating, [[dyspepsia]], and seizures.<ref>[http://www.alzforum.org/dis/tre/drc/detail.asp?id=76 Alzheimer Research Forum]</ref>  The carbamate [[functional group]] readily hydrolyses in water, and in bodily conditions. The metabolite thus formed from physostigmine and some other alkaloids (e.g. cymserine) is [[eseroline]], which research has suggested may be neurotoxic to humans.<ref>Somani, SM; Kutty, RK; Krishna, G (1990). "Eseroline, a metabolite of physostigmine, induces neuronal cell death". Toxicology and applied pharmacology 106 (1): 28–37. doi:10.1016/0041-008X(90)90102-Z. {{PMID|2251681}}.</ref> Death can result from failure of the respiratory system and paralysis of the heart.

== See also ==
* [[Calabar Bean]]
* [[Cymserine]]
* [[Efik people]]
* [[Thomas Richard Fraser]]

== References ==
{{Reflist|30em}}

{{Opthalmologicals}}
{{Antidotes}}
{{Cholinergics}}

[[:Category:Acetylcholinesterase inhibitors]]
[[:Category:Antidotes]]
[[:Category:Alkaloids]]
[[:Category:Carbamates]]
[[:Category:Pyrroloindoles]]
[[:Category:Alkaloids found in Fabaceae]]

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