Acetylcholinesterase inhibitor

Acetylcholinesterase inhibitor

An acetylcholinesterase inhibitor (often abbreviated AChEI) or anti-cholinesterase is a chemical that inhibits the cholinesterase enzyme from breaking down acetylcholine, increasing both the level and duration of action of the neurotransmitter acetylcholine.



Acetylcholinesterase inhibitors:


Reversible inhibitor

Compounds which function as reversible competitive or noncompetitive inhibitors of cholinesterase are those most likely to have therapeutic uses. These include:

Comparison table

Comparison of reversible acetylcholinesterase inhibitors
Inhibitor Duration Main site of action Clinical use Adverse effects
Edrophonium short (10 min.)[3] neuromuscular junction[3] diagnosis of myasthenia gravis[3]
Neostigmine medium (1-2 hrs.)[3] neuromuscular junction[3] visceral[3]
Physostigmine medium (0.5-5 hrs.)[3] postganglionic parasympathetic[3] treat glaucoma (eye drops)[3]
Pyridostigmine medium (2-3 hrs.)[3] neuromuscular junction[3]
Dyflos long[3] postganglionic parasympathetic[3] historically to treat glaucoma (eye drops)[3] toxic[3]
Ecothiopate long[3] postganglionic parasympathetic[3] treat glaucoma (eye drops)[3] systemic effects[3]
Parathion (irreversible) long[3] none[3] toxic[3]

Quasi-irreversible inhibitor

Compounds which function as quasi-irreversible inhibitors of cholinesterase are those most likely to have use as chemical weapons or pesticides. These include:

Natural Compounds


Some major effects of cholinesterase inhibitors:

  • Actions on the autonomic nervous system, that is parasympathetic nervous system will cause bradycardia, hypotension, hypersecretion, bronchoconstriction, GI tract hypermotility, and decrease intraocular pressure.
  • SLUDGE syndrome.
  • Actions on the neuromuscular junction will result in prolonged muscle contraction.

Administration of reversible cholinoesterase inhibitors is contraindicated with those that have urinary retention due to obstruction.

Titration phase

When used in the central nervous system to alleviate neurological symptoms, such as rivastigmine in Alzheimer's disease, all cholinesterase inhibitors require doses to be increased gradually over several weeks, and this is usually referred to as the titration phase.[4]

See also


  1. ^ Eubanks LM, Rogers CJ, Beuscher AE, et al. (2006). "A molecular link between the active component of marijuana and Alzheimer's disease pathology". Mol. Pharm. 3 (6): 773–7. doi:10.1021/mp060066m. PMC 2562334. PMID 17140265. 
  2. ^ Rhee IK, I; Appels N, Hofte B, Karabatak B, Erkelens C, Stark LM, Flippin LA, Verpoorte R (November 2004). "Isolation of the Acetylcholinesterase Inhibitor Ungeremine from Nerine bowdenii by Preparative HPLC Coupled On-Line to a Flow Assay System". Biological & Pharmaceutical Bulletin 27 (11): 1804–1809. PMID 15516727. 
  3. ^ a b c d e f g h i j k l m n o p q r s t u v w x y Rang, H. P. (2003). Pharmacology. Edinburgh: Churchill Livingstone. ISBN 0-443-07145-4.  Page 156
  4. ^ Inglis, F (2002). "The tolerability and safety of cholinesterase inhibitors in the treatment of dementia.". International journal of clinical practice. Supplement (127): 45–63. PMID 12139367. 

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