Benzatropine was approved for medical use in the United States in 1954.[4] It is available as ageneric medication.[4] In 2020, it was the 229th most commonly prescribed medication in the United States, with more than 2million prescriptions.[8][9] It is sold under the brand nameCogentin among others.[4]
Benzatropine is used to reduceextrapyramidal side effects ofantipsychotic treatment. Benzatropine is also a second-line drug for the treatment ofParkinson's disease. It improvestremor, and may alleviaterigidity andbradykinesia.[10] Benzatropine is also sometimes used for the treatment ofdystonia, a rare disorder that causes abnormal muscle contraction, resulting in twisting postures of limbs, trunk, or face.
While some studies suggest that use ofanticholinergics increases the risk oftardive dyskinesia (a long-term side effect ofantipsychotics),[11][12] other studies have found no association between anticholinergic exposure and risk of developing tardive dyskinesia,[13] although symptoms may be worsened.[14]
Drugs that decrease cholinergic transmission may impair storage of new information into long-term memory. Anticholinergic agents can also impair time perception.[15]
Benzatropine is acentrally actinganticholinergic andantihistamine. In terms of its anticholinergic activity, it is specifically anantimuscarinic and acts aselectivemuscarinic acetylcholineM1 andM3 receptorantagonist.[16] Benzatropine partially blocks cholinergic activity in thebasal ganglia. Animal studies have indicated that anticholinergic activity of benzatropine is approximately one-half that of atropine, while its antihistamine activity approaches that ofmepyramine. Its anticholinergic effects have been established as therapeutically significant in the management of Parkinsonism. Benzatropine antagonizes the effect ofacetylcholine, decreasing the imbalance between the neurotransmitters acetylcholine anddopamine, which may improve the symptoms of early Parkinson's disease.[17]
Benzatropine has been also identified, by a high throughput screening approach, as a potent differentiating agent foroligodendrocytes, possibly working throughM1 andM3muscarinic receptors. In preclinical models for multiple sclerosis, benzatropine decreased clinical symptoms and enhanced re-myelination.[18]
In addition to its anticholinergic activity, benztropine has been found to increase the availability of dopamine by blocking itsreuptake and storage in central sites, and as a result, increasingdopaminergic activity. Benzatropine andanalogues are atypicaldopamine reuptake inhibitors,[19] which might make them useful for people withakathisia secondary to antipsychotic therapy.[20]
Since 1959, benzatropine is the officialinternational nonproprietary name of the medication under the INN scheme, the medication naming system coordinated by theWorld Health Organization; it is also theBritish Approved Name (BAN) given in theBritish Pharmacopoeia,[2][3] and has been the official nonproprietary name in Australia since 2015.[23] Regional variations of the "a" spelling are also used in French, Italian, Portuguese, and Spanish, as well asLatin (all medications are assigned a Latin name by WHO).[3]
"Benztropine" is the officialUnited States Adopted Name (USAN), the medication naming system coordinated by the USAN Council, co-sponsored by the American Medical Association (AMA), the United States Pharmacopeial Convention (USP), and the American Pharmacists Association (APhA). It is also theJapanese Accepted Name (JAN)[24] and was used in Australia until 2015, when it was harmonized with the INN.[23]
Both names may be modified to account for themethanesulfonate salt as which the medication is formulated: the modified INN (INNm) and BAN (BANM) isbenzatropine mesilate, while the modified USAN isbenztropine mesylate.[25] The modified JAN is a hybrid form,benztropine mesilate.[24]
The misspelling benzotropine is also occasionally seen in the literature.
^DiMascio A, Bernardo DL, Greenblatt DJ, Marder JE (May 1976). "A controlled trial of amantadine in drug-induced extrapyramidal disorders".Archives of General Psychiatry.33 (5):599–602.doi:10.1001/archpsyc.1976.01770050055008.PMID5066.
^Wszola BA, Newell KM, Sprague RL (August 2001). "Risk factors for tardive dyskinesia in a large population of youths and adults".Experimental and Clinical Psychopharmacology.9 (3):285–296.doi:10.1037/1064-1297.9.3.285.PMID11534539.
^van Harten PN, Hoek HW, Matroos GE, Koeter M, Kahn RS (April 1998). "Intermittent neuroleptic treatment and risk for tardive dyskinesia: Curaçao Extrapyramidal Syndromes Study III".The American Journal of Psychiatry.155 (4):565–567.doi:10.1176/ajp.155.4.565.PMID9546009.
^Yassa R (September 1988). "Tardive dyskinesia and anticholinergic drugs. A critical review of the literature".L'Encéphale. 14 Spec No (Spec No):233–239.PMID3063514.
^Gelenberg AJ, Van Putten T, Lavori PW, Wojcik JD, Falk WE, Marder S, et al. (June 1989). "Anticholinergic effects on memory: benztropine versus amantadine".Journal of Clinical Psychopharmacology.9 (3):180–185.doi:10.1097/00004714-198906000-00004.PMID2661606.S2CID27308127.
^Lakstygal AM, Kolesnikova TO, Khatsko SL, Zabegalov KN, Volgin AD, Demin KA, et al. (May 2019). "DARK Classics in Chemical Neuroscience: Atropine, Scopolamine, and Other Anticholinergic Deliriant Hallucinogens".ACS Chem Neurosci.10 (5):2144–2159.doi:10.1021/acschemneuro.8b00615.PMID30566832.
^Adler LA, Peselow E, Rosenthal M, Angrist B (1993). "A controlled comparison of the effects of propranolol, benztropine, and placebo on akathisia: an interim analysis".Psychopharmacology Bulletin.29 (2):283–286.PMID8290678.
^Wilson DV, Nickels FA, Williams MA (November 1991). "Pharmacologic treatment of priapism in two horses".Journal of the American Veterinary Medical Association.199 (9):1183–1184.doi:10.2460/javma.1991.199.09.1183.PMID1752772.
N
Y (what is this?) (verify)
