Benztropine mesylate - CAS 132-17-2
Catalog number: 132-17-2
Category: Inhibitor
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Molecular Formula:
C21H25NO.CH4SO3
Molecular Weight:
403.53
COA:
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Targets:
mAChR
Description:
Benztropine inhibits MTSET-induced inhibition of [3H]WIN binding to Wild-type dopamine transporter with EC50 of 28 μM in concentration-dependent manner.
Purity:
>98%
Synonyms:
Benztropine Mesylate; Cogentin; Cogentin mesylate; MLS000737056; Benztropine methanesulfonate; NSC42199; ST50997629; Benzotropine mesylate
MSDS:
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InChIKey:
CPFJLLXFNPCTDW-UHFFFAOYSA-N
InChI:
InChI=1S/C21H25NO.CH4O3S/c1-22-18-12-13-19(22)15-20(14-18)23-21(16-8-4-2-5-9-16)17-10-6-3-7-11-17;1-5(2,3)4/h2-11,18-21H,12-15H2,1H3;1H3,(H,2,3,4)
Canonical SMILES:
CN1C2CCC1CC(C2)OC(C3=CC=CC=C3)C4=CC=CC=C4.CS(=O)(=O)O
1.Persistence of racial disparities in prescription of first-generation antipsychotics in the USA.
Cook TB1, Reeves GM2, Teufel J1, Postolache TT2,3,4. Pharmacoepidemiol Drug Saf. 2015 Nov;24(11):1197-206. doi: 10.1002/pds.3819. Epub 2015 Jul 1.
PURPOSE: The aim of this study was to estimate the prevalence of first-generation antipsychotics (FGA) prescribed for treatment of psychiatric and neurological conditions and use of benztropine to reduce extrapyramidal side effects (EPS) by patient race/ethnicity in a nationally representative sample of adult outpatient visits.
2.α-Synuclein-induced myelination deficit defines a novel interventional target for multiple system atrophy.
Ettle B1, Kerman BE2,3, Valera E4, Gillmann C5, Schlachetzki JC1,6, Reiprich S7, Büttner C8, Ekici AB8, Reis A8, Wegner M7, Bäuerle T5, Riemenschneider MJ9, Masliah E4, Gage FH2, Winkler J10. Acta Neuropathol. 2016 Apr 8. [Epub ahead of print]
Multiple system atrophy (MSA) is a rare atypical parkinsonian disorder characterized by a rapidly progressing clinical course and at present without any efficient therapy. Neuropathologically, myelin loss and neurodegeneration are associated with α-synuclein accumulation in oligodendrocytes, but underlying pathomechanisms are poorly understood. Here, we analyzed the impact of oligodendrocytic α-synuclein on the formation of myelin sheaths to define a potential interventional target for MSA. Post-mortem analyses of MSA patients and controls were performed to quantify myelin and oligodendrocyte numbers. As pre-clinical models, we used transgenic MSA mice, a myelinating stem cell-derived oligodendrocyte-neuron co-culture, and primary oligodendrocytes to determine functional consequences of oligodendrocytic α-synuclein overexpression on myelination. We detected myelin loss accompanied by preserved or even increased numbers of oligodendrocytes in post-mortem MSA brains or transgenic mouse forebrains, respectively, indicating an oligodendrocytic dysfunction in myelin formation.
3.Drug-induced parkinsonism following chronic methamphetamine use by a patient on haloperidol decanoate.
Matthew BJ1, Gedzior JS2. Int J Psychiatry Med. 2015;50(4):405-11. doi: 10.1177/0091217415612736. Epub 2015 Nov 2.
This report attempts to highlight that use of an antipsychotic and concurrent chronic use of methamphetamine can cause drug-induced parkinsonism. Methamphetamine is usually not encountered in the list of agents that induce drug-induced parkinsonism and so its consideration particularly during chronic use by a patient who is also on an antipsychotic is worthwhile because of its popularity as an illegal narcotic. This case report describes just such a case of drug-induced parkinsonism which is a subacute syndrome that mimics Parkinson's disease. Although less alarming than dystonia, it is more common, more difficult to treat and can be the cause of significant disability during maintenance treatment especially in the elderly. In most cases, symptoms are reversible in days or weeks, but occasionally, especially in the elderly, or if long-acting injectable antipsychotics are used-as in this case-symptoms may last for weeks or months. The report also illustrates the neuronal workings due to chronic methamphetamine-use and the additive effects of dopamine blockade by antipsychotics such as haloperidol.
4.2-Substituted 3β-Aryltropane Cocaine Analogs Produce Atypical Effects without Inducing Inward-Facing Dopamine Transporter Conformations.
Hong WC1, Kopajtic TA1, Xu L1, Lomenzo SA1, Jean B1, Madura JD1, Surratt CK1, Trudell ML1, Katz JL2. J Pharmacol Exp Ther. 2016 Mar;356(3):624-34. doi: 10.1124/jpet.115.230722. Epub 2016 Jan 14.
Previous structure-activity relationship studies indicate that a series of cocaine analogs, 3β-aryltropanes with 2β-diarylmethoxy substituents, selectively bind to the dopamine transporter (DAT) with nanomolar affinities that are 10-fold greater than the affinities of their corresponding 2α-enantiomers. The present study compared these compounds to cocaine with respect to locomotor effects in mice, and assessed their ability to substitute for cocaine (10 mg/kg, i.p.) in rats trained to discriminate cocaine from saline. Despite nanomolar DAT affinity, only the 2β-Ph2COCH2-3β-4-Cl-Ph analog fully substituted for cocaine-like discriminative effects. Whereas all of the 2β compounds increased locomotion, only the 2β-(4-ClPh)PhCOCH2-3β-4-Cl-Ph analog had cocaine-like efficacy. None of the 2α-substituted compounds produced either of these cocaine-like effects. To explore the molecular mechanisms of these drugs, their effects on DAT conformation were probed using a cysteine-accessibility assay.
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CAS 132-17-2 Benztropine mesylate

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