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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/04/15 02:23:03」(JST)

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Thiethylperazine (Torecan) is an antiemetic of the phenothiazine class. Though it was never licensed or used as an antipsychotic, it may have such effects.

Thiethylperazine activates the transport protein ABCC1 that clears beta-amyloid from brains of mice. ^[1]

References

^ Science Daily (September 1, 2011). "Alzheimer Disease: Transport Protein ABCC1 Plays Key Role in Clearing Beta-Amyloid from Brains of Mice.". Retrieved September 1, 2011.

Bourquin, J. P.; Schwarb, G.; Gamboni, G.; Rischer, R.; Ruesch, L.; Uldimann, S. G.; Theuss, U.; Schenke, E.; Renz, J.; Helv. Chim. Acta 1958, 41, 1072.

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English Journal

[Noncardiogenic pulmonary edema in the course of poisoning with clozapine, ketoprofen and thiethylperazine].

Majewska M, Kołodziej M, Szponar J, Drelich G, Danielewicz P, Kostek H.Author information Samodzielny Publiczny Szpital Wojewódzki im. Jana Bozego w Lublinie, Regionalny Ośrodek Toksykologii Klinicznej.AbstractPulmonary edema is a severe, potentially fatal clinical condition. It happens, when interstitial fluid is accumulating in the alveoli, impeding proper gas exchange. Typically we distinguish cardiogenic and noncardiogenic pulmonary edema. The article describes the case of severe pulmonary edema, which occurred in a young woman, free of cardiac diseases, about 30 hours after a suicidal drug poisoning (clozapine, ketoprofen, thiethylperazine). Both clozapine and ketoprofen intoxication, may be severe. Complications in these poisonings affect not only the central nervous system, but also the circulatory or respiratory system and may even occur several hours after the overdose of these drugs. The study considered the causes and possible mechanisms of pulmonary edema in poisoning with these drugs.
Przegla̧d lekarski.Przegl Lek.2012;69(8):618-20.
Pulmonary edema is a severe, potentially fatal clinical condition. It happens, when interstitial fluid is accumulating in the alveoli, impeding proper gas exchange. Typically we distinguish cardiogenic and noncardiogenic pulmonary edema. The article describes the case of severe pulmonary edema, whic
PMID 23243946

Cerebral amyloid-β proteostasis is regulated by the membrane transport protein ABCC1 in mice.

Krohn M, Lange C, Hofrichter J, Scheffler K, Stenzel J, Steffen J, Schumacher T, Brüning T, Plath AS, Alfen F, Schmidt A, Winter F, Rateitschak K, Wree A, Gsponer J, Walker LC, Pahnke J.Author information Department of Neurology, Neurodegeneration Research Laboratory, University of Rostock, Rostock, Germany.AbstractIn Alzheimer disease (AD), the intracerebral accumulation of amyloid-β (Aβ) peptides is a critical yet poorly understood process. Aβ clearance via the blood-brain barrier is reduced by approximately 30% in AD patients, but the underlying mechanisms remain elusive. ABC transporters have been implicated in the regulation of Aβ levels in the brain. Using a mouse model of AD in which the animals were further genetically modified to lack specific ABC transporters, here we have shown that the transporter ABCC1 has an important role in cerebral Aβ clearance and accumulation. Deficiency of ABCC1 substantially increased cerebral Aβ levels without altering the expression of most enzymes that would favor the production of Aβ from the Aβ precursor protein. In contrast, activation of ABCC1 using thiethylperazine (a drug approved by the FDA to relieve nausea and vomiting) markedly reduced Aβ load in a mouse model of AD expressing ABCC1 but not in such mice lacking ABCC1. Thus, by altering the temporal aggregation profile of Aβ, pharmacological activation of ABC transporters could impede the neurodegenerative cascade that culminates in the dementia of AD.
The Journal of clinical investigation.J Clin Invest.2011 Oct;121(10):3924-31. doi: 10.1172/JCI57867. Epub 2011 Sep 1.
In Alzheimer disease (AD), the intracerebral accumulation of amyloid-β (Aβ) peptides is a critical yet poorly understood process. Aβ clearance via the blood-brain barrier is reduced by approximately 30% in AD patients, but the underlying mechanisms remain elusive. ABC transporters have been impli
PMID 21881209

Enhancement of vancomycin activity by phenothiazines against vancomycin-resistant Enterococcus faecium in vitro.

Rahbar M, Mehrgan H, Hadji-nejad S.Author information Department of Microbiology, Reference Health Laboratories, Ministry of Health, Tehran, Iran.AbstractThe antimicrobial and resistance-reversal activities of seven phenothiazine derivatives were evaluated against vancomycin-sensitive Enterococcus faecalis ATCC 29212, vancomycin resistant E. faecalis ATCC 51299 and ten vancomycin-resistant E. faecium strains originating from human infections. Minimum inhibitory concentrations (MIC) of the compounds were determined by agar dilution method, and synergy between phenothiazines and vancomycin was investigated using Checkerboard (microbroth dilution) technique. We found that all enterococci strains, regardless of their susceptibility to vancomycin, were inhibited by phenothiazines at concentrations varying from 8 to 256 microg/ml, with thiethylperazine being the most potent inhibitory agent. Besides, all the phenothiazines showed partial synergy with vancomycin and could lessen MIC of vancomycin from 512 to 8 microg/ml at their sub-inhibitory concentrations. The highest reduction in MIC was observed with chlorpromazine (32 times); however, thiethylperazine and promethazine stood next (24 times). Although resistance modification was observed at concentrations higher than those that phenothiazines reach in vivo, the potential offered by non-antibiotics justify further animal experiments as well as clinical trials to establish their clinical relevance.
Basic & clinical pharmacology & toxicology.Basic Clin Pharmacol Toxicol.2010 Aug;107(2):676-9. doi: 10.1111/j.1742-7843.2010.00558.x. Epub 2010 Mar 28.
The antimicrobial and resistance-reversal activities of seven phenothiazine derivatives were evaluated against vancomycin-sensitive Enterococcus faecalis ATCC 29212, vancomycin resistant E. faecalis ATCC 51299 and ten vancomycin-resistant E. faecium strains originating from human infections. Minimum
PMID 20353486

Related Pictures

★リンクテーブル★

リンク元	「チエチルペラジン」「thiethylperazine maleate」「リンゴ酸チエチルペラジン」
関連記事	「thiethylperazine」

「チエチルペラジン」

Thiethylperazine
Systematic (IUPAC) name
	2-(ethylthio)-10-[3-(4-methylpiperazin-1-yl)propyl]-10H-phenothiazine
Clinical data
AHFS/Drugs.com	Micromedex Detailed Consumer Information
Legal status	?
Pharmacokinetic data
Protein binding	60%
Identifiers
CAS number	1420-55-9
ATC code	R06AD03
PubChem	CID 5440
DrugBank	DB00372
ChemSpider	5245
UNII	8ETK1WAF6R
KEGG	D02354
ChEBI	CHEBI:9544
ChEMBL	CHEMBL1378
Chemical data
Formula	C22H29N3S2
Mol. mass	399.618 g/mol
	SMILES S(c2cc1N(c3c(Sc1cc2)cccc3)CCCN4CCN(C)CC4)CC;
	InChI InChI=1S/C22H29N3S2/c1-3-26-18-9-10-22-20(17-18)25(19-7-4-5-8-21(19)27-22)12-6-11-24-15-13-23(2)14-16-24/h4-5,7-10,17H,3,6,11-16H2,1-2H3 ; Key:XCTYLCDETUVOIP-UHFFFAOYSA-N ;
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