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Key Documents

H0100000

Haloperidol

European Pharmacopoeia (EP) Reference Standard

Synonyme(s) :

4-[4-(4-Chlorophenyl)-4-hydroxy-1-piperidinyl]-1-(4-fluorophenyl)-1-butanone, 4-[4-(4-Chlorophenyl)-4-hydroxypiperidino]-4′-fluorobutyrophenone, 4-[4-(p-Chlorophenyl)-4-hydroxypiperidino]-4′-fluorobutyrophenone

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About This Item

Formule empirique (notation de Hill):
C21H23ClFNO2
Numéro CAS:
Poids moléculaire :
375.86
Numéro MDL:
Code UNSPSC :
41116107
ID de substance PubChem :
Nomenclature NACRES :
NA.24

Qualité

pharmaceutical primary standard

Famille d'API

haloperidol

Fabricant/nom de marque

EDQM

Application(s)

pharmaceutical (small molecule)

Format

neat

Température de stockage

2-8°C

Chaîne SMILES 

OC1(CCN(CCCC(=O)c2ccc(F)cc2)CC1)c3ccc(Cl)cc3

InChI

1S/C21H23ClFNO2/c22-18-7-5-17(6-8-18)21(26)11-14-24(15-12-21)13-1-2-20(25)16-3-9-19(23)10-4-16/h3-10,26H,1-2,11-15H2

Clé InChI

LNEPOXFFQSENCJ-UHFFFAOYSA-N

Informations sur le gène

human ... HTR2A(3356)

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Description générale

This product is provided as delivered and specified by the issuing Pharmacopoeia. All information provided in support of this product, including SDS and any product information leaflets have been developed and issued under the Authority of the Issuing Pharmacopoeia. For further information and support please go to the website of the issuing Pharmacopoeia.

Application

Haloperidol EP Reference standard, intended for use in laboratory tests only as specifically prescribed in the European Pharmacopoeia.

Conditionnement

The product is delivered as supplied by the issuing Pharmacopoeia. For the current unit quantity, please visit the EDQM reference substance catalogue.

Autres remarques

Sales restrictions may apply.

Pictogrammes

Skull and crossbonesHealth hazard

Mention d'avertissement

Danger

Classification des risques

Acute Tox. 3 Oral - Eye Irrit. 2 - Repr. 2 - Skin Irrit. 2 - Skin Sens. 1 - STOT SE 3

Organes cibles

Respiratory system

Code de la classe de stockage

6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


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Lot/Batch Number

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Consulter la Bibliothèque de documents

Katarzyna J Radomska et al.
Human molecular genetics, 22(7), 1373-1382 (2013-01-17)
Linkage, association and expression studies previously pointed to the human QKI, KH domain containing, RNA-binding (QKI) as a candidate gene for schizophrenia. Functional studies of the mouse orthologue Qk focused mainly on its role in oligodendrocyte development and myelination, while
Dan Shan et al.
Schizophrenia research, 144(1-3), 1-8 (2013-01-30)
Glutamate transporters facilitate the buffering, clearance and cycling of glutamate and play an important role in maintaining synaptic and extrasynaptic glutamate levels. Alterations in glutamate transporter expression may lead to abnormal glutamate neurotransmission contributing to the pathophysiology of schizophrenia. In
Mark C Fok et al.
International journal of geriatric psychiatry, 30(4), 333-344 (2015-02-03)
To summarize the effect of antipsychotics for preventing postoperative delirium. We conducted a literature search using Medline, EMBASE, Cochrane Central Register of Controlled Trials, Cochrane Database of Systematic Reviews and clinicaltrials.gov. We included randomized controlled trials of adults undergoing surgery
Norma Adán et al.
The Journal of clinical investigation, 123(9), 3902-3913 (2013-08-03)
Chondrocytes are the only cells in cartilage, and their death by apoptosis contributes to cartilage loss in inflammatory joint diseases, such as rheumatoid arthritis (RA). A putative therapeutic intervention for RA is the inhibition of apoptosis-mediated cartilage degradation. The hormone
Robin Nguyen et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 34(45), 14948-14960 (2014-11-08)
Hyperactivity within the ventral hippocampus (vHPC) has been linked to both psychosis in humans and behavioral deficits in animal models of schizophrenia. A local decrease in GABA-mediated inhibition, particularly involving parvalbumin (PV)-expressing GABA neurons, has been proposed as a key

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