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C1900000

Chlorpromazine hydrochloride

European Pharmacopoeia (EP) Reference Standard

Sinónimos:

2-Chloro-10-(3-dimethylaminopropyl)phenothiazine hydrochloride, CPZ, Largactil

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About This Item

Fórmula empírica (notación de Hill):
C17H19ClN2S · HCl
Número de CAS:
69-09-0
Peso molecular:
355.33
Beilstein/REAXYS Number:
3779989
MDL number:
MFCD00012654
UNSPSC Code:
41116107
PubChem Substance ID:
329774913
NACRES:
NA.24

grade

pharmaceutical primary standard

API family

chlorpromazine

manufacturer/tradename

EDQM

application(s)

pharmaceutical (small molecule)

format

neat

SMILES string

Cl[H].CN(C)CCCN1c2ccccc2Sc3ccc(Cl)cc13

InChI

1S/C17H19ClN2S.ClH/c1-19(2)10-5-11-20-14-6-3-4-7-16(14)21-17-9-8-13(18)12-15(17)20;/h3-4,6-9,12H,5,10-11H2,1-2H3;1H

InChI key

FBSMERQALIEGJT-UHFFFAOYSA-N

Gene Information

human ... DRD2(1813) , DRD3(1814) , DRD4(1815) , HTR2A(3356)

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General description

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

Substitute for benzidine, o-dianisidine, and o-tolidine in the determination of microquantities of hemoglobin and peroxidase.

Biochem/physiol Actions

Chlorpromazine demonstrates cytotoxic and antiproliferative activity against leukemic cells, but does not affect the viability of normal lymphocytes.
Phenothiazine antipsychotic; D2 dopamine receptor antagonist, H1 histamine receptor antagonist; inhibits calmodulin-dependent stimulation of cyclic nucleotide phosphodiesterase and nitric oxide synthase.

Packaging

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

Other Notes

Sales restrictions may apply.

Related product

Referencia del producto
Descripción
Precios

pictograms

Skull and crossbones
GHS06

signalword

Danger

hcodes

H301,H330

Hazard Classifications

Acute Tox. 1 Inhalation - Acute Tox. 3 Oral

Storage Class

6.1A - Combustible acute toxic Cat. 1 and 2 / very toxic hazardous materials

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

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Certificados de análisis (COA)

Lot/Batch Number

Lo sentimos, en este momento no disponemos de COAs para este producto en línea.

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Mihail Lucian Pascu et al.
PloS one, 8(2), e55767-e55767 (2013-02-14)
Phenothiazines when exposed to white light or to UV radiation undergo a variety of reactions that result in degradation of parental compound and formation of new species. This process is slow and may be sped up with exposure to high
Rosanne Varkevisser et al.
Pflugers Archiv : European journal of physiology, 465(2), 247-259 (2012-11-30)
Drug-induced ion channel trafficking disturbance can cause cardiac arrhythmias. We showed that the antiprotozoic pentamidine decreased K(IR)2.x carried I(K1) current and that inhibiting protein degradation in the lysosome increased intracellular K(IR)2.1 levels. In this study, we aim to identify and
Soon Young Shin et al.
Carcinogenesis, 34(9), 2080-2089 (2013-05-22)
2-Chloro-10-[3(-dimethylamino)propyl]phenothiazine mono hydrochloride (chlorpromazine; CPZ) is an antipsychotic agent that was originally developed to control psychotic disorders. The cytotoxic properties of the CPZ are well known, but its mechanism of action is poorly understood. In this study, we investigated the
Stephanie L MacAllister et al.
Canadian journal of physiology and pharmacology, 91(1), 56-63 (2013-02-02)
Chlorpromazine (CPZ), a member of the largest class of first-generation antipsychotic agents, is known to cause hepatotoxicity in the form of cholestasis and hepatocellular necrosis in some patients. The mechanism of CPZ hepatotoxicity is unclear, but is thought to result
Jessica M D'Amico et al.
Journal of neurophysiology, 109(6), 1473-1484 (2012-12-12)
In animals, the recovery of motoneuron excitability in the months following a complete spinal cord injury is mediated, in part, by increases in constitutive serotonin (5-HT2) and norepinephrine (α1) receptor activity, which facilitates the reactivation of calcium-mediated persistent inward currents
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