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P4099900

Pyridostigmine bromide

European Pharmacopoeia (EP) Reference Standard

Synonyme(s) :

3-(Dimethylaminocarbonyloxy)-1-methylpyridinium bromide

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About This Item

Formule empirique (notation de Hill):
C9H13BrN2O2
Numéro CAS:
101-26-8
Poids moléculaire :
261.12
Numéro MDL:
MFCD00079283
Code UNSPSC :
41116107
ID de substance PubChem :
329820197
Nomenclature NACRES :
NA.24

Qualité

pharmaceutical primary standard

Famille d'API

pyridostigmine

Fabricant/nom de marque

EDQM

Application(s)

pharmaceutical (small molecule)

Format

neat

Température de stockage

2-8°C

Chaîne SMILES 

[Br-].CN(C)C(=O)Oc1ccc[n+](C)c1

InChI

1S/C9H13N2O2.BrH/c1-10(2)9(12)13-8-5-4-6-11(3)7-8;/h4-7H,1-3H3;1H/q+1;/p-1

Clé InChI

VNYBTNPBYXSMOO-UHFFFAOYSA-M

Informations sur le gène

human ... ACHE(43)

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Catégories apparentées

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

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

Actions biochimiques/physiologiques

Acetylcholinesterase inhibitor.

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.

Produit(s) apparenté(s)

Réf. du produit
Description
Tarif

Pictogrammes

Skull and crossbones
GHS06

Mention d'avertissement

Danger

Mentions de danger

H300 + H310 + H330,H317

Classification des risques

Acute Tox. 1 Inhalation - Acute Tox. 2 Dermal - Acute Tox. 2 Oral - Skin Sens. 1

Code de la classe de stockage

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

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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Certificats d'analyse (COA)

Lot/Batch Number

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Retrouvez la documentation relative aux produits que vous avez récemment achetés dans la Bibliothèque de documents.

Consulter la Bibliothèque de documents

João Paulo J Sabino et al.
Autonomic neuroscience : basic & clinical, 173(1-2), 58-64 (2012-12-12)
Sympathetic hyperactivity and its outcome in heart failure have been thoroughly investigated to determine the focus of pharmacologic approaches targeting the sympathetic nervous system in the treatment of this pathophysiological condition. On the other hand, therapeutic approaches aiming to protect
Adil E Bharucha et al.
Gut, 62(5), 708-715 (2012-06-09)
Chronic constipation in diabetes mellitus is associated with colonic motor dysfunction and is managed with laxatives. Cholinesterase inhibitors increase colonic motility. This study evaluated the effects of a cholinesterase inhibitor on gastrointestinal and colonic transit and bowel function in diabetic
H Zach et al.
European journal of neurology, 20(4), 708-713 (2013-01-03)
Several small retrospective studies have observed that patients with a purely ocular manifestation of myasthenia gravis (MG) are significantly less likely to convert to a generalized disease when treated early on with corticosteroids. However, given the limited number of reported
Renata M Lataro et al.
American journal of physiology. Regulatory, integrative and comparative physiology, 305(8), R908-R916 (2013-08-21)
Heart failure (HF) is characterized by elevated sympathetic activity and reduced parasympathetic control of the heart. Experimental evidence suggests that the increase in parasympathetic function can be a therapeutic alternative to slow HF evolution. The parasympathetic neurotransmission can be improved
Renske I Wadman et al.
Neurology, 79(20), 2050-2055 (2012-11-02)
Spinal muscular atrophy (SMA) is pathologically characterized by degeneration of anterior horn cells. Recent observations in animal models of SMA and muscle tissue from patients with SMA suggest additional abnormalities in the development and maturation of the neuromuscular junction. We
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