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Key Documents

Y0000106

Pilocarpine nitrate for system suitability

European Pharmacopoeia (EP) Reference Standard

Synonym(s):

Pilocarpine nitrate salt

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About This Item

Empirical Formula (Hill Notation):
C11H16N2O2 · HNO3
CAS Number:
Molecular Weight:
271.27
Beilstein:
4171406
MDL number:
UNSPSC Code:
41116107
PubChem Substance ID:
NACRES:
NA.24

grade

pharmaceutical primary standard

API family

pilocarpine

manufacturer/tradename

EDQM

application(s)

pharmaceutical (small molecule)

format

neat

storage temp.

2-8°C

SMILES string

O[N+]([O-])=O.CC[C@H]1[C@H](COC1=O)Cc2cncn2C

InChI

1S/C11H16N2O2.HNO3/c1-3-10-8(6-15-11(10)14)4-9-5-12-7-13(9)2;2-1(3)4/h5,7-8,10H,3-4,6H2,1-2H3;(H,2,3,4)/t8-,10-;/m0./s1

InChI key

PRZXEPJJHQYOGF-GNAZCLTHSA-N

Gene Information

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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

Pilocarpine nitrate for system suitability EP Reference standard, intended for use in laboratory tests only as specifically prescribed in the European Pharmacopoeia.

Biochem/physiol Actions

Nonselective muscarinic acetylcholine receptor agonist; used to produce an experimental model of epilepsy.

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.

Pictograms

Flame over circleSkull and crossbones

Signal Word

Danger

Hazard Statements

Hazard Classifications

Acute Tox. 2 Inhalation - Acute Tox. 4 Oral - Ox. Sol. 2

Storage Class Code

5.1B - Oxidizing hazardous materials

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


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Linda Holtman et al.
Epilepsia, 54(4), 589-595 (2013-02-13)
Brain inflammation occurs during epileptogenesis and may contribute to the development and progression of temporal lobe epilepsy. Recently, several studies have indicated that seizures may also increase specific blood plasma cytokine levels in animal models as well as in human
Olav B Smeland et al.
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 33(7), 1090-1097 (2013-04-25)
Although certain metabolic characteristics such as interictal glucose hypometabolism are well established for temporal lobe epilepsy (TLE), its pathogenesis still remains unclear. Here, we performed a comprehensive study of brain metabolism in a mouse model of TLE, induced by pilocarpine-status
Jay R Vargas et al.
Journal of neuropathology and experimental neurology, 72(10), 919-932 (2013-09-18)
Astrocytes have emerged as active participants of synaptic transmission and are increasingly implicated in neurologic disorders including epilepsy. Adult glial fibrillary acidic protein (GFAP)-positive hippocampal astrocytes are not known for ionotropic glutamate receptor expression under basal conditions. Using a chemoconvulsive
Shuo-Bin Jou et al.
Seizure, 22(3), 221-229 (2013-01-15)
Bilateral electrical stimulation of anterior nuclei of thalamus (ANT) has shown promising effects on epileptic seizures. However, bilateral implantation increases the risk of surgical complications and side effects. This study was undertaken to access the effectiveness of a stimulation paradigm
Manuela Mazzuferi et al.
Annals of neurology, 74(4), 560-568 (2013-05-21)
Epigenetic mechanisms involved in transcriptional regulation of multiple molecular pathways are potentially attractive therapeutic interventions for epilepsy, because single target therapies are unlikely to provide both anticonvulsant and disease-modifying effects. A selection of epilepsy-related gene expression data sets were retrieved

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