TEVA-SELEGILINE TABLET

国: カナダ

言語: 英語

ソース: Health Canada

有効成分:

SELEGILINE HYDROCHLORIDE

から入手可能:

TEVA CANADA LIMITED

ATCコード:

N04BD01

INN（国際名）:

SELEGILINE

投薬量:

5MG

医薬品形態:

TABLET

構図:

SELEGILINE HYDROCHLORIDE 5MG

投与経路:

ORAL

パッケージ内のユニット:

60/100/300/500/1000

処方タイプ:

Prescription

治療領域:

MONOAMINE OXIDASE B INHIBITORS

製品概要:

Active ingredient group (AIG) number: 0131374001; AHFS:

認証ステータス:

APPROVED

承認日:

2014-05-15

製品の特徴

PRODUCT MONOGRAPH
TEVA-SELEGILINE
(Selegiline Hydrochloride)
5 mg Tablets
Teva Standard
Antiparkinsonian Agent
Teva Canada Limited
Date of Revision:
Toronto, Canada
July 14, 2015
Control Number: 185193
2
PRODUCT MONOGRAPH
TEVA-SELEGILINE
(Selegiline Hydrochloride)
5 mg Tablets
Teva Standard
THERAPEUTIC CLASSIFICATION
Antiparkinsonian Agent
ACTION AND CLINICAL PHARMACOLOGY
TEVA-SELEGILINE (selegiline hydrochloride) is an irreversible
inhibitor of the enzyme
monoamine oxidase (MAO). Because selegiline has greater affinity for
type B than type
A MAO, it can serve as a selective inhibitor of MAO-B if it is
administered at the
recommended dose.
Selegiline may have pharmacological effects unrelated to MAO-B
inhibition. There is
some evidence that it may increase dopaminergic activity by
interfering with dopamine re-
uptake at the synapse. Effects resulting from selegiline
administration may also be
mediated through its metabolites. Two of its three principle
metabolites, amphetamine
and methamphetamine, have pharmacological actions of their own, they
interfere with
neuronal re-uptake and enhance the release of several
neurotransmitters (e.g.,
norepinephrine, dopamine, serotonin). The extent to which these
neurotransmitters
contribute to selegiline's effects are unknown.
Rationale for the use of selective MAO-B inhibitors in Parkinson's
disease: Many of the
prominent symptoms of Parkinson's Disease are due to deficiency of
striatal dopamine that
is the consequence of a progressive degeneration and loss of a
population of dopaminergic
3
neurons which originate in the substantia nigra and project to the
striatum. Early in the
course of the disease, the deficit in the capacity of these neurons to
synthesize dopamine
can be overcome by the administration of exogenous levodopa. After
several years of
levodopa therapy, the response to a given dose of levodopa is often
accompanied by side
effects (dyskinesia, on-off phenomena, freezing).
MAO-B inhibitors may be useful under these conditions because by
blocking the
catabolism o