RILUTEK TABLET 50 mg

国: シンガポール

言語: 英語

ソース: HSA (Health Sciences Authority)

有効成分:

RILUZOLE

から入手可能:

SANOFI-AVENTIS SINGAPORE PTE. LTD.

ATCコード:

N07XX02

投薬量:

50 mg

医薬品形態:

TABLET, FILM COATED

構図:

RILUZOLE 50 mg

投与経路:

ORAL

処方タイプ:

Prescription Only

製:

Opella Healthcare International SAS

認証ステータス:

ACTIVE

承認日:

1997-07-31

情報リーフレット

RILUTEK
_® _
(RILUZOLE)_ _TABLETS 

 [sanofi-aventis logo] 

RILUTEK
_® _
(RILUZOLE)TABLETS 
RX ONLY 

DESCRIPTION 
RILUTEK
_® _
(riluzole) is a member of the benzonthiazole class. Chemically
riluzole is 2-amino-6-
(trifluoromethoxy) benzonthiazole. Its molecular formula is C
8
H
5
F
3
N
2
OS and its molecular weight 
is 234.2. Its structural formula is as follows:
_ _

_        _
_ _
Riluzole is a white to slightly yellow powder that is
very soluble in dimethyformamide, 
dimethysolfuxide and methanol, freely soluble in
dichloromethane, sparingly soluble in 0.1N HCl 
and very slightly soluble in water and 0.1N NaOH. RILUTEK
is available as a capsule shaped, 
white, film coated tablet for oral administration containing 50mg of riluzole. Each tablet is 
engraved with  “RPR 202”  on one side. 
INACTIVE INGREDIENTS: CORE : anhydrous dibasic calcium phosphate,
USP; microcrystalline 
cellulose, NF; anhydrous colloidal silica, NF; magnesium stearate,
NF; croscarmellose sodium, 
NF.  
FILM COATING: Hydroxypropyl methylcellulose, USP;
polyethylene glycol 6000; titanium 
dioxide, USP. 

CLINICAL PHARMACOLOGY 
MECHANISM OF ACTION 
The etiology and pathogenesis of amyotropic lateral
sclerosis (ALS) are not known, although a 
number of hypotheses have been advanced. One
hypothesis is that motor neurons, made 
vulnerable through either genetic predisposition or environmental
factors, are injured by 
glutamate. In some cases of familial ALS, the enzyme superoxide
dismutase has been found to 
be defective. 
The mode of action of 
RILUTEK is unknown.  Its pharmacological
properties include the following, 
some of which may be related to its effect:   1) an
inhibitory effect on glutamate release,              
2) inactivation of voltage-dependent sodium channels, and
3) ability to interfere with intracellular 
events that follow transmitter

製品の特徴

RILUTEK
_® _
(
RILUZOLE)_ _TABLETS
[sanofi-aventis logo]
RILUTEK
_® _
(
RILUZOLE)TABLETS
RX ONLY
DESCRIPTION
RILUTEK
_® _
(
riluzole) is a member of the benzonthiazole class. Chemically riluzole
is 2-amino-6-
(trifluoromethoxy) benzonthiazole. Its molecular formula is C
8
H
5
F
3
N
2
OS and its molecular weight
is 234.2. Its structural formula is as follows:
_ _
_ _
_ _
Riluzole is a white to slightly yellow powder that is very soluble in
dimethyformamide,
dimethysolfuxide and methanol, freely soluble in dichloromethane,
sparingly soluble in 0.1N HCl
and very slightly soluble in water and 0.1N NaOH. RILUTEK is available
as a capsule shaped,
white, film coated tablet for oral administration containing 50mg of
riluzole. Each tablet is
engraved with “RPR 202” on one side.
INACTIVE INGREDIENTS: CORE : anhydrous dibasic calcium phosphate, USP;
microcrystalline
cellulose, NF; anhydrous colloidal silica, NF; magnesium stearate, NF;
croscarmellose sodium,
NF. FILM COATING: Hydroxypropyl methylcellulose, USP; polyethylene
glycol 6000; titanium
dioxide, USP.
CLINICAL PHARMACOLOGY
MECHANISM OF ACTION
The etiology and pathogenesis of amyotropic lateral sclerosis (ALS)
are not known, although a
number of hypotheses have been advanced. One hypothesis is that motor
neurons, made
vulnerable through either genetic predisposition or environmental
factors, are injured by
glutamate. In some cases of familial ALS, the enzyme superoxide
dismutase has been found to
be defective.
The mode of action of RILUTEK is unknown. Its pharmacological
properties include the following,
some of which may be related to its effect: 1) an inhibitory effect on
glutamate release,
2) inactivation of voltage-dependent sodium channels, and 3) ability
to interfere with intracellular
events that follow transmitter binding at excitatory amino acid
receptors.
Riluzole has also been shown, in a single study, to delay median time
to death in a transgenic
mouse model of ALS. These mice express human superoxide dismutase
bearing one of the
mutations found in