PHL-FENOFIBRATE SUPRA TABLET

国: カナダ

言語: 英語

ソース: Health Canada

有効成分:

FENOFIBRATE

から入手可能:

PHARMEL INC

ATCコード:

C10AB05

INN（国際名）:

FENOFIBRATE

投薬量:

100MG

医薬品形態:

TABLET

構図:

FENOFIBRATE 100MG

投与経路:

ORAL

パッケージ内のユニット:

100

処方タイプ:

Prescription

治療領域:

FRIBIC ACID DERIVATIVES

製品概要:

Active ingredient group (AIG) number: 0118895002; AHFS:

認証ステータス:

CANCELLED PRE MARKET

承認日:

2017-09-13

製品の特徴

PRODUCT MONOGRAPH
PR
PHL-FENOFIBRATE SUPRA
fenofibrate
microcoated formulation
film-coated tablets
100 mg, 160 mg tablets
Lipid Metabolism Regulator
PHARMEL INC.
Date of Preparation:
8699, 8e Avenue
March 29, 2004
Montreal, Quebec
H1Z 2X4
CONTROL NO.: 090588
- 2 -
PRODUCT MONOGRAPH
PR
PHL-FENOFIBRATE SUPRA
fenofibrate
microcoated formulation
film-coated tablets
100 mg and 160 mg
PHARMACOLOGICAL CLASSIFICATION
Lipid metabolism regulator
ACTIONS AND CLINICAL PHARMACOLOGY
phl-FENOFIBRATE SUPRA (fenofibrate) lowers elevated serum lipids by
decreasing the low density
lipoprotein (LDL) fraction rich in cholesterol and the very low
density lipoprotein (VLDL) fraction rich in
triglycerides. In addition, fenofibrate increases the high density
lipoprotein (HDL) cholesterol fraction.
Fenofibrate appears to have a greater depressant effect on the very
low density lipoproteins (VLDL) than on
the low density lipoproteins (LDL). Therapeutic doses of fenofibrate
produce elevations of HDL cholesterol,
a reduction in the content of the low density lipoproteins
cholesterol, and a substantial reduction in the
triglyceride content of very low density lipoproteins.
Recent findings suggest that the lipid modulating effects of
fenofibrate are mediated by the activation of a
specific nuclear receptor called peroxisome proliferator activated
receptor alpha (PPAR
α
) which produces:
¾
a reduction in apo C-III, and therefore a reduction in the level of
dense atherogenic LDL particles;
¾
a stimulation of mitochondrial beta-oxidation, and therefore a
reduction in triglyceride secretion;
¾
a rise in lipoprotein lipase production, and therefore an acceleration
of triglyceride rich lipoprotein
breakdown;
¾
a rise in apo A-I and apo A-II production, and a corresponding rise in
HDL.
After oral administration, fenofibrate is rapidly hydrolysed to
fenofibric acid, the active metabolite.
Fenofibrate’s absorption is low and variable when the product is
administered under fasting conditions.
Fenofibrate’s absorption is increased when the compo