RIVA-PRAVASTATIN TABLET

Ülke: Kanada

Dil: İngilizce

Kaynak: Health Canada

Aktif bileşen:

PRAVASTATIN SODIUM

Mevcut itibaren:

LABORATOIRE RIVA INC.

ATC kodu:

C10AA03

INN (International Adı):

PRAVASTATIN

Doz:

20MG

Farmasötik formu:

TABLET

Kompozisyon:

PRAVASTATIN SODIUM 20MG

Uygulama yolu:

ORAL

Paketteki üniteler:

100

Reçete türü:

Prescription

Terapötik alanı:

HMG-COA REDUCTASE INHIBITORS

Ürün özeti:

Active ingredient group (AIG) number: 0122563002; AHFS:

Yetkilendirme durumu:

CANCELLED POST MARKET

Yetkilendirme tarihi:

2005-06-30

Ürün özellikleri

PRODUCT MONOGRAPH
RIVA PRAVASTATIN
(PRAVASTATIN SODIUM TABLETS)
10, 20, AND 40 MG
LIPID METABOLISM REGULATOR
Laboratoires Riva Inc.
660 boul. Industriel
Blainville (Québec)
J7C 3V4
Date of Preparation: July 28, 2004
Control#: 092967
2
PRODUCT MONOGRAPH
NAME OF DRUG
RIVA PRAVASTATIN
(PRAVASTATIN SODIUM TABLETS)
10, 20 and 40 mg
THERAPEUTIC CLASSIFICATION
Lipid Metabolism Regulator
ACTIONS AND CLINICAL PHARMACOLOGY
_Riva _
PRAVASTATIN (Pravastatin Sodium) is one of a new class of
lipid-lowering compounds known as
HMG-CoA
reductase
inhibitors
(statins)
that
reduce
cholesterol
biosynthesis.
These
agents
are
competitive inhibitors of 3-hydroxy- 3-methylglutaryl-coenzyme A
(HMG-CoA) reductase, the enzyme
catalyzing
the
early
rate-limiting
step
in
cholesterol
biosynthesis,
conversion
of
HMG-CoA
to
mevalonate. Pravastatin is isolated from a strain of
_Penicillium citrinum. _
The active drug substance is the
hydroxyacid form.
_Riva _
PRAVASTATIN produces its lipid-lowering effect in two ways. First, as
a consequence of its
reversible inhibition of HMG-CoA reductase activity, it effects modest
reductions in intracellular pools of
cholesterol. This results in an increase in the number of Low Density
Lipoproteins (LDL) - receptors on
cell surfaces and enhanced receptor-mediated catabolism and clearance
of circulating LDL. Second,
3
pravastatin inhibits LDL production by inhibiting hepatic synthesis of
Very Low Density Lipoproteins
(VLDL), the LDL precursor.
Epidemiologic and clinical investigations have associated the risk of
coronary artery disease (CAD) with
elevated levels of Total-C, LDL-C, and decreased levels of HDL-C.
These abnormalities of lipoprotein
metabolism are considered as major contributors to the development of
the disease. Other factors, e.g.
interactions between lipids/lipoproteins and endothelium, platelets
and macrophages, have also been
incriminated in the development of human atherosclerosis and of its
complications.
In long-term, prospective clinical trials effective treatment of
hypercholesterolemia