ZOCOR TABLET 10 mg

País: Cingapura

Língua: inglês

Origem: HSA (Health Sciences Authority)

Ingredientes ativos:

SIMVASTATIN

Disponível em:

ORGANON SINGAPORE PTE. LTD.

Código ATC:

C10AA01

Dosagem:

10.0 mg

Forma farmacêutica:

TABLET, FILM COATED

Composição:

SIMVASTATIN 10.0 mg

Via de administração:

ORAL

Tipo de prescrição:

Prescription Only

Fabricado por:

Organon Pharma (UK) Limited

Status de autorização:

ACTIVE

Data de autorização:

1990-02-01

Folheto informativo - Bula

ZOCOR                                          
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                SG-MK0733-T-072014 
(SIMVASTATIN) 

PHYSICIANS CIRCULAR

Tablets             Trademark 
ZOCOR® 
(simvastatin)

ZOCOR (simvastatin) is a lipid-lowering agent derived
synthetically from a fermentation product of 
_Aspergillus terreus_. 

After oral ingestion, ZOCOR, an inactive lactone, is hydrolyzed
to the corresponding β-hydroxyacid form. 
This is a principal metabolite and an
inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) 
reductase, the enzyme that catalyzes an early and
rate-limiting step in the biosynthesis of cholesterol. 
Clinical studies show ZOCOR to be highly effective in reducing
total plasma cholesterol (total-C), low-
density lipoprotein cholesterol (LDL-C), triglycerides (TG), and
very-low-density lipoprotein cholesterol 
(VLDL-C) concentrations, and
increasing high-density lipoprotein  cholesterol (HDL-C) in
heterozygous 
familial and non-familial forms of hypercholesterolemia, and in
mixed hyperlipidemia when elevated 
cholesterol was cause for concern and diet alone has been
insufficient. Marked responses are seen 
within 2 weeks, and maximum therapeutic responses occur within
4-6 weeks. The response is 
maintained during continuation of therapy. When therapy with ZOCOR is stopped, cholesterol and lipids

return to pretreatment levels. 

The active form of simvastatin is a
specific inhibitor of HMG-CoA reductase, the enzyme which
catalyzes 
the conversion of HMG-CoA to mevalonate.  Because the conversion of HMG-CoA to mevalonate is an 
early step in the
biosynthetic pathway of cholesterol, therapy with ZOCOR would
not be expected to 
cause an accumulation of potentially toxic sterols.  In
addition, HMG-CoA is also metabolized readily 
back to acetyl

Características técnicas

ZOCOR
SG-OG0733-T-052023
(simvastatin)
PHYSICIANS CIRCULAR
Tablets Trademark
ZOCORⓇ
(simvastatin)
ZOCOR (simvastatin) is a lipid-lowering agent derived synthetically
from a fermentation product of
Aspergillus terreus
.
After oral ingestion, ZOCOR, an inactive lactone, is hydrolyzed to the
corresponding β-hydroxyacid form.
This is a principal metabolite and an inhibitor of
3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA)
reductase, the enzyme that catalyzes an early and rate-limiting step
in the biosynthesis of cholesterol.
Clinical studies show ZOCOR to be highly effective in reducing total
plasma cholesterol (total-C), low-
density lipoprotein cholesterol (LDL-C), triglycerides (TG), and
very-low-density lipoprotein cholesterol
(VLDL-C) concentrations, and increasing high-density lipoprotein
cholesterol (HDL-C) in heterozygous
familial and non-familial forms of hypercholesterolemia, and in mixed
hyperlipidemia when elevated
cholesterol was cause for concern and diet alone has been
insufficient. Marked responses are seen within
2 weeks, and maximum therapeutic responses occur within 4-6 weeks. The
response is maintained during
continuation
of
therapy.
When
therapy
with
ZOCOR
is
stopped,
cholesterol
and
lipids
return
to
pretreatment levels.
The active form of simvastatin is a specific inhibitor of HMG-CoA
reductase, the enzyme which catalyzes
the conversion of HMG-CoA to mevalonate. Because the conversion of
HMG-CoA to mevalonate is an
early step in the biosynthetic pathway of cholesterol, therapy with
ZOCOR would not be expected to cause
an accumulation of potentially toxic sterols. In addition, HMG-CoA is
also metabolized readily back to
acetyl-CoA, which participates in many biosynthetic processes in the
body.
In animal studies, after oral dosing, simvastatin had high selectivity
for the liver, where it achieved
substantially higher concentrations than in non-target tissues.
Simvastatin undergoes extensive first-pass
extraction in the liver, the primary site of action, with subsequent
excretion of drug in the