|
Lipanthyl®
supra 160
NAME OF THE MEDICINAL PRODUCT
LIPANTHYL® SUPRA 160 mg
PHARMACEUTICAL FORM
Film-coated tablet.
COMPOSITION FOR ONE TABLET
Active ingredient: Fenofibrate (INN) 160 mg.
Excipients: Sodium laurilsulfate, lactose monohydrate, povidone, cellulose
microcrystalline, silica colloidal anhydrous, crospovidone, sodium stearyl
fumarate.
Composition of the coating: polyvinyl alcohol, titanium dioxide (E171),
talc, (soybean) lecithin, xanthan gum.
PHARMACOLOGICAL PROPERTIES
Serum Lipid Reducing Agents/Cholesterol and Triglycerides Reducers/Fibrates.
ATC code: C10 AB 05
Fenofibrate is a fibric acid derivative whose lipid modifying effects
reported in humans are mediated via activation of Peroxisome Proliferator
Activated Receptor type alpha (PPARα ).
Through activation of PPARα
, fenofibrate increases the lipolysis and elimination of atherogenic
triglyceride-rich particles from plasma by activating lipoprotein lipase and
reducing production of apoprotein CIII. Activation of PPARα also induces
an increase in the synthesis of apoproteins AI and AII.
The above stated effects of fenofibrate on lipoproteins lead to a reduction
in very low- and low density fractions (VLDL and LDL) containing apoprotein
B and an increase in the high density lipoprotein fraction (HDL) containing
apoprotein AI and AII.
In addition, through modulation of the synthesis and
the catabolism of VLDL fractions, fenofibrate increases the LDL clearance
and reduces small and dense LDL, the levels of which are elevated in the
atherogenic lipoprotein phenotype, a common disorder in patients at risk for
coronary heart disease.
During clinical trials with fenofibrate, total cholesterol was reduced by 20
to 25%, triglycerides by 40 to 55% and HDL cholesterol was increased by 10
to 30%.
In hypercholesterolaemic patients, where LDL cholesterol levels are reduced
by 20 to 35%, the overall effect on cholesterol results in a decrease in the
ratios of total cholesterol to HDL cholesterol, LDL cholesterol to HDL
cholesterol, or Apo B to Apo AI, all of which are markers of atherogenic
risk.
Because of its significant effect on LDL cholesterol and triglycerides,
treatment with fenofibrate should be beneficial in hypercholesterolaemic
patients with or without hypertriglyceridaemia, including secondary
hyperlipoproteinaemia such as type 2 diabetes mellitus.
At the present time, no results of long-term controlled clinical trials are
available to demonstrate the efficacy of fenofibrate in the primary or
secondary prevention of atherosclerotic complications. Extravascular
deposits of cholesterol (tendinous and tuberous xanthoma) may be markedly
reduced or even entirely eliminated during fenofibrate therapy.
Patients with raised levels of fibrinogen treated with fenofibrate have
shown significant reductions in this parameter, as have those with raised
levels of Lp(a). Other inflammatory markers such as C Reactive Protein are
reduced with fenofibrate treatment.
The uricosuric effect of fenofibrate
leading to reduction in uric acid levels of approximately 25% should be of
additional benefit in those dyslipidaemic patients with hyperuricaemia.
Fenofibrate has been shown to possess an anti-aggregatory effect on
platelets in animals and in a clinical study, which showed a reduction in
platelet aggregation induced by ADP, arachidonic acid and epinephrine.
Pharmacokinetic properties
LIPANTHYL® SUPRA 160 mg is a film-coated tablet containing 160 mg of micronised fenofibrate and is suprabioavailable (larger bioavailability)
compared to the previous formulations.
Absorption: Maximum plasma concentrations occur within 4 to 5 hours after
oral administration. Plasma concentrations are stable during continuous
treatment in any given individual. The absorption of fenofibrate is
increased when administered with food.
Distribution: Fenofibric acid is strongly bound to plasma albumin (more than
99%).
Plasma half-life: The plasma elimination half-life of fenofibric acid is
approximately 20 hours.
Metabolism and excretion: No unchanged fenofibrate can be detected in the
plasma where the principal metabolite is fenofibric acid. The drug is
excreted mainly in the urine. Practically all the drug is eliminated within
6 days. Fenofibrate is mainly excreted in the form of fenofibric acid and
its glucuronide conjugate. In elderly patients, the fenofibric acid apparent
total plasma clearance is not modified. Kinetic studies following the
administration of a single dose and continuous treatment have demonstrated
that the drug does not accumulate. Fenofibric acid is not eliminated by
haemodialysis.
INDICATIONS
Hypercholesterolaemia and hypertriglyceridaemia alone or combined (types IIa,
IIb, IV dyslipidaemias, as well as types III and V dyslipidaemias) in
patients unresponsive to dietary and other non-drug therapeutic measures
(e.g. weight reduction or increased physical activity), particularly when
there is evidence of associated risk. The treatment of secondary
hyperlipoproteinaemias is indicated if the hyperlipoproteinaemia persists
despite effective treatment of the underlying disease (e.g. dyslipidaemia in
diabetes mellitus).
Dietary measures initiated before therapy should be
continued.
CONTRA-INDICATIONS
LIPANTHYL® SUPRA 160 mg is contra-indicated in children, during pregnancy
or lactation, in patients with liver insufficiency (including biliary
cirrhosis and unexplained persistent liver function abnormality), severe
renal insufficiency (creatinine clearance < 20ml/min), in patients
hypersensitive to fenofibrate and/or excipients, known photoallergy or
phototoxic reaction during treatment with fibrates or ketoprofen, chronic or
acute pancreatitis with the exception of acute pancreatitis due to severe
hypertriglyceridemia, gallbladder disease.. LIPANTHYL® SUPRA 160 mg should
not be taken in patients allergic to peanut or arachis oil or soya lecithin
or related products due to the risk of hypersensitivity reactions.
1
2
|
