Traykor 145 mg 30 pcs. film-coated tablets

Composition and release form

10 pcs in blister; in a cardboard pack there are 1, 2, 3, 5, 9 and 10 blisters; or in a blister 14 pcs.; in a cardboard pack there are 2, 6 and 7 blisters; or in a blister 10 pcs.; There are 28 and 30 blisters in a cardboard box (for hospitals).

10 pcs in blister; in a cardboard pack there are 1, 2, 3, 5, 9 and 10 blisters; or in a blister 14 pcs.; in a cardboard pack there are 2, 6 and 7 blisters.

Pharmacodynamics

Fenofibrate is a derivative of fibric acid, the ability of which to change lipid levels in the human body is mediated by activation of PPARα. By activating PPARα receptors (peroxisome proliferator-activated receptor alpha), fenofibrate enhances lipolysis and the removal from plasma of atherogenic lipoproteins with a high triglyceride content by activating lipoprotein lipase and reducing the synthesis of apolipoprotein CIII. Activation of PPARα also leads to increased synthesis of apolipoproteins AI and AII.

The effects of fenofibrate on lipoproteins described above lead to a decrease in the content of the LDL and VLDL fraction, which includes apolipoprotein B, and an increase in the content of the HDL fraction, which includes apolipoproteins AI and AII.

In addition, by correcting disturbances in VLDL synthesis and catabolism, fenofibrate increases LDL clearance and reduces the content of dense and small LDL particles, an increase in which is observed in patients with an atherogenic lipid phenotype (a common disorder in patients at risk of coronary heart disease).

In clinical studies, fenofibrate was observed to reduce total cholesterol by 20–25% and triglycerides by 40–55% while increasing HDL cholesterol by 10–30%. In patients with hypercholesterolemia, in whom LDL-cholesterol levels are reduced by 20-35%, fenofibrate use led to a decrease in the ratios: "total cholesterol/HDL-cholesterol", "LDL-cholesterol/HDL-cholesterol" and "Apo B/Apo AI" ", which are markers of atherogenic risk.

Given the effect of fenofibrate on LDL cholesterol and triglyceride levels, the use of the drug is effective in patients with hypercholesterolemia, both accompanied and not accompanied by hypertriglyceridemia, including secondary hyperlipoproteinemia, for example, type 2 diabetes mellitus.

During treatment with fenofibrate, extravascular cholesterol deposits (tendon and tuberous xanthomas) may significantly decrease and even completely disappear.

Patients with elevated fibrinogen levels treated with fenofibrate showed a significant decrease in this indicator, as did patients with elevated Lp(a) levels. Other markers of inflammation, such as C-reactive protein, also decrease with fenofibrate treatment.

For patients with dyslipidemia and hyperuricemia, an additional benefit is the uricosuric effect of fenofibrate, resulting in a reduction in uric acid concentrations of approximately 25%.

Fenofibrate has been shown to reduce platelet aggregation caused by adenosine diphosphate, arachidonic acid and epinephrine in a clinical study and in animal experiments.

Pharmacological properties of the drug Traykor 145 mg

fenofibrate is a fibric acid derivative. Its effects on lipid profiles observed in humans are mediated by activation of peroxisome proliferator-activated receptor alpha (PPARα). Through activation of PPARα, fenofibrate increases the intensity of lipolysis and the removal of TG-rich particles from the blood plasma by activating lipoprotein lipase and reducing the formation of apoprotein CIII. Activation of PPARα also causes an increase in the synthesis of apoproteins AI and AII. The above-mentioned effects of fenofibrate on LP lead to a decrease in the VLDL and LDL fractions that contain apoprotein B, and an increase in the HDL fraction that contains apoproteins AI and AII. In addition, by modifying the synthesis and catabolism of the VLDL fraction, fenofibrate increases the clearance of LDL and reduces the amount of LDL, which is elevated in the atherogenic lipoprotein phenotype, which is often noted in patients at risk for CAD. During clinical trials of fenofibrate, total cholesterol levels decreased by 20–25%, TG levels by 40–55%, and HDL cholesterol levels increased by 10–30%. In patients with hypercholesterolemia, in whom LDL cholesterol levels were reduced by 20–35%, the overall effect relative to cholesterol was a reduction in the ratios of total cholesterol to HDL cholesterol, LDL cholesterol to HDL cholesterol, or apoprotein B to apoprotein AI, which are markers of atherogenic risk. Due to its effect on LDL cholesterol and TG, treatment with fenofibrate has a positive effect both in patients with hypercholesterolemia in combination with hypertriglyceridemia and without it, including secondary hyperlipoproteinemia, the same as that detected in type II diabetes mellitus. To date, there are no results from long-term controlled studies to demonstrate the effectiveness of fenofibrate in the primary and secondary prevention of complications of atherosclerosis. Extravascular cholesterol deposits (xanthoma tendinosum et tuberosum) may significantly decrease or even completely disappear during fenofibrate therapy. Patients with elevated fibrinogen levels who were treated with fenofibrate showed a significant decrease in this parameter. Other markers of inflammation, such as CRP, are also reduced by fenofibrate treatment. The uricosuric effect of fenofibrate, which leads to a 25% reduction in uric acid levels, can be considered as an additional beneficial effect in patients with dyslipidemia in combination with hyperuricemia. It has been found that fenofibrate can reduce platelet aggregation induced by adenosine diphosphate, arachidonic acid and epinephrine. Trikor 145 mg tablets contain fenofibrate in the form of nanoparticles. Absorption Maximum plasma concentrations are achieved 2–4 hours after oral administration. Plasma concentrations are stable with continuous treatment. Unlike other fenofibrate preparations, the maximum plasma concentration and overall absorption of the drug, which contains fenofibrate nanoparticles, are not affected by food intake. Therefore, Traykor 145 mg tablets can be taken regardless of meals. A drug absorption study, which involved administering 145 mg tablets to healthy men and women on an empty stomach and with a high-fat meal, showed that the absorption rates (AUC and maximum plasma concentration) of fenofibric acid were not affected by food intake. Distribution Fenofibric acid has a high degree of binding to plasma albumin (more than 99%). Metabolism and Excretion Following oral administration, fenofibrate is rapidly hydrolyzed by esterases to the active metabolite fenofibric acid. Fenofibrate is not detected unchanged in blood plasma. Fenofibrate is not a substrate for CYP3A4 and does not participate in hepatic microsomal metabolism. Fenofibrate is excreted primarily in the urine. Almost completely eliminated in 6 days. It is excreted primarily in the form of fenofibric acid and its glucuronide conjugate. In elderly patients, the total plasma clearance of fenofibric acid does not change. Kinetic studies after a single dose and during long-term treatment showed that fenofibrate does not accumulate in the body. Fenofibric acid is not excreted by hemodialysis. The half-life of fenofibric acid from blood plasma is 20 hours.

Pharmacokinetics

Trikor® 145 mg film-coated tablets contain 145 mg of micronized fenofibrate in the form of nanoparticles.

The parent fenofibrate is not detectable in plasma. The main plasma metabolite is fenofibric acid.

Cmax in blood plasma is achieved 2–4 hours after oral administration. With long-term use, the concentration of the drug in plasma remains stable, regardless of the individual characteristics of the patient.

Unlike previous dosage forms of fenofibrate, the maximum plasma concentration and overall effect of nanoparticle fenofibrate are independent of food intake. Therefore, Trikor® 145 mg can be taken at any time, regardless of meals.

Fenofibric acid binds strongly to plasma albumin (more than 99%).

T1/2 of fenofibric acid is about 20 hours.

After oral administration, fenofibrate is rapidly hydrolyzed by esterases. Only the main active metabolite of fenofibrate, fenofibric acid, is detected in plasma. Fenofibrate is not a CYP3A4 substrate. Does not take part in microsomal metabolism.

Excreted primarily in urine as fenofibric acid and glucuronide conjugate. Within 6 days, fenofibrate is eliminated almost completely. The overall clearance of fenofibric acid, determined in elderly patients, does not change.

The drug does not accumulate after a single dose or with long-term use.

It is not excreted during hemodialysis.

Trikor® 160 mg film-coated tablets have higher bioavailability compared to earlier dosage forms of fenofibrate.

The parent fenofibrate is not detectable in plasma. The main plasma metabolite is fenofibric acid.

Cmax in blood plasma is achieved 4–5 hours after oral administration. With long-term use, the concentration of the drug in plasma remains stable. The absorption of fenofibrate is enhanced when taken simultaneously with food.

Fenofibric acid binds strongly to plasma albumin (more than 99%).

T1/2 of fenofibric acid is about 20 hours.

Only the main metabolite of fenofibrate, fenofibric acid, is detected in plasma. Excreted primarily in urine as fenofibric acid and glucuronide conjugate. Within 6 days, fenofibrate is eliminated almost completely. The overall clearance of fenofibric acid, determined in elderly patients, does not change.

The drug does not accumulate after a single dose or with long-term use.

It is not excreted during hemodialysis.

Traykor 145 mg 30 pcs. film-coated tablets

pharmachologic effect

Lipid-lowering agent - fibrate.

Composition and release form Traykor 145 mg 30 pcs. film-coated tablets

Tablets - 1 tablet:

• Active ingredient: fenofibrate (micronized) - 145.0 mg;
• Excipients: sucrose - 145.0 mg; sodium lauryl sulfate - 10.2 mg; lactose monohydrate - 132.0 mg; crospovidone - 75.5 mg; microcrystalline silicated cellulose - 86.0 mg; hypromellose - 29.0 mg; docusate sodium - 2.9 mg; magnesium stearate - 0.9 mg;
• Film coating: Opadry® OY-B-28920: [polyvinyl alcohol - 11.43 mg; titanium dioxide - 8.03 mg; talc 5.02 mg; soy lecithin - 0.50 mg; xanthan gum - 0.12 mg] - 25.1 mg.

10 tablets in PVC/PE/PVDC/Al blister. 1,2, 3, 5, 9, 10 blisters in a cardboard box along with instructions for use.

14 tablets per PVC/PE/PVDC/Al blister. 2, 6, 7 blisters in a cardboard box along with instructions for use.

10 tablets in PVC/PE/PVDC/Al blister. 28, 30 blisters in cardboard packs (packaging for hospitals). The cardboard pack contains an equal number of instructions for medical use.

Description of the dosage form

White, oblong, film-coated tablets with “145” written on one side and the F logo on the other side.

Directions for use and doses

It is necessary to continue to follow the cholesterol-lowering diet that the patient followed before starting treatment with Trikor 145 mg.

Traykor 145 mg tablets should be swallowed whole, without chewing, with water. Trikor 145 mg can be taken at any time of the day, regardless of meal times.

Adults.

One tablet of Traykor 145 mg once a day.

Patients taking one capsule of micronized fenofibrate 200 mg or one tablet of micronized fenofibrate 160 mg (Traykor 160 mg may be used) per day can switch to taking 1 tablet of Traykor 145 mg without additional dose adjustment.

Elderly patients without renal impairment

It is recommended to take the standard dose for adults (1 tablet per day).

The effectiveness of therapy should be assessed by the concentration of lipids (total cholesterol, LDL, triglycerides) in the blood serum. If there is no therapeutic effect after several months of therapy (usually after 3 months), the advisability of prescribing concomitant or alternative therapy should be considered.

Patients with liver dysfunction

Due to the insufficient amount of accumulated data on the use of the drug Traykor in patients with impaired liver function, it is not possible to give recommendations on the use of the drug in this category of patients.

Patients with impaired renal function

Patients with mild chronic renal failure (creatinine clearance above 60 ml/min) do not require dose adjustment.

Pharmacodynamics

Fenofibrate is a derivative of fibric acid, the ability of which to change lipid levels in the human body is mediated by activation of PPARalpha. By activating PPARalpha receptors (peroxisome proliferator-activated receptor alpha), fenofibrate enhances lipolysis and the elimination of atherogenic lipoproteins with high triglyceride content from plasma by activating lipoprotein lipase and reducing the synthesis of apolipoprotein CIII. Activation of PPARalpha also leads to increased synthesis of apolipoproteins AI and AII. The effects of fenofibrate on lipoproteins described above lead to a decrease in the content of the LDL and VLDL fraction, which includes apolipoprotein B, and an increase in the content of the HDL fraction, which includes apolipoproteins AI and AII. In addition, by correcting disturbances in VLDL synthesis and catabolism, fenofibrate increases LDL clearance and reduces the content of dense and small LDL particles, an increase in which is observed in patients with an atherogenic lipid phenotype (a common disorder in patients at risk of coronary heart disease).

In clinical studies, it was noted that the use of fenofibrate reduced total cholesterol by 20-25% and triglycerides by 40-55% while increasing HDL cholesterol by 10-30%. In patients with hypercholesterolemia, in whom LDL-cholesterol levels are reduced by 20-35%, the use of fenofibrate led to a decrease in the ratios: "total cholesterol/HDL-cholesterol", "LDL-cholesterol/HDL-cholesterol" and "Apo B/Apo AI" ", which are markers of atherogenic risk. Given the effect of fenofibrate on LDL cholesterol and triglyceride levels, the use of the drug is effective in patients with hypercholesterolemia, both accompanied and not accompanied by hypertriglyceridemia, including secondary hyperlipoproteinemia, for example, type 2 diabetes mellitus.

During treatment with fenofibrate, extravascular cholesterol deposits (tendon and tuberous xanthomas) may significantly decrease and even completely disappear. Patients with elevated fibrinogen levels treated with fenofibrate showed a significant decrease in this indicator, as did patients with elevated Lp(a) levels. Other markers of inflammation, such as C-reactive protein, also decrease with fenofibrate treatment. For patients with dyslipidemia and hyperuricemia, an additional benefit is the uricosuric effect of fenofibrate, resulting in a reduction in uric acid concentrations of approximately 25%. Fenofibrate has been shown to reduce platelet aggregation caused by adenosine diphosphate, arachidonic acid and epinephrine in a clinical study and in animal experiments.

Pharmacokinetics

Trikor® 145 mg film-coated tablets contain 145 mg of micronized fenofibrate in the form of nanoparticles. The parent fenofibrate is not detectable in plasma. The main plasma metabolite is fenofibric acid. Cmax in blood plasma is achieved 2-4 hours after oral administration. With long-term use, the concentration of the drug in plasma remains stable, regardless of the individual characteristics of the patient. Unlike previous dosage forms of fenofibrate, the maximum plasma concentration and overall effect of nanoparticle fenofibrate are independent of food intake.

Therefore, Trikor® 145 mg can be taken at any time, regardless of meals. Fenofibric acid binds strongly to plasma albumin (more than 99%). T1/2 of fenofibric acid is about 20 hours. After oral administration, fenofibrate is quickly hydrolyzed by esterases. Only the main active metabolite of fenofibrate, fenofibric acid, is detected in plasma. Fenofibrate is not a CYP3A4 substrate. Does not take part in microsomal metabolism. Excreted primarily in urine as fenofibric acid and glucuronide conjugate. Within 6 days, fenofibrate is eliminated almost completely. The total clearance of fenofibric acid, determined in elderly patients, does not change. The drug does not accumulate after a single dose or with long-term use. It is not excreted during hemodialysis.

Trikor® 160 mg film-coated tablets have higher bioavailability compared to earlier dosage forms of fenofibrate. The parent fenofibrate is not detectable in plasma. The main plasma metabolite is fenofibric acid. Cmax in blood plasma is achieved 4-5 hours after oral administration. With long-term use, the concentration of the drug in plasma remains stable. The absorption of fenofibrate is enhanced when taken simultaneously with food. Fenofibric acid binds strongly to plasma albumin (more than 99%). T1/2 of fenofibric acid is about 20 hours. Only the main metabolite of fenofibrate, fenofibric acid, is found in plasma. Excreted primarily in urine as fenofibric acid and glucuronide conjugate. Within 6 days, fenofibrate is eliminated almost completely. The overall clearance of fenofibric acid, determined in elderly patients, does not change. The drug does not accumulate after a single dose or with long-term use. It is not excreted during hemodialysis.

Indications for use Traykor 145 mg 30 pcs. film-coated tablets

Hypercholesterolemia (type IIa), endogenous hypertriglyceridemia (type IV) and their combination (types IIb and III) with insufficient effectiveness of the selected diet, hypercholesterolemia due to diet and/or in the presence of associated risk factors.

Contraindications

Hypersensitivity, pregnancy, lactation, childhood.

With caution. Liver and/or renal failure, cholelithiasis or nephrourolithiasis, liver cirrhosis, alcoholism.

Application of Traykor 145 mg 30 pcs. film-coated tablets during pregnancy and breastfeeding

Contraindicated during pregnancy, lactation period, and children.

special instructions

Before starting treatment with Trikor 145 mg, appropriate treatment should be carried out to eliminate the cause of secondary hypercholesterolemia, for example, in diseases such as uncontrolled type 2 diabetes mellitus, hypothyroidism, nephrotic syndrome, dysproteinemia, obstructive liver diseases, consequences of drug therapy, alcoholism.

In patients with hyperlipidemia taking estrogens or hormonal contraceptives containing estrogens, it is necessary to determine whether the hyperlipidemia is of a primary or secondary nature. In such cases, an increase in lipid concentrations may be caused by estrogen intake.

Effect on cardiovascular morbidity and mortality

The ACCORD clinical randomized placebo-controlled trial was conducted in 5518 patients with type 2 diabetes mellitus who received fenofibrate in addition to simvastatin therapy. The fenofibrate plus simvastatin group demonstrated a statistically nonsignificant 8% reduction in the relative risk of major cardiovascular events, including nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death, compared with simvastatin alone (hazard ratio 0.92, 95% CI 0.79-1.08, P=0.32; absolute risk reduction: 0.74%). A subgroup analysis of patients with dyslipidemia (triglycerides (TG) ≥ 2.3 mmol/L and high-density lipoprotein (HDL) cholesterol ≤ 0.88 mmol/L) demonstrated a statistically significant 31% reduction in the relative risk of major cardiovascular events in fenofibrate plus simvastatin group compared with simvastatin monotherapy group (hazard ratio 0.69, 95% CI 0.49-0.97, P=0.03; absolute risk reduction: 4.95%). Another subgroup analysis revealed a statistically significant difference between sexes (P=0.01), indicating a possible benefit of combination therapy in men (P=0.037) but a potentially higher risk in women (P=0.069) compared with simvastatin monotherapy.

The 5-year randomized, placebo-controlled FIELD trial was conducted in 9795 patients with type 2 diabetes treated with fenofibrate. Fenofibrate demonstrated a non-significant 11% reduction in the primary cardiovascular outcome (hazard ratio 0.89, 95% CI 0.75-1.05, P=0.16) and a statistically significant 11% reduction in the secondary outcome of overall cardiovascular disease. vascular system (risk ratio 0.89% (0.80-0.99), P = 0.04). There was a nonsignificant increase in all-cause mortality by 11% (hazard ratio 1.11, 95% CI 0.95-1.29, P=0.18) and a nonsignificant increase in mortality from coronary heart disease by 19% (hazard ratio 1.19, 95% CI 0.90-1.57, P=0.22) with fenofibrate versus placebo.

Liver function

When taking the drug Traykor and other drugs that reduce lipid concentrations, some patients have described an increase in the activity of “liver” transaminases. In most cases, this increase was temporary, minor and asymptomatic. It is recommended to monitor the activity of transaminases (alanine aminotransferase (ALT), aspartate aminotransferase (AST)) every 3 months during the first 12 months and periodically during further treatment. Patients whose activity of “liver” transaminases has increased during treatment require attention, and if the activity of ALT and AST increases by more than 3 times compared to the upper limit of normal, the drug is stopped. If symptoms of hepatitis appear (jaundice, itching), laboratory tests should be performed and, if the diagnosis of hepatitis is confirmed, the drug Traykor should be discontinued.

Pancreatitis

Cases of the development of pancreatitis have been described during treatment with Traykor. Possible causes of pancreatitis in these cases were: insufficient effectiveness of the drug in patients with severe hypertriglyceridemia, direct effects of the drug, as well as secondary phenomena associated with the presence of stones or sedimentation in the bile ducts, accompanied by obstruction of the common bile duct.

Muscles

When taking Trikor and other drugs that reduce lipid concentrations, cases of toxic effects on muscle tissue, with or without renal dysfunction, including very rare cases of rhabdomyolysis, have been described. The incidence of this disorder increases in the case of hypoalbuminemia and a history of impaired renal function.

Toxic effects on muscle tissue can be suspected based on patient complaints of weakness, diffuse myalgia, myositis, muscle spasms and cramps, and/or a marked increase in creatinine phosphokinase (CPK) activity (more than 5 times the upper limit of normal). In these cases, treatment with Trikor 145 mg should be discontinued.

The risk of developing rhabdomyolysis may increase in patients with a predisposition to myopathy and/or rhabdomyolysis, including age over 70 years, a family history of hereditary muscle diseases, hypothyroidism, and alcohol abuse. Such patients should be prescribed the drug only if the expected benefit outweighs the possible risk of developing rhabdomyolysis.

When taking Trikor 145 mg concomitantly with HMG-CoA reductase inhibitors or other fibrates, the risk of serious toxic effects on muscle fibers increases, especially if the patient had a muscle disease before starting treatment. In this regard, the joint prescription of Trikor 145 mg and a statin is permissible only if the patient has severe mixed dyslipidemia and high cardiovascular risk, in the absence of a history of muscle disease and under conditions of close monitoring aimed at identifying signs of the development of toxic effects on muscle tissue.

Renal function

If the creatinine concentration increases by more than 50% above the upper limit of normal, treatment should be suspended. It is recommended to determine creatinine concentrations in the first 3 months and periodically during further treatment.

Hematological disorders

After initiation of fenofibrate therapy, patients experienced a mild to moderate decrease in hemoglobin levels, a decrease in hematocrit, and a decrease in white blood cell count. However, with long-term use of the drug, the values ​​of these indicators stabilize. Thrombocytopenia and agranulocytosis have been reported in individual patients receiving fenofibrate. During the first twelve months from the start of therapy with Traykor, periodic monitoring of the level of red blood cells and white blood cells is recommended.

Hypersensitivity reactions

Immediate hypersensitivity

Cases of anaphylaxis and angioedema have been reported during post-marketing use of fenofibrate. In some cases, such reactions were life-threatening for the patient and required emergency treatment. If signs or symptoms of immediate hypersensitivity are observed, consult a doctor immediately and stop using fenofibrate.

Delayed hypersensitivity

During post-marketing use of fenofibrate, cases of serious adverse skin reactions to the drug have been reported, including Stevens-Johnson syndrome, toxic epidermal necrolysis, and drug reaction with eosinophilia and systemic manifestations (DRESS syndrome). Such reactions developed over a period of time ranging from several days to several weeks from the start of fenofibrate therapy. Cases of DRESS syndrome have been accompanied by skin reactions such as rash or exfoliative dermatitis, and a combination of eosinophilia and fever involving the renal, hepatic or respiratory systems. If serious adverse skin reactions to the drug are suspected, fenofibrate should be discontinued and specific treatment should be initiated.

Thromboembolic complications

In the FIELD study, patients receiving fenofibrate had a comparatively higher incidence of pulmonary embolism and deep vein thrombosis than patients receiving placebo. Of the 9795 patients enrolled in the FIELD trial, 4900 patients were randomized to placebo and 4985 patients were randomized to fenofibrate. In the group of patients receiving placebo, 48 cases (1.0%) of deep vein thrombosis were reported, and in the group of patients receiving fenofibrate, 67 such cases (1.4%) were recorded; P=0.074. In the placebo group, 32 cases (0.7%) of pulmonary embolism were reported; in the group of patients receiving fenofibrate - 53 cases (1.0%); P=0.022.

Paradoxical reduction in HDL cholesterol

In clinical studies and post-marketing use, cases of marked reductions in HDL cholesterol levels (less than 2 mg/dL) after initiation of fibrate therapy in patients with and without diabetes have been described. The decrease in HDL cholesterol was accompanied by a decrease in apolipoprotein A1. This reduction usually developed between 2 weeks and several years after initiation of fibrates. HDL cholesterol levels remained low as long as fibrate therapy was continued. A rapid and sustained response was observed after discontinuation of fibrate therapy.

The clinical significance of this reduction in HDL cholesterol has not been established. It is recommended to monitor HDL cholesterol levels during the first few months after initiating fibrate therapy. If there is a significant decrease in HDL cholesterol levels, the drug should be discontinued and HDL cholesterol levels should continue to be monitored until they return to baseline values. Fibrates should not be re-prescribed in such patients.

Impact on the ability to drive vehicles and operate machinery

Traykor 145 mg has no or minimal effect on the ability to drive a vehicle and operate machinery (risk of developing dizziness).

Overdose

Cases of overdose have not been described. A specific antidote is unknown. If an overdose is suspected, symptomatic and, if necessary, supportive treatment should be prescribed. Hemodialysis is ineffective.

Side effects Traykor 145 mg 30 pcs. film-coated tablets

Dyspepsia, nausea, vomiting, diarrhea, cholelithiasis, increased activity of liver transaminases and CPK, myalgia, myositis, rhabdomyolysis, dizziness, excessive fatigue, decreased potency, allergic skin reactions.

Drug interactions

Oral anticoagulants: fenofibrate enhances the effect of oral anticoagulants and may increase the risk of bleeding, which is associated with the displacement of the anticoagulant from sites of binding to plasma proteins. At the beginning of treatment with fenofibrate, it is recommended to reduce the dose of anticoagulants by approximately one third, followed by gradual titration of the dose. Dose selection is recommended to be done under the control of INR levels.

Cyclosporine: Several severe cases of reversible decline in renal function have been reported during concomitant treatment with fenofibrate and cyclosporine. Therefore, it is necessary to monitor the status of renal function in such patients and discontinue fenofibrate in case of serious changes in laboratory parameters.

HMG-CoA reductase inhibitors and other fibrates: When fenofibrate is taken concomitantly with HMG-CoA reductase inhibitors or other fibrates, the risk of serious toxic effects on muscle fibers increases (see section "Special Instructions").

Cytochrome P450 enzymes: In vitro studies of human liver microsomes have shown that fenofibrate and fenofibric acid are not inhibitors of the following cytochrome P450 isoenzymes: CYP3A4, CYP2D6, CYP2E1 or CYP1A2. At therapeutic concentrations, these compounds are weak inhibitors of the CYP2C19 and CYP2A6 isoenzymes and weak to moderate inhibitors of CYP2C9.

Indications for the drug Traykor

hypercholesterolemia and hypertriglyceridemia isolated or mixed (dyslipidemia type IIa, IIb, III, IV, V) (table 145 mg) and (dyslipidemia type IIa, IIb, III*, IV, V*) (table 160 mg) in patients for whom diet or other non-drug treatment interventions (for example, weight loss or increased physical activity) have been ineffective, especially in the presence of risk factors associated with dyslipidemia, such as hypertension and smoking;

secondary hyperlipoproteinemia in cases where hyperlipoproteinemia persists despite effective treatment of the underlying disease (for example, dyslipidemia in diabetes mellitus).

When using the drug Trikor®, patients should adhere to the diet that they followed before starting treatment.

* Clinical studies included only a few patients with dyslipidemia types III and V.

Contraindications

hypersensitivity to fenofibrate or other components of the drug;

severe liver failure (including liver cirrhosis);

severe renal failure (Cl creatinine <20 ml/min);

age under 18 years;

a history of photosensitivity or phototoxicity during treatment with fibrates or ketoprofen;

gallbladder diseases;

breastfeeding period;

congenital galactosemia, lactase deficiency, impaired absorption of glucose and galactose (the drug contains lactose);

congenital fructosemia, sucrase-isomaltase deficiency (the drug contains sucrose) (table 145 mg);

history of an allergic reaction to peanuts, peanut butter, soy lecithin or related products (due to the risk of developing a hypersensitivity reaction).

Carefully:

liver and/or kidney failure;

hypothyroidism;

patients who abuse alcohol;

elderly patients;

patients with a history of hereditary muscle diseases;

simultaneous use of oral anticoagulants, HMG-CoA reductase inhibitors (see section “Interaction”).

Contraindications to the use of the drug Traykor 145 mg

Liver failure (including biliary cirrhosis); renal failure; childhood; hypersensitivity to fenofibrate or other components of the drug; photosensitivity or phototoxic reactions during treatment with fibrates or ketoprofen in the past; gallbladder disease (cholelithiasis). Trikor 145 mg should not be taken by patients with allergies to peanut butter or soy lecithin, or related products (possible risk of hypersensitivity reactions).

Use during pregnancy and breastfeeding

There are limited data on the use of fenofibrate in pregnant women. In animal experiments, the teratogenic effect of fenofibrate was not observed. Embryotoxicity has been observed when doses toxic to the mother were administered during preclinical trials. The potential risk to humans is unknown. Therefore, during pregnancy, Trikor® tablets can be used only after a careful assessment of the risk-benefit ratio.

Due to the lack of data on the safety of use, the drug is contraindicated for use during breastfeeding.

Side effects

The frequency of the adverse reactions listed below was determined as follows: very often (≥1/10), often (>1/100, <1/10); sometimes (>1/1000, <1/100); rare (>1/10000, <1/1000); very rare (<1/10000), including isolated reports.

From the gastrointestinal tract: often - abdominal pain, nausea, vomiting, diarrhea and moderate flatulence; sometimes - cases of pancreatitis.

From the liver: often - a moderate increase in the concentration of serum transaminases; sometimes - the formation of gallstones; very rarely - episodes of hepatitis. If symptoms of hepatitis appear (jaundice, itching), laboratory tests should be performed and, if hepatitis is confirmed, fenofibrate should be discontinued. (See "Special Instructions").

From the musculoskeletal system and connective tissue: rarely - diffuse myalgia, myositis, muscle spasms and weakness; very rarely - rhabdomyolysis (acute necrosis of skeletal muscles).

Vascular disorders: sometimes - venous thromboembolism (pulmonary embolism, deep vein thrombosis).

From the circulatory and lymphatic system: rarely - increased levels of hemoglobin and leukocytes.

From the nervous system: rarely - sexual dysfunction, headache.

From the respiratory system: very rarely - interstitial pneumopathy.

From the skin and subcutaneous fat: sometimes - rash, itching, urticaria or photosensitivity reactions; rarely - alopecia; very rarely - photosensitivity, accompanied by erythema, the formation of blisters or nodules on areas of the skin exposed to sunlight or artificial UV irradiation, such as a quartz lamp (in some cases, after many months of use without any complications).

Laboratory tests: sometimes - increased levels of creatinine and urea in the serum.

Interaction

Oral anticoagulants: fenofibrate enhances the effect of oral anticoagulants and may increase the risk of bleeding, which is associated with the displacement of the anticoagulant from sites of binding to plasma proteins.

At the beginning of treatment with fenofibrate, it is recommended to reduce the dose of anticoagulants by approximately one third, followed by gradual titration of the dose. Dose selection is recommended to be done under the control of INR levels.

Cyclosporine: Several severe cases of reversible decline in renal function have been reported during concomitant treatment with fenofibrate and cyclosporine. Therefore, it is necessary to monitor the status of renal function in such patients and discontinue fenofibrate in case of serious changes in laboratory parameters.

HMG-CoA reductase inhibitors and other fibrates: When fenofibrate is taken concomitantly with HMG-CoA reductase inhibitors or other fibrates, the risk of serious toxic effects on muscle fibers increases (see section "Special Instructions").

Cytochrome P450 enzymes: In vitro studies of human liver microsomes have shown that fenofibrate and fenofibric acid are not inhibitors of the following cytochrome P450 isoenzymes: CYP3A4, CYP2D6, CYP2E1 or CYP1A2. At therapeutic concentrations, these compounds are weak inhibitors of the CYP2C19 and CYP2A6 isoenzymes and weak to moderate inhibitors of CYP2C9.

Interactions of the drug Traykor 145 mg

Oral anticoagulants Fenofibrate enhances the effect of oral anticoagulants and may increase the risk of bleeding. It is recommended to reduce the dose of anticoagulants by 1/3 at the beginning of treatment and then gradually increase it, if necessary, under the control of INR (international normalized ratio). Cyclosporine Several severe cases of renal impairment have been reported with concomitant use of fenofibrate and cyclosporine, and renal function should be closely monitored in these patients. Treatment with Trikor 145 mg should be discontinued in case of significant deviations in laboratory parameters. HMG-CoA reductase inhibitors and other fibrates The risk of serious muscle toxicity is increased when used concomitantly with HMG-CoA reductase inhibitors or other fibrates. This combination should be used with caution and carefully monitored for signs of muscle toxicity (see WARNINGS). Cytochrome P450 Enzymes An in vitro using human liver microsomes showed that fenofibrate and fenofibric acid are not inhibitors of cytochrome (CYP) P450 isoforms CYP 3A4, CYP 2D6, CYP 2E1 or CYP 1A2. They are weak inhibitors of CYP 2C19 and CYP 2A6 and have a weak to moderate inhibitory effect on CYP 2C9 at therapeutic concentrations, which must be taken into account when coadministered with drugs that are metabolized by these cytochrome P450 isoforms.

Directions for use and doses

Orally, swallowing whole, without chewing, with a glass of water, at any time of the day, regardless of meals (table 145 mg) and simultaneously with meals (table 160 mg).

Adults, 1 tablet. 1 time per day. Patients taking 1 caps. Lipantil 200 M or 1 tablet. Trikora® 160 mg/day, can switch to taking 1 tablet. Trikora® 145 mg without additional dose adjustment. Patients taking 1 caps. Lipantil 200 M per day, can switch to taking 1 tablet. Trikora® 160 mg without additional dose adjustment.

Elderly patients: it is recommended to take the standard dose for adults (1 tablet of Trikor® 1 time per day).

Patients with renal failure require a dose reduction (see section "Special Instructions").

The use of the drug in patients with liver diseases has not been studied.

The drug should be taken for a long time, while continuing to follow the diet that the patient followed before starting treatment with Trikor®. The effectiveness of drug treatment should be periodically assessed by a doctor.

The effectiveness of therapy should be assessed by the content of lipids (total cholesterol, LDL, triglycerides) in the blood serum. If there is no therapeutic effect after several months of therapy (usually after 3 months), the advisability of prescribing concomitant or alternative therapy should be considered.

Use of the drug Traykor 145 mg

In combination with diet therapy, the drug is intended for long-term treatment, the effectiveness of which must be periodically monitored by determining the level of lipids in the blood serum (total cholesterol, LDL cholesterol, TG). If, after using the drug for several months (for example, 3 months), serum lipid levels have not decreased sufficiently, additional treatment or other types of therapy should be considered. Doses Adults The recommended dose is 145 mg (1 tablet) 1 time per day. Patients taking fenofibrate at a dose of 200 mg can replace it with 1 tablet of Trikor 145 mg without additional dose adjustment. Elderly Patients The usual adult dose is recommended for elderly patients. Patients with renal failure Patients with renal failure require dose reduction. Such patients are recommended to take drugs that contain lower doses of fenofibrate (100 mg or 67 mg). Children Traykor 145 mg is contraindicated for the treatment of children. Liver diseases The use of the drug in patients with liver diseases has not been studied. Directions for use The tablets must be swallowed whole with a glass of water. Trikor 145 mg tablets can be taken at any time throughout the day, regardless of meals.

special instructions

Before starting treatment with Trikor®, appropriate treatment should be carried out to eliminate the cause of secondary hypercholesterolemia, for example, in such conditions and diseases as uncontrolled diabetes mellitus type 2, hypothyroidism, nephrotic syndrome, dysproteinemia, obstructive liver diseases, consequences of drug therapy, alcoholism.

The effectiveness of therapy should be assessed by the content of lipids (total cholesterol, LDL, triglycerides) in the blood serum. If there is no therapeutic effect after several months of therapy (usually after 3 months), the advisability of prescribing concomitant or alternative therapy should be considered.

In patients with hyperlipidemia taking estrogens or hormonal contraceptives containing estrogens, it is necessary to determine whether the hyperlipidemia is of a primary or secondary nature. In such cases, the increase in lipid levels may be caused by estrogen intake.

Liver function: When taking Trikor® and other drugs that reduce lipid concentrations, increased levels of hepatic transaminases have been described in some patients. In most cases, this increase was temporary, minor and asymptomatic. During the first 12 months of treatment, it is recommended to monitor transaminase levels (ALT, AST) every 3 months. Patients whose transaminase concentrations have increased during treatment require attention, and if the concentrations of ALT and AST increase more than 3 times compared to the upper limit of normal, the drug should be stopped.

Pancreatitis: cases of pancreatitis developing during treatment with Trikor® have been described. Possible causes of pancreatitis in these cases were: insufficient effectiveness of the drug in patients with severe hypertriglyceridemia, direct effects of the drug, as well as secondary phenomena associated with the presence of stones or sediment formation in the gallbladder, accompanied by obstruction of the common bile duct.

Muscles: When taking Trikor® and other drugs that reduce lipid concentrations, cases of toxic effects on muscle tissue, including very rare cases of rhabdomyolysis, have been described. The incidence of this disorder increases in the case of hypoalbuminemia and a history of renal failure. The possibility of this complication increases in cases of hypoalbuminemia and renal failure.

Toxic effects on muscle tissue can be suspected based on patient complaints of weakness, diffuse myalgia, myositis, muscle spasms and cramps, and/or a marked increase in creatine phosphokinase activity (more than 5 times the upper limit of normal). In these cases, treatment with Trikor® must be stopped.

The risk of developing rhabdomyolysis may increase in patients with a predisposition to myopathy and/or rhabdomyolysis, including age over 70 years, a family history of hereditary muscle diseases, impaired renal function, hypothyroidism, and alcohol abuse. Such patients should be prescribed the drug only if the expected benefit outweighs the possible risk of developing rhabdomyolysis.

When taking Trikor® concomitantly with HMG-CoA reductase inhibitors or other fibrates, the risk of serious toxic effects on muscle fibers increases, especially if the patient had a muscle disease prior to treatment. In this regard, the joint prescription of Trikor® and a statin is permissible only if the patient has severe mixed dyslipidemia and high cardiovascular risk, in the absence of a history of muscle disease and under conditions of close monitoring aimed at identifying signs of the development of a toxic effect on muscle tissue.

Renal function: If creatinine concentration increases to more than 50% above the upper limit of normal, treatment should be suspended. In the first 3 months of treatment, it is recommended to determine creatinine concentrations.

When using the drug, there was no effect on the ability to drive a car or operate machinery.

Special instructions for the use of the drug Traykor 145 mg

The prescription of Traykor 145 mg is especially indicated in the presence of obvious concomitant risk factors, such as hypertension (arterial hypertension) and smoking. In case of hypercholesterolemia of secondary origin, before starting treatment with Trikor 145 mg, it is necessary to carry out adequate therapy for the conditions that caused it, or eliminate other possible causes, which include, for example, decompensated type II diabetes mellitus, hypothyroidism, nephrotic syndrome, dysproteinemia (for example, in myeloma ), hyperbilirubinemia, pharmacotherapy (oral contraceptives, corticosteroids, antihypertensive drugs, protease inhibitors for the treatment of HIV infection), alcoholism. The effect of treatment should be monitored by determining the level of lipids in the blood serum (total cholesterol, LDL, TG). If an adequate effect has not been achieved within several months (for example, 3 months), additional treatment or other types of therapy should be considered. In patients with hyperlipidemia who are taking estrogen preparations or contraceptives containing estrogens, it is necessary to check whether the hyperlipidemia is primary or secondary in origin, since lipid levels may increase with the use of oral estrogens. Liver function As with the use of other lipid-lowering drugs, increased transaminase activity was observed in some patients. In most cases it was transient, minor and asymptomatic. It is recommended to check transaminase activity every 3 months during the first 12 months of treatment. It is necessary to monitor the condition of patients in whom increased transaminase levels are detected. If the level of ALT and AST increases by more than 3 times compared to the upper limit of normal, the drug must be discontinued. Pancreatitis Cases of pancreatitis have been reported in patients taking fenofibrate. Its occurrence may be the result of treatment failure in patients with severe hypertriglyceridemia, a direct effect of a drug, or due to another cause, such as a bile duct stone or blockage of the common bile duct. Muscle Toxic effects on muscle, including very rare cases of rhabdomyolysis, have been reported during therapy with fibrates and other lipid-lowering drugs. Its frequency increases with hypoalbuminemia or renal failure. The possible toxic effect on muscles should be taken into account in patients with diffuse myalgia, cramps and muscle weakness, as well as with a pronounced increase in CPK (5 times compared to normal). In these cases, treatment with Trikor 145 mg should be discontinued. If there are factors that predict susceptibility to myopathy and/or rhabdomyolysis, including age over 70 years, hereditary muscle disease in the patient or family members, kidney disease, hypothyroidism, or alcohol abuse, patients may be at increased risk of developing rhabdomyolysis. In such patients, it is necessary to carefully evaluate the benefits and risks of treatment with Trikor 145 mg. The risk of muscle toxicity may be increased if the drug is co-administered with another fibrate or HMG-CoA reductase inhibitor, especially in the presence of concomitant muscle diseases. Therefore, it is advisable to prescribe the combination of fenofibrate and a statin only to patients with severe combined dyslipidemia and a high risk of cardiovascular disease in the absence of a history of muscle diseases and to carry out treatment under careful monitoring of possible toxic effects on muscles. Renal function Treatment should be discontinued if creatinine levels increase by more than 50% above the upper limit of normal. It is recommended to consider the need to monitor creatinine levels during the first months after starting treatment. Trikor 145 mg contains lactose, therefore patients with hereditary diseases such as galactose intolerance, Lapp lactase deficiency or glucose-galactose malabsorption should not take this drug. Trikor 145 mg contains sucrose, therefore patients with hereditary diseases such as fructose intolerance, glucose-galactose malabsorption or sucrase-isomaltase deficiency should not take this drug. Use during pregnancy and lactation There are no adequate data on the use of fenofibrate during pregnancy. Animal studies have not established teratogenic effects. Embryotoxic effects have been detected at maternally toxic doses. The potential risk for humans is unknown, therefore Trikor 145 mg can be used during pregnancy only after a careful assessment of the benefit/risk ratio. There are no data on the excretion of fenofibrate and/or its metabolites into breast milk, therefore Trikor 145 mg should not be taken by mothers who are breastfeeding. The ability to influence reaction speed when driving vehicles or working with other mechanisms. No effects were noted.