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Tricor (Fenofibrate)

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Tricor is the medication of high quality, which is taken in treatment of high triglyceride levels and high cholesterol with diet changes. Tricor is acting by increasing enzyme which breaks down fats in the blood. It is fibrate (lipid-lowering agent).

Other names for this medication:
Antara, Antilip, Apteor, Catalip, Controlip, Craveril, Docfenofi, Durafenat, Einecs, Elipsia, Evothyl, Febira, Fegenor, Felosma, Fenobeta, Fenobrat, Fenobrate, Fenocap, Fenofib, Fenofibrat, Fenofibrate, Fenofibrato, Fenofibratum, Fenofix, Fenogal, Fenoglide, Fenohexal, Fenolid, Fenolip, Fenoratio, Fenosup, Fenox, Fibrafen, Fibral, Fulcro, Grofibrat, Hafenthyl, Hyperchol, Katalip, Lexemin, Lifen, Lifibrat, Lipanthyl, Lipantil, Liparison, Lipcor, Liperial, Lipicard, Lipidcare, Lipidil, Lipidof, Lipilfen, Lipirate, Lipired, Lipirex, Lipivim, Lipofen, Lipofene, Lipofib, Lipohexal, Lipolin, Lipsin, Lofat, Lofibra, Lowlip, Minuslip, Naftilan, Nofiate, Nolipax, Normalip, Normolip, Nubrex, Nuozhituo, Phenofibrate, Procetofen, Procetoken, Proctofene, Secalip, Stanlip, Supralip, Suprelip, Tilene, Trigent, Triglide, Trilipix, Trolip, Versamid, Xafenor, Yosenob, Zumafib

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Also known as:  Fenofibrate.


Tricor is the medication of high quality, which is taken in treatment of high triglyceride levels and high cholesterol with diet changes.

The target of this perfect remedy is the treatment of high triglyceride levels and high cholesterol with diet changes.

Tricor is also known as Fenofibrate, Fenofibric acid, Lipicard, Lofibra, Lipanthyl, Fenocor-67.

Tricor is acting by increasing enzyme which breaks down fats in the blood. It is fibrate (lipid-lowering agent).

Generic name of Tricor is Fenofibrate.

Brand names of Tricor are Tricor, Tricor, Antara, Triglide, Lofibra, Lipofen.


Tricor can be taken once a day. Take Tricor capsules orally with water at the same time every day, with food.

If you are taking colestipol (such as Colestid) or cholestyramine (such as Questran) while using Tricor you should take these medicines at least 1 hour after using Tricor or 4-6 hours before using Tricor.

Follow low-fat diet, low-cholesterol.

If you want to achieve most effective results do not stop taking Tricor suddenly.


If you overdose Tricor and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Tricor if you are allergic to its components.

Do not take Tricor if you're pregnant or you plan to have a baby, or you are a nursing mother. Tricor can ham your baby.

Be careful with Tricor if you suffer from liver cirrhosis, hepatitis, severe kidney disease, gallbladder disease, diabetes, kidney, liver, heart disease, hypothyroidism.

Be careful with Tricor if you are taking such medicines as blood thinner (warfarin (such as Coumadin)); fluvastatin (such as Lescol), cholesterol-lowering medicines (lovastatin (such as Mevacor), simvastatin (such as Zocor), cerivastatin (such as Baycol), pravastatin (such as Pravachol), atorvastatin (such as Lipitor), cyclosporine (such as Gengraf, Neoral, Sandimmune).

If you experience drowsiness and dizziness while taking Tricor you should avoid any activities such as driving or operating machinery.

Avoid alcohol.

Elderly people should be very careful with Tricor.

Keep low-cholesterol and low-fat diet.

Do not stop taking Tricor suddenly.

tricor and alcohol

Fenofibrate-loaded LFCS Type III SNEDDS formulations could be a potential oral pharmaceutical product for administering the poorly water-soluble drug, fenofibrate, with an enhanced oral BA.

tricor cholesterol medicine

Alterations in Abcb4(-/-) mice, compared with wild-type mice, included deregulation of genes that control lipid synthesis, storage, and oxidation; decreased serum levels of cholesterol and phospholipids; and reduced hepatic long-chain fatty acyl-CoAs (LCA-CoA). Feeding Abcb4(-/-) mice the side chain-modified bile acid 24-norursodeoxycholic acid (norUDCA) reversed their liver injury and fibrosis, increased serum levels of lipids, lowered phospholipase and triglyceride hydrolase activities, and restored hepatic LCA-CoA and triglyceride levels. Additional genetic and nutritional studies indicated that lipid metabolism contributed to chronic cholestatic liver injury; crossing peroxisome proliferator-activated receptor (PPAR)-α-deficient mice with Abcb4(-/-) mice (to create double knockouts) or placing Abcb4(-/-) mice on a high-fat diet protected against liver injury, with features similar to those involved in the response to norUDCA. Placing pregnant Abcb4(-/-) mice on high-fat diets prevented liver injury in their offspring. However, fenofibrate, an activator of PPARα, aggravated liver injury in Abcb4(-/-) mice.

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Fenofibrate was associated with a 19% reduction in serum urate after 3 weeks of treatment (mean+/-S.E. 0.37+/-0.04 vs 0.30+/-0.02 mM/l; P=0.004). The effect was reversed after a 3-week fenofibrate withdrawal period (0.30+/-0.02 vs 0.38+/-0.03 mM/l). There was a rise in uric acid clearance with fenofibrate treatment of 36% (7.2+/-0.9 vs 11.4+/-1.6 ml/min, normal range 6-11; P=0.006) without a significant change in creatinine clearance. Both total cholesterol and serum triglycerides were also reduced. No patient developed acute gout whilst taking fenofibrate.

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In the primary prevention of atherosclerosis and risk of lipoproteinemia, is of primordial importance. Therefore, adequate food and physical activities are necessary. If no good result is evident thereafter medicinal treatment should be prescribed. In our open random study performed in two different centres, we evaluated the efficiency and tolerance of Gemfibrozile and Phenofibrate in 77 patients with IIa, IIb, and IV stage of hyperlipoproteinaemia. The study included the patients in whom the 8-week diet gave no expected results. The evaluation of Gemfibrosile (900 mg daily) and Phenofibrate (300 m daily) efficiency lasted 12 weeks. During that time 11 patients were excluded from the study because of administration of other relevant drugs or for lack of control examinations. The efficiency was evaluated in 66 patients: 33 to Gemfibrozile and 31 to Phenofibrate. At the end of treatment the following results were obtained: decreased cholesterol level by 17% in Gemfibrozile patients and by 6% in Phenofibrate subjects; LDL-cholesterol by 15% i.e. 3% and triglycerides by 48% in Gemfibrozile cases and by 27% in Phenofibrate individuals. At the end of treatment HDL-cholesterol was increased by 29% in patients treated with Gemfibrozile and by 9% in those treated with Phenofibrate. Apoprotein A-1 was increased after Phenofibrate treatment and decreased after Gemfibrozile administration. Apoprotein B was increased in both groups. No harmful clinical or laboratory effects were observed. On the basis of these results it can be concluded that the effect of Gemfibrozile was more favourable on lipod composition in the plasma then that of Phenofibrate. No significant differences in drug tolerance were observed.

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We observed statistically significant increases in concentrations of serum creatinine (P < 0.005) and cystatin C(P < 0.01). Concentrations of both analytes increased in 10 (83.3%) of the patients. In these patients, the median increases were 15.1% (range 5.5-23.2%) for creatinine and 9.9% (range 1.1-26.1%) for cystatin C.

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The blood-brain barrier contributes to maintain brain cholesterol metabolism and protects this uniquely balanced system from exchange with plasma lipoprotein cholesterol. Brain capillary endothelial cells, representing a physiological barrier to the central nervous system, express apolipoprotein A-I (apoA-I, the major high-density lipoprotein (HDL)-associated apolipoprotein), ATP-binding cassette transporter A1 (ABCA1), and scavenger receptor, class B, type I (SR-BI), proteins that promote cellular cholesterol mobilization. Liver X receptors (LXRs) and peroxisome-proliferator activated receptors (PPARs) are regulators of cholesterol transport, and activation of LXRs and PPARs has potential therapeutic implications for lipid-related neurodegenerative diseases. To clarify the functional impact of LXR/PPAR activation, sterol transport along the: (i) ABCA1/apoA-I and (ii) SR-BI/HDL pathway was investigated in primary, polarized brain capillary endothelial cells, an in vitro model of the blood-brain barrier. Activation of LXR (24(S)OH-cholesterol, TO901317), PPARalpha (bezafibrate, fenofibrate), and PPARgamma (troglitazone, pioglitazone) modulated expression of apoA-I, ABCA1, and SR-BI on mRNA and/or protein levels without compromising transendothelial electrical resistance or tight junction protein expression. LXR-agonists and troglitazone enhanced basolateral-to-apical cholesterol mobilization in the absence of exogenous sterol acceptors. Along with the induction of cell surface-located ABCA1, several agonists enhanced cholesterol mobilization in the presence of exogenous apoA-I, while efflux of 24(S)OH-cholesterol (the major brain cholesterol metabolite) in the presence of exogenous HDL remained unaffected. Summarizing, in cerebrovascular endothelial cells apoA-I, ABCA1, and SR-BI represent drug targets for LXR and PPAR-agonists to interfere with cholesterol homeostasis at the periphery of the central nervous system.

tricor drug classification

To assess the efficacy and safety of K-877 (Pemafibrate), a novel selective peroxisome proliferator-activated receptor α modulator (SPPARMα) that possesses unique PPARα activity and selectivity, compared with placebo and fenofibrate in dyslipidaemic patients with high triglyceride (TG) and low high-density lipoprotein cholesterol (HDL-C) levels.

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The effect of fenofibrate, a ligand of peroxisome proliferator-activated receptor (PPAR) alpha, on the growth and metastatic potential of Bomirski hamster melanoma s.c. tumors, pigmented line (BHM Ma) was investigated in vivo. RT-PCR and Western-blot analyses revealed the presence of mRNA and protein of PPAR alpha in BHM Ma cells. The animals treated orally with fenofibrate developed significantly fewer metastatic foci in the lungs, as compared to the control group; however, primary tumor growth remained unaltered. This observation is interesting in respect of the potential use of fenofibrate in melanoma chemoprevention.

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We show that PPARalpha protein, like primary human monocytes, is also expressed in the human monocytic THP-1 cell line. Fenofibric acid, WY14643, and GW2331 inhibited TF mRNA upregulation after stimulation of THP-1 cells with lipopolysaccharide or interleukin-1ss. In primary human monocytes and macrophages, the lipopolysaccharide- or interleukin-1ss-mediated induction of TF activity was also inhibited by fenofibric acid, WY14643, or GW2331.

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The effects on serum lipoproteins were studied in 8 patients with familial heterozygous hypercholesterolemia and 9 patients with familial combined hyperlipidemia during an 8-week treatment with fenofibrate. VLDL, IDL, LDL and HDL were isolated by ultracentrifugation and precipitation. Lipids and apolipoproteins A-I and B were determined by enzymatic and immunonephelometric techniques, respectively. In hypercholesterolemia, administration of fenofibrate resulted in decreases of VLDL, IDL, and LDL (cholesterol -58.3%, -28.6%, and -24.4%), while, in combined hyperlipidemia, treatment with the drug lowered VLDL and IDL (-33.3% and -42.9%). HDL cholesterol and apolipoprotein A-I increased only in hypercholesterolemia (+22.9% and +6.9%).

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tricor 50 mg 2017-12-23

Compared with placebo, fenofibrate decreased total cholesterol, non-HDL cholesterol, apolipoprotein B, and triglycerides and increased HDL cholesterol and apolipoprotein A-I (all P < 0.001) while tending to decrease LDL cholesterol (P = 0.069). Fenofibrate significantly improved percent flow-mediated dilator response to hyperemia by 48 +/- 5% (P < 0.001) and lowered plasma levels of high-sensitivity C-reactive protein (hsCRP) relative to baseline measurements from 0.80 to 0.70 mg/l (P = 0.001) and fibrinogen levels by 16 +/- 3% (P < 0.001). Compared with placebo, fenofibrate therapy significantly increased plasma levels of adiponectin by 14 +/- 5% (P = 0.008) and increased Penisole Pills insulin sensitivity (assessed by quantitative insulin sensitivity check index [QUICKI]) by 6 +/- 2% (P = 0.048). There were significant correlations between percent changes in adiponectin levels and percent changes in flow-mediated dilation (r = 0.401, P = 0.006), hsCRP (r = -0.443, P = 0.002), or QUICKI (r = 0.292, P = 0.049). Multivariate regression analysis showed that only changes in adiponectin levels persisted as an independent predictor of changes in flow-mediated dilation (r = 0.504, P = 0.013). Overall, we observed similar results in 24 patients with metabolic syndrome.

tricor 48mg tab 2016-09-22

Primate and rodent models show that peroxisome proliferator-activated receptor-alpha (PPAR-α) ligands, including fibrate medications, reduce nicotine reinforcement, reward, and related effects. We tested fenofibrate, the most common U.S. Food and Drug Administration-approved fibrate for lipid control versus placebo for initial evidence of efficacy in smoking cessation using a validated cross-over procedure for early Phase 2 evaluations Cenforce 100 Dosage .

tricor 215 mg 2015-07-20

A human ovarian cancer cell line (SKOV3) as the research object, was incubated with serum-free media for 24 h. These cells were then treated by appropriate concentrations of fenofibrate for different time, including control and experimental groups. Cell proliferation was evaluated by MTT assay. Apoptosis was detected by Hoechst/PI and Annexin-V/PI fluorescent assay. The migration of cells was measured by the scratch-wound healing Buy Cenforce 50 assay.

tricor drug 2017-04-10

Management of a lipophilic-hydrophilic balance is a key element in drug design to achieve desirable pharmacokinetic characters. Therefore we have created unique modular molecules, symmetrically branched oligoglycerols (BGL), as an alternative way to endow hydrophobic molecules with sufficient hydrophilicity. We Coumadin Dosing Protocol have successfully demonstrated amelioration of the water solubility and thermal stability of several hydrophobic agents by covalent conjugation to BGL so far. However, it has not been clarified whether the molecular modification by BGL also improves the pharmacological and/or pharmacokinetic properties indeed. Recently, we synthesized a novel BGL-prodrug derivative of fenofibrate, which is an antihyperlipidemic agent and one of the most hydrophobic medicinal compounds currently used clinically, by conjugating fenofibric acid to symmetrically branched glycerol trimer (BGL003), the simplest BGL. We have previously demonstrated that the hydrophilicity and water solubility of fenofibrate are improved more than 2000 times just by conjugation to the BGL003. To verify our hypothesis that the prodrug strategy with BGL should improve pharmacological efficacy and pharmacokinetic properties of extremely hydrophobic agents such as fenofibrate by the rise in hydrophilicity, we evaluated the BGL003-prodrug derivative of fenofibrate (FF-BGL) using rodent models. Here we demonstrate that the lipid-lowering effects of fenofibrate are much potentiated by chemical conjugation to BGL003 without exhibiting significant toxicity. Plasma concentration of fenofibric acid, an active metabolite of fenofibrate, after single oral administration of FF-BGL was more than 3 times higher than that of fenofibrate, in accordance. In fasting rats, plasma concentration of fenofibric acid after fenofibrate administration was curtailed into less than half of that in ad libitum-fed rats, while FF-BGL showed about the same plasma level even in the starving rats. This is the first report showing that BGL-prodrug improves pharmacological and pharmacokinetic properties as well as hydrophilicity of highly hydrophobic compounds. Furthermore, prodrug strategy using BGL suggests the possibility of diminishing the food-drug interaction effects, which should be advantageous for promoting drug compliance. BGL will be a suitable prodrug strategy to ameliorate physical, pharmacological, and pharmacokinetic characteristics of extremely hydrophobic compounds.

tricor dose 2015-01-13

Micronized fenofibrate lowers total cholesterol and low-density lipoprotein cholesterol to a similar extent as statins but raises high-density lipoprotein cholesterol and lowers triglycerides to a greater extent. The comparative lipid-modifying efficacy of micronized fenofibrate and pravastatin has not been evaluated in dyslipidemic patients. This prospective, multicenter, randomized trial compared the efficacy of 3 months' treatment with micronized fenofibrate (200 mg once daily) or pravastatin (20 mg once daily) in hypercholesterolemic type IIa and mixed dyslipidemic type IIb patients. Two hundred sixty-five male and female patients (18-75 years) were recruited from 28 European centers, and 151 were analyzed. Micronized fenofibrate was at least as effective as Lioresal 20 Mg pravastatin in reducing levels of low-density lipoprotein cholesterol and total cholesterol in primary dyslipidemia but was significantly more effective than pravastatin in raising high-density lipoprotein cholesterol (respectively, 13.2% vs. 5.6%; p = 0.0084) and lowering triglycerides (-38.7% vs. -11.8%; p = 0.0001). In type IIa dyslipidemia, micronized fenofibrate was as effective as pravastatin in raising high-density lipoprotein cholesterol (+8.6% vs. +8.0%) but was fivefold more effective in lowering triglycerides (-34.3% vs. -7.2%; p = 0.0001). In type IIb dyslipidemic patients with low baseline high-density lipoprotein cholesterol levels, micronized fenofibrate was 10-fold and nearly 3-fold superior to pravastatin in raising high-density lipoprotein cholesterol and lowering triglycerides, respectively. Micronized fenofibrate may be considered an effective first-line therapy for patients with primary hyperlipidemia, particularly those with type IIb mixed dyslipidemia or type 2 diabetes.

tricor dosage instructions 2016-09-13

A literature survey reveals that both lipid lowering drugs - statins and fibrates--and hypothyroidism are documented causes of muscle disorders including rhabdomyolysis leading to acute renal failure. We describe a case of fenofibrate monotherapy (Lipicard) induced dialysis dependent acute renal failure in an undiagnosed hypothyroid patient which is the first case to be reported from Sri Lanka Flonase Generic Price . We strongly recommend that all patients who are receiving statins and/or fibrates should be screened for occult hypothyroidism which seems to aggravate the muscle damage due to the above drugs, with or without other risk factors.

tricor cost 2017-08-07

The results confirmed the efficacy of the combination of fenofibrate and simvastatin. The combined Coumadin Missed Dose therapeutic approach was shown to be safe for the treatment of primary mixed hyperlipidaemia, at least in patients with normal hepatic and renal function.

medication tricor 2015-02-06

Ensuring the physical stability of drug nanosuspensions prepared via wet media Viagra Pills milling has been a challenge for pharmaceutical scientists. The aim of this study is to assess the combined use of non-ionic cellulosic polymers and anionic surfactants in stabilizing multiple drug nanosuspensions. Particle size of five drugs, i.e. azodicarbonamide (AZD), fenofibrate (FNB), griseofulvin (GF), ibuprofen (IBU) and phenylbutazone (PB) was reduced separately in an aqueous solution of hydroxypropyl cellulose (HPC) with/without sodium dodecyl sulfate (SDS) via a stirred media mill. Laser diffraction, scanning electron microscopy, thermal analysis, rheometry and electrophoresis were used to evaluate the breakage kinetics, storage stability, electrostatic repulsion and stabilizer adsorption. Without SDS, drug particles exhibited aggregation to different extents; FNB and GF particles aggregated the most due to low zeta potential and insufficient steric stabilization. Although aggregation in all milled suspensions was reduced due to HPC-SDS combination, FNB and IBU showed notable growth during 7-day storage. It is concluded that the combination of non-ionic cellulosic polymers and anionic surfactants is generally viable for ensuring the physical stability of wet-milled drug nanosuspensions, provided that the surfactant concentration is optimized to mitigate the Ostwald ripening, whereas cellulosic polymers alone may provide stability for some drug suspensions.

tricor 45 mg 2015-12-03

Renal insufficiency is characterized by lipoprotein abnormalities including elevated triglyceride levels. Lexapro Typical Dosage

tricor drug class 2016-08-24

Moderate evidence showed that the fibrate class can be effective in the secondary prevention of composite outcome of non-fatal stroke, non-fatal MI, and vascular death. However, this beneficial effect relies on the inclusion of clofibrate data, a drug that was discontinued in 2002 due to its unacceptably large adverse effects. Further trials of the use of fibrates in populations with previous stroke and also against a background treatment with statins (standard of care) are required.

tricor and alcohol 2017-09-17

Fenofibrate did not alleviate thermal injury-induced hepatic ER stress and dysfunction, but it reduced hepatic steatosis by modulating hepatic genes related to fat metabolism.

tricor 345 mg 2016-05-06

Expression of integrin CD18 (in all leukocyte populations), lipopolysaccharide receptor and VLA-4 (on lymphocytes only) was significantly higher in patients than in controls. Both treatments resulted in significant decrease in CD18 and CD14 expression; LFA-1 and VLA-4 were not influenced.