An antilipemic agent that lowers CHOLESTEROL and TRIGLYCERIDES. It decreases LOW DENSITY LIPOPROTEINS and increases HIGH DENSITY LIPOPROTEINS.
Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.
TRANSCRIPTION FACTORS that are activated by ligands and heterodimerize with RETINOID X RECEPTORS and bind to peroxisome proliferator response elements in the promoter regions of target genes.
An antilipemic agent that is the biologically active metabolite of CLOFIBRATE.
Compounds that either share the structure of fibric acid in their molecular arrangement or are considered variants of the fibric acid structure.
A lipid-regulating agent that lowers elevated serum lipids primarily by decreasing serum triglycerides with a variable reduction in total cholesterol.
An antilipemic agent which reduces both CHOLESTEROL and TRIGLYCERIDES in the blood.
A condition of elevated levels of TRIGLYCERIDES in the blood.
A flavoprotein oxidoreductase that has specificity for long-chain fatty acids. It forms a complex with ELECTRON-TRANSFERRING FLAVOPROTEINS and conveys reducing equivalents to UBIQUINONE.
A fibric acid derivative used in the treatment of HYPERLIPOPROTEINEMIA TYPE III and severe HYPERTRIGLYCERIDEMIA. (From Martindale, The Extra Pharmacopoeia, 30th ed, p986)
Enlargement of the liver.
Errors in the metabolism of LIPIDS resulting from inborn genetic MUTATIONS that are heritable.
A nuclear transcription factor. Heterodimerization with RETINOID X RECEPTOR GAMMA is important to metabolism of LIPIDS. It is the target of FIBRATES to control HYPERLIPIDEMIAS.
'Fluorobenzenes' are aromatic hydrocarbons consisting of a benzene ring substituted with one or more fluorine atoms, characterized by the presence of the highly electronegative fluorine atom(s) that influence the compound's chemical reactivity and physical properties.
Compounds that inhibit HMG-CoA reductases. They have been shown to directly lower cholesterol synthesis.
Triglycerides are the most common type of fat in the body, stored in fat cells and used as energy; they are measured in blood tests to assess heart disease risk, with high levels often resulting from dietary habits, obesity, physical inactivity, smoking, and alcohol consumption.
A group of compounds that contain the structure SO2NH2.
A family of 6-membered heterocyclic compounds occurring in nature in a wide variety of forms. They include several nucleic acid constituents (CYTOSINE; THYMINE; and URACIL) and form the basic structure of the barbiturates.
The regular recurrence, in cycles of about 24 hours, of biological processes or activities, such as sensitivity to drugs and stimuli, hormone secretion, sleeping, and feeding.
A derivative of LOVASTATIN and potent competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It may also interfere with steroid hormone production. Due to the induction of hepatic LDL RECEPTORS, it increases breakdown of LDL CHOLESTEROL.

Heterotropic effectors exert more significant strain on monoligated than on unligated hemoglobin. (1/221)

The effect of allosteric effectors, such as inositol hexakisphosphate and/or bezafibrate, has been investigated on the unliganded human adult hemoglobin both spectroscopically (employing electronic absorption, circular dichroism, resonance Raman, and x-ray absorption near-edge spectroscopies) and functionally (following the kinetics of the first CO binding step up to a final 4% ligand saturation degree). All data indicate that the unliganded T-state is not perturbed by the interaction with either one or both effectors, suggesting that their functional influence is only exerted when a ligand molecule is bound to the heme. This is confirmed by the observation that CO dissociation from partially liganded hemoglobin ( +info)

Variation of liver-type fatty acid binding protein content in the human hepatoma cell line HepG2 by peroxisome proliferators and antisense RNA affects the rate of fatty acid uptake. (2/221)

The liver-type fatty acid binding protein (L-FABP), a member of a family of mostly cytosolic 14-15 kDa proteins known to bind fatty acids in vitro and in vivo, is discussed to play a role in fatty acid uptake. Cells of the hepatoma HepG2 cell line endogenously express this protein to approximately 0.2% of cytosolic proteins and served as a model to study the effect of L-FABP on fatty acid uptake, by manipulating L-FABP expression in two approaches. First, L-FABP content was more than doubled upon treating the cells with the potent peroxisome proliferators bezafibrate and Wy14,643 and incubation of these cells with [1-14C]oleic acid led to an increase in fatty acid uptake rate from 0.55 to 0.74 and 0.98 nmol/min per mg protein, respectively. In the second approach L-FABP expression was reduced by stable transfection with antisense L-FABP mRNA yielding seven clones with L-FABP contents ranging from 0.03% to 0.14% of cytosolic proteins. This reduction to one sixth of normal L-FABP content reduced the rate of [1-14C]oleic acid uptake from 0.55 to 0. 19 nmol/min per mg protein, i.e., by 66%. The analysis of peroxisome proliferator-treated cells and L-FABP mRNA antisense clones revealed a direct correlation between L-FABP content and fatty acid uptake.  (+info)

Coupling of the oxygen-linked interaction energy for inositol hexakisphosphate and bezafibrate binding to human HbA0. (3/221)

The energetics of signal propagation between different functional domains (i.e. the binding sites for O2, inositol hexakisphospate (IHP), and bezafibrate (BZF)) of human HbA0 was analyzed at different heme ligation states and through the use of a stable, partially heme ligated intermediate. Present data allow three main conclusions to be drawn, and namely: (i) IHP and BZF enhance each others binding as the oxygenation proceeds, the coupling free energy going from close to zero in the deoxy state to -3.4 kJ/mol in the oxygenated form; (ii) the simultaneous presence of IHP and BZF stabilizes the hemoglobin T quaternary structure at very low O2 pressures, but as oxygenation proceeds it does not impair the transition toward the R structure, which indeed occurs also under these conditions; (iii) under room air pressure (i.e. pO2 = 150 torr), IHP and BZF together induce the formation of an asymmetric dioxygenated hemoglobin tetramer, whose features appear reminiscent of those suggested for transition state species (i.e. T- and R-like tertiary conformation(s) within a quaternary R-like structure).  (+info)

A comparison of the use, effectiveness and safety of bezafibrate, gemfibrozil and simvastatin in normal clinical practice using the New Zealand Intensive Medicines Monitoring Programme (IMMP). (4/221)

AIMS: Because of the importance of treating dyslipidaemia in the prevention of ischaemic heart disease and because patient selection criteria and outcomes in clinical trials do not necessarily reflect what happens in normal clinical practice, we compared outcomes from bezafibrate, gemfibrozil and simvastatin therapy under conditions of normal use. METHODS: A random sample of 200 patients was selected from the New Zealand Intensive Medicines Monitoring Programme's (IMMP) patient cohorts for each drug. Questionnaires sent to prescribers requested information on indications, risk factors for ischaemic heart disease, lipid profiles with changes during treatment and reasons for stopping therapy. RESULTS: 80% of prescribers replied and 83% of these contained useful information. The three groups were similar for age, sex and geographical region, but significantly more patients on bezafibrate had diabetes and/or hypertension than those on gemfibrozil or simvastatin. After treatment and taking the initial measure into account, the changes in serum lipid values were consistent with those generally observed, but with gemfibrozil being significantly less effective than expected. More patients (15.8%S) stopped gemfibrozil because of an inadequate response compared with bezafibrate (5.4%) and simvastatin (1.6%). Gemfibrozil treatment was also withdrawn significantly more frequently due to a possible adverse reaction compared with the other two drugs. CONCLUSIONS: In normal clinical practice in New Zealand gemfibrozil appears less effective and more frequently causes adverse effects leading to withdrawal of treatment than either bezafibrate or simvastatin.  (+info)

Phytanic acid is ligand and transcriptional activator of murine liver fatty acid binding protein. (5/221)

Branched-chain phytanic acid is metabolized in liver peroxisomes. Sterol carrier protein 2/sterol carrier protein x (SCP2/SCPx) knockout mice, which develop a phenotype with a deficiency in phytanic acid degradation, accumulate dramatically high concentrations of this fatty acid in serum (Seedorf at al. 1998. Genes Dev. 12: 1189-1201) and liver. Concomitantly, a 6.9-fold induction of liver fatty acid binding protein (L-FABP) expression is observed in comparison to wild-type animals fed standard chow, possibly mediated by the peroxisome proliferator-activated receptor alpha (PPARalpha). Cytosolic transport of phytanic acid to either peroxisomal membranes or to the nucleus for activation of PPARalpha may be mediated by L-FABP, which gives rise to the question whether phytanic acid is a transactivator of this protein. Here we show first that phytanic acid binds to recombinant L-FABP with high affinity. Then the increase of the in vivo phytanic acid concentration by phytol feeding to mice results in a 4-fold induction of L-FABP expression in liver, which is in the order of that attained with bezafibrate, a known peroxisome proliferator. Finally to test in vitro whether this induction is conferred by phytanic acid, we cotransfected HepG2 cells with an expression plasmid for murine PPARalpha and a CAT-reporter gene with 176 bp of the murine L-FABP promoter, containing the peroxisome proliferator responsive element (PPRE). After incubation with phytanic acid, we observed a 3.2-fold induction of CAT expression. These findings, both in vivo and in vitro, demonstrate that phytanic acid is a transcriptional activator of L-FABP expression and that this effect is mediated via PPARalpha.  (+info)

The effect of peroxisome proliferators on mitochondrial bioenergetics. (6/221)

Peroxisome proliferators are a group of structurally diverse chemicals that cause the proliferation of peroxisomes in rodents. The purpose of this investigation was to test the hypothesis that the shared effect of these compounds on peroxisome proliferation is mediated through a common inhibitory effect on mitochondrial bioenergetics. Freshly isolated rat liver mitochondria were energized with succinate. The effect of the chemicals on mitochondrial bioenergetics was analyzed by monitoring calcium-induced changes in membrane potential and swelling, as well as changes in mitochondrial respiration. Mitochondrial membrane potential was measured with a TPP(+)-sensitive electrode, and swelling was recorded spectrophotometrically. Mitochondrial oxygen uptake was monitored with a Clark-type oxygen electrode. Gemfibrozil and WY-14,643 induced the mitochondrial permeability transition as characterized by calcium-induced swelling and depolarization of membrane potential, both of which were inhibited by cyclosporine A. Fenofibrate, clofibrate, ciprofibrate and diethylhexyl phthalate, on the other hand, caused a direct dose-dependent depolarization of mitochondrial membrane potential. However, the mechanism of membrane depolarization varied among the test chemicals. Bezafibrate and trichloroethylene elicited no effect on succinate-supported mitochondrial bioenergetics. The results of this investigation demonstrate that although most, but not all, peroxisome proliferators interfere with mitochondrial bioenergetics, the specific biomolecular mechanism differs among the individual compounds.  (+info)

Activators of peroxisome proliferator-activated receptor-alpha induce the expression of the uncoupling protein-3 gene in skeletal muscle: a potential mechanism for the lipid intake-dependent activation of uncoupling protein-3 gene expression at birth. (7/221)

The recently identified uncoupling protein-3 (UCP-3) gene, predicted to encode a new member of the family of uncoupling proteins, is preferentially expressed in skeletal muscle and has been related to phenotypes of obesity and type 2 diabetes. We have established that during mouse ontogeny, the expression of the UCP-3 gene is switched on in skeletal muscle just after birth. The induction of UCP-3 gene expression is dependent on the initiation of suckling and particularly on lipid intake. Treatment of newborn mice with activators of peroxisome proliferator-activated receptors (PPARs), such as clofibrate, bezafibrate, or (4-chloro-6-(2,3-xylidine)-pirimidinylthio)acetic acid (WY 14,643), mimics the action of food intake on UCP-3 gene expression. The specific ligand of PPAR-alpha WY 14,643 induces UCP-3 gene expression in a time- and dose-dependent manner, whereas the thiazolidinedione BRL 49653, specific for PPAR-gamma, has no effect. These treatments act without altering circulating free fatty acids. During development, skeletal muscle expresses constitutive levels of PPAR-delta mRNA, whereas expression of the PPAR-gamma gene is undetectable. PPAR-alpha gene expression is developmentally regulated in muscle as it is first expressed at birth, just before UCP-3 gene induction occurs. The induction of UCP-3 gene expression by WY 14,643 is impaired in skeletal muscle of premature neonates, which do not express PPAR-alpha. It is proposed that the UCP-3 gene is predominantly regulated in neonatal muscle by PPAR-alpha activation.  (+info)

Effects of fibrate compounds on expression of plasminogen activator inhibitor-1 by cultured endothelial cells. (8/221)

The consistent positive correlation between triglyceride and plasminogen activator inhibitor-1 (PAI-1) levels in plasma and the fact that very low density lipoprotein (VLDL) induces secretion of PAI-1 from cultured human umbilical vein endothelial cells (HUVECs) and human hepatoblastoma cells have raised the question of whether fibrate treatment, the main effect of which is a profound lowering of plasma concentrations of VLDL, might improve fibrinolytic function by reducing the plasma levels of PAI-1. However, the findings of controlled clinical trials using various fibrate compounds have been discrepant. ECs express PAI-1 under normal conditions in humans. We therefore examined the effects of several fibrate compounds on PAI-1 expression and secretion by cultured HUVECs and the HUVEC-derived cell line EA.hy926. All fibrate compounds examined had significant effects on PAI-1 gene transcription in the EA.hy926 cells. Low concentrations of clofibric acid and bezafibrate increased PAI-1 transcription and secretion, whereas Wy-14643 increased PAI-1 synthesis in a dose-dependent way. In contrast, both fenofibric acid and gemfibrozil markedly decreased PAI-1 transcription and secretion from HUVECs and EA.hy926 cells. Thus, stimulation of the transcriptional activity of the PAI-1 gene by some fibrates is linked to increased secretion of PAI-1 protein by the cells, whereas the opposite effects occur with other fibrate compounds. Whether the different effects on PAI-1 transcription and secretion by ECs in vitro also reflect differences in treatment effects on the regulation of plasma PAI-1 activity in vivo will have to be determined in larger-scale, controlled clinical trials.  (+info)

Bezafibrate is a medication that belongs to a class of drugs called fibrates. It is primarily used to treat high cholesterol and related conditions, such as hyperlipidemia and mixed dyslipidemia. The medication works by reducing the levels of triglycerides and increasing the levels of "good" cholesterol (HDL) in the blood.

Bezafibrate achieves this effect by activating certain receptors in the body, known as peroxisome proliferator-activated receptors (PPARs), which play a role in regulating lipid metabolism. By binding to these receptors, bezafibrate helps to promote the breakdown of fats and reduce the production of cholesterol in the liver.

It is important to note that bezafibrate should be used in conjunction with lifestyle modifications, such as a healthy diet and regular exercise, to effectively manage high cholesterol and related conditions. Additionally, it may interact with other medications, so it is essential to inform your healthcare provider of all the drugs you are taking before starting bezafibrate therapy.

As with any medication, bezafibrate can cause side effects, including gastrointestinal symptoms such as nausea, diarrhea, and abdominal pain, as well as headaches, muscle cramps, and skin rashes. In rare cases, it may also cause more serious side effects, such as liver or kidney damage, so regular monitoring of liver and kidney function is recommended during treatment.

Overall, bezafibrate is a valuable tool in the management of high cholesterol and related conditions, but it should be used under the guidance and supervision of a healthcare professional to ensure safe and effective use.

Hypolipidemic agents are a class of medications that are used to lower the levels of lipids (fats) in the blood, particularly cholesterol and triglycerides. These drugs work by reducing the production or increasing the breakdown of fats in the body, which can help prevent or treat conditions such as hyperlipidemia (high levels of fats in the blood), atherosclerosis (hardening and narrowing of the arteries), and cardiovascular disease.

There are several different types of hypolipidemic agents, including:

1. Statins: These drugs block the action of an enzyme called HMG-CoA reductase, which is necessary for the production of cholesterol in the liver. By reducing the amount of cholesterol produced, statins can help lower LDL (bad) cholesterol levels and increase HDL (good) cholesterol levels.
2. Bile acid sequestrants: These drugs bind to bile acids in the intestines and prevent them from being reabsorbed into the bloodstream. This causes the liver to produce more bile acids, which requires it to use up more cholesterol, thereby lowering LDL cholesterol levels.
3. Nicotinic acid: Also known as niacin, this drug can help lower LDL and VLDL (very low-density lipoprotein) cholesterol levels and increase HDL cholesterol levels. It works by reducing the production of fatty acids in the liver.
4. Fibrates: These drugs are used to treat high triglyceride levels. They work by increasing the breakdown of fats in the body and reducing the production of VLDL cholesterol in the liver.
5. PCSK9 inhibitors: These drugs block the action of a protein called PCSK9, which helps regulate the amount of LDL cholesterol in the blood. By blocking PCSK9, these drugs can help lower LDL cholesterol levels.

It's important to note that hypolipidemic agents should only be used under the guidance and supervision of a healthcare provider, as they can have side effects and may interact with other medications.

Peroxisome Proliferator-Activated Receptors (PPARs) are a group of nuclear receptor proteins that function as transcription factors, regulating the expression of specific genes. They play crucial roles in the regulation of energy homeostasis, lipid metabolism, glucose homeostasis, and inflammation.

There are three major subtypes of PPARs: PPAR-α, PPAR-β/δ, and PPAR-γ. These subtypes have different tissue distributions and functions:

1. PPAR-α: Predominantly expressed in the liver, heart, kidney, and brown adipose tissue. It regulates fatty acid oxidation, lipoprotein metabolism, and glucose homeostasis.
2. PPAR-β/δ: Expressed more widely in various tissues, including the brain, muscle, adipose tissue, and skin. It is involved in fatty acid oxidation, cell differentiation, and wound healing.
3. PPAR-γ: Primarily expressed in adipose tissue, macrophages, and the colon. It plays a central role in adipocyte differentiation, lipid storage, insulin sensitivity, and inflammation.

PPARs are activated by specific ligands, such as fatty acids, eicosanoids, and synthetic compounds like fibrates (PPAR-α agonists) and thiazolidinediones (PPAR-γ agonists). These agonists have been used in the treatment of metabolic disorders, including dyslipidemia and type 2 diabetes.

Clofibric acid is the main metabolic product of clofibrate, a medication that belongs to the class of drugs called fibrates. It works by lowering levels of total and LDL (low-density lipoprotein) cholesterol and triglycerides in the blood, while increasing HDL (high-density lipoprotein) cholesterol levels. Clofibric acid is an antihyperlipidemic agent that is used primarily for the treatment of hypertriglyceridemia and mixed dyslipidemia. It may also be used to prevent pancreatitis caused by high triglyceride levels.

Clofibric acid is detectable in the urine and can be used as a biomarker for clofibrate exposure or use. However, it's important to note that clofibrate has largely been replaced by newer fibrates and statins due to its adverse effects profile and lower efficacy compared to these newer agents.

Fibric acids, also known as fibric acid derivatives, are a class of medications that are primarily used to lower elevated levels of triglycerides (a type of fat) in the blood. They work by increasing the breakdown and removal of triglycerides from the bloodstream, and reducing the production of very-low-density lipoprotein (VLDL), a type of particle that carries triglycerides in the blood.

Examples of fibric acids include gemfibrozil, fenofibrate, and clofibrate. These medications are often prescribed for people with high triglyceride levels who are at risk for pancreatitis (inflammation of the pancreas) or other complications related to high triglycerides.

Fibric acids may also have a modest effect on raising levels of high-density lipoprotein (HDL), or "good" cholesterol, and lowering levels of low-density lipoprotein (LDL), or "bad" cholesterol, in some people. However, they are generally not as effective at lowering LDL cholesterol as statins, another class of cholesterol-lowering medications.

It's important to note that fibric acids can interact with other medications and may cause side effects such as stomach upset, muscle pain, and an increased risk of gallstones. As with any medication, it's important to use fibric acids under the guidance of a healthcare provider.

Gemfibrozil is a medication that belongs to a class of drugs called fibrates. It is primarily used to lower elevated levels of triglycerides (a type of fat found in the blood) and increase levels of "good" cholesterol (HDL-C) in the blood.

Gemfibrozil works by reducing the production of triglycerides in the body, increasing the breakdown of fats in the liver, and improving the way the body handles fats and sugar. It is often prescribed for people with high triglyceride levels who are at risk for pancreatitis (inflammation of the pancreas) or those who have not responded well to other cholesterol-lowering medications, such as statins.

It's important to note that while gemfibrozil can help manage triglyceride and cholesterol levels, it is not a substitute for a healthy lifestyle. Regular exercise, a balanced diet, limiting alcohol consumption, and avoiding smoking are all crucial components of maintaining good cardiovascular health.

As with any medication, gemfibrozil should be taken under the supervision of a healthcare provider, who can monitor its effectiveness and potential side effects. Common side effects of gemfibrozil include stomach pain, diarrhea, and muscle or joint pain. Rare but serious side effects may include liver damage, kidney problems, and an increased risk of gallstones.

Fenofibrate is a medication that belongs to the class of drugs known as fibrates. It is primarily used to lower levels of cholesterol and other fats (triglycerides) in the blood. Fenofibrate works by increasing the breakdown and elimination of these fats from the body, which can help reduce the risk of heart disease and stroke.

Fenofibrate is available in various forms, including tablets and capsules, and is typically taken once or twice a day with meals. Common side effects of fenofibrate include headache, nausea, and muscle pain. More serious side effects are rare but can include liver damage, kidney problems, and an increased risk of gallstones.

It's important to note that fenofibrate should be used in conjunction with a healthy diet, regular exercise, and other lifestyle changes to manage high cholesterol and triglyceride levels effectively. Additionally, patients taking fenofibrate should be monitored regularly by their healthcare provider to ensure that the medication is working properly and to check for any potential side effects.

Hypertriglyceridemia is a medical condition characterized by an elevated level of triglycerides in the blood. Triglycerides are a type of fat (lipid) found in your blood that can increase the risk of developing heart disease, especially when levels are very high.

In general, hypertriglyceridemia is defined as having triglyceride levels greater than 150 milligrams per deciliter (mg/dL) of blood. However, the specific definition of hypertriglyceridemia may vary depending on individual risk factors and medical history.

Hypertriglyceridemia can be caused by a variety of factors, including genetics, obesity, physical inactivity, excessive alcohol consumption, and certain medications. In some cases, it may also be a secondary consequence of other medical conditions such as diabetes or hypothyroidism. Treatment for hypertriglyceridemia typically involves lifestyle modifications such as dietary changes, increased exercise, and weight loss, as well as medication if necessary.

Acyl-CoA dehydrogenase, long-chain (LCHAD) is a medical term that refers to an enzyme found in the body that plays a crucial role in breaking down fatty acids for energy. This enzyme is responsible for catalyzing the first step in the beta-oxidation of long-chain fatty acids, which involves the removal of hydrogen atoms from the fatty acid molecule to create a double bond.

Mutations in the gene that encodes LCHAD can lead to deficiencies in the enzyme's activity, resulting in an accumulation of unmetabolized long-chain fatty acids in the body. This can cause a range of symptoms, including hypoglycemia (low blood sugar), muscle weakness, and liver dysfunction. In severe cases, LCHAD deficiency can lead to serious complications such as heart problems, developmental delays, and even death.

LCHAD deficiency is typically diagnosed through newborn screening or genetic testing, and treatment may involve dietary modifications, supplementation with medium-chain triglycerides (MCTs), and avoidance of fasting to prevent the breakdown of fatty acids for energy. In some cases, LCHAD deficiency may require more intensive treatments such as carnitine supplementation or liver transplantation.

Clofibrate is a medication that belongs to the class of drugs known as fibrates. It is primarily used to lower elevated levels of cholesterol and other fats (lipids) in the blood, specifically low-density lipoprotein (LDL), or "bad" cholesterol, and triglycerides, while increasing high-density lipoprotein (HDL), or "good" cholesterol. Clofibrate works by reducing the production of very-low-density lipoproteins (VLDL) in the liver, which in turn lowers triglyceride levels and indirectly reduces LDL cholesterol levels.

Clofibrate is available in oral tablet form and is typically prescribed for patients with high cholesterol or triglycerides who are at risk of cardiovascular disease, such as those with a history of heart attacks, strokes, or peripheral artery disease. It is important to note that clofibrate should be used in conjunction with lifestyle modifications, including a healthy diet, regular exercise, and smoking cessation.

Like all medications, clofibrate can have side effects, some of which may be serious. Common side effects include stomach upset, diarrhea, gas, and changes in taste. Less commonly, clofibrate can cause more severe side effects such as liver or muscle damage, gallstones, and an increased risk of developing certain types of cancer. Patients taking clofibrate should be monitored regularly by their healthcare provider to ensure that the medication is working effectively and to monitor for any potential side effects.

Hepatomegaly is a medical term that refers to an enlargement of the liver beyond its normal size. The liver is usually located in the upper right quadrant of the abdomen and can be felt during a physical examination. A healthcare provider may detect hepatomegaly by palpating (examining through touch) the abdomen, noticing that the edge of the liver extends past the lower ribcage.

There are several possible causes for hepatomegaly, including:
- Fatty liver disease (both alcoholic and nonalcoholic)
- Hepatitis (viral or autoimmune)
- Liver cirrhosis
- Cancer (such as primary liver cancer, metastatic cancer, or lymphoma)
- Infections (e.g., bacterial, fungal, or parasitic)
- Heart failure and other cardiovascular conditions
- Genetic disorders (e.g., Gaucher's disease, Niemann-Pick disease, or Hunter syndrome)
- Metabolic disorders (e.g., glycogen storage diseases, hemochromatosis, or Wilson's disease)

Diagnosing the underlying cause of hepatomegaly typically involves a combination of medical history, physical examination, laboratory tests, and imaging studies like ultrasound, CT scan, or MRI. Treatment depends on the specific cause identified and may include medications, lifestyle changes, or, in some cases, surgical intervention.

Inborn errors of lipid metabolism refer to genetic disorders that affect the body's ability to break down and process lipids (fats) properly. These disorders are caused by defects in genes that code for enzymes or proteins involved in lipid metabolism. As a result, toxic levels of lipids or their intermediates may accumulate in the body, leading to various health issues, which can include neurological problems, liver dysfunction, muscle weakness, and cardiovascular disease.

There are several types of inborn errors of lipid metabolism, including:

1. Disorders of fatty acid oxidation: These disorders affect the body's ability to convert long-chain fatty acids into energy, leading to muscle weakness, hypoglycemia, and cardiomyopathy. Examples include medium-chain acyl-CoA dehydrogenase deficiency (MCAD) and very long-chain acyl-CoA dehydrogenase deficiency (VLCAD).
2. Disorders of cholesterol metabolism: These disorders affect the body's ability to process cholesterol, leading to an accumulation of cholesterol or its intermediates in various tissues. Examples include Smith-Lemli-Opitz syndrome and lathosterolosis.
3. Disorders of sphingolipid metabolism: These disorders affect the body's ability to break down sphingolipids, leading to an accumulation of these lipids in various tissues. Examples include Gaucher disease, Niemann-Pick disease, and Fabry disease.
4. Disorders of glycerophospholipid metabolism: These disorders affect the body's ability to break down glycerophospholipids, leading to an accumulation of these lipids in various tissues. Examples include rhizomelic chondrodysplasia punctata and abetalipoproteinemia.

Inborn errors of lipid metabolism are typically diagnosed through genetic testing and biochemical tests that measure the activity of specific enzymes or the levels of specific lipids in the body. Treatment may include dietary modifications, supplements, enzyme replacement therapy, or gene therapy, depending on the specific disorder and its severity.

PPAR-alpha (Peroxisome Proliferator-Activated Receptor alpha) is a type of nuclear receptor protein that functions as a transcription factor, regulating the expression of specific genes involved in lipid metabolism. It plays a crucial role in the breakdown of fatty acids and the synthesis of high-density lipoproteins (HDL or "good" cholesterol) in the liver. PPAR-alpha activation also has anti-inflammatory effects, making it a potential therapeutic target for metabolic disorders such as diabetes, hyperlipidemia, and non-alcoholic fatty liver disease (NAFLD).

Fluorobenzenes are a group of organic compounds that consist of a benzene ring (a cyclic structure with six carbon atoms in a hexagonal arrangement) substituted with one or more fluorine atoms. The general chemical formula for a fluorobenzene is C6H5F, but this can vary depending on the number of fluorine atoms present in the molecule.

Fluorobenzenes are relatively stable and non-reactive compounds due to the strong carbon-fluorine bond. They are used as starting materials in the synthesis of various pharmaceuticals, agrochemicals, and other specialty chemicals. Some fluorobenzenes also have potential applications as refrigerants, fire extinguishing agents, and solvents.

It is worth noting that while fluorobenzenes themselves are not considered to be particularly hazardous, some of their derivatives can be toxic or environmentally harmful, so they must be handled with care during production and use.

Hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitors, also known as statins, are a class of cholesterol-lowering medications. They work by inhibiting the enzyme HMG-CoA reductase, which plays a central role in the production of cholesterol in the liver. By blocking this enzyme, the liver is stimulated to take up more low-density lipoprotein (LDL) cholesterol from the bloodstream, leading to a decrease in LDL cholesterol levels and a reduced risk of cardiovascular disease.

Examples of HMG-CoA reductase inhibitors include atorvastatin, simvastatin, pravastatin, rosuvastatin, and fluvastatin. These medications are commonly prescribed to individuals with high cholesterol levels, particularly those who are at risk for or have established cardiovascular disease.

It's important to note that while HMG-CoA reductase inhibitors can be effective in reducing LDL cholesterol levels and the risk of cardiovascular events, they should be used as part of a comprehensive approach to managing high cholesterol, which may also include lifestyle modifications such as dietary changes, exercise, and weight management.

Triglycerides are the most common type of fat in the body, and they're found in the food we eat. They're carried in the bloodstream to provide energy to the cells in our body. High levels of triglycerides in the blood can increase the risk of heart disease, especially in combination with other risk factors such as high LDL (bad) cholesterol, low HDL (good) cholesterol, and high blood pressure.

It's important to note that while triglycerides are a type of fat, they should not be confused with cholesterol, which is a waxy substance found in the cells of our body. Both triglycerides and cholesterol are important for maintaining good health, but high levels of either can increase the risk of heart disease.

Triglyceride levels are measured through a blood test called a lipid panel or lipid profile. A normal triglyceride level is less than 150 mg/dL. Borderline-high levels range from 150 to 199 mg/dL, high levels range from 200 to 499 mg/dL, and very high levels are 500 mg/dL or higher.

Elevated triglycerides can be caused by various factors such as obesity, physical inactivity, excessive alcohol consumption, smoking, and certain medical conditions like diabetes, hypothyroidism, and kidney disease. Medications such as beta-blockers, steroids, and diuretics can also raise triglyceride levels.

Lifestyle changes such as losing weight, exercising regularly, eating a healthy diet low in saturated and trans fats, avoiding excessive alcohol consumption, and quitting smoking can help lower triglyceride levels. In some cases, medication may be necessary to reduce triglycerides to recommended levels.

Sulfonamides are a group of synthetic antibacterial drugs that contain the sulfonamide group (SO2NH2) in their chemical structure. They are bacteriostatic agents, meaning they inhibit bacterial growth rather than killing them outright. Sulfonamides work by preventing the bacteria from synthesizing folic acid, which is essential for their survival.

The first sulfonamide drug was introduced in the 1930s and since then, many different sulfonamides have been developed with varying chemical structures and pharmacological properties. They are used to treat a wide range of bacterial infections, including urinary tract infections, respiratory tract infections, skin and soft tissue infections, and ear infections.

Some common sulfonamide drugs include sulfisoxazole, sulfamethoxazole, and trimethoprim-sulfamethoxazole (a combination of a sulfonamide and another antibiotic called trimethoprim). While sulfonamides are generally safe and effective when used as directed, they can cause side effects such as rash, nausea, and allergic reactions. It is important to follow the prescribing physician's instructions carefully and to report any unusual symptoms or side effects promptly.

Pyrimidines are heterocyclic aromatic organic compounds similar to benzene and pyridine, containing two nitrogen atoms at positions 1 and 3 of the six-member ring. They are one of the two types of nucleobases found in nucleic acids, the other being purines. The pyrimidine bases include cytosine (C) and thymine (T) in DNA, and uracil (U) in RNA, which pair with guanine (G) and adenine (A), respectively, through hydrogen bonding to form the double helix structure of nucleic acids. Pyrimidines are also found in many other biomolecules and have various roles in cellular metabolism and genetic regulation.

A circadian rhythm is a roughly 24-hour biological cycle that regulates various physiological and behavioral processes in living organisms. It is driven by the body's internal clock, which is primarily located in the suprachiasmatic nucleus (SCN) of the hypothalamus in the brain.

The circadian rhythm controls many aspects of human physiology, including sleep-wake cycles, hormone secretion, body temperature, and metabolism. It helps to synchronize these processes with the external environment, particularly the day-night cycle caused by the rotation of the Earth.

Disruptions to the circadian rhythm can have negative effects on health, leading to conditions such as insomnia, sleep disorders, depression, bipolar disorder, and even increased risk of chronic diseases like cancer, diabetes, and cardiovascular disease. Factors that can disrupt the circadian rhythm include shift work, jet lag, irregular sleep schedules, and exposure to artificial light at night.

Simvastatin is a medication that belongs to a class of drugs called statins, which are used to lower cholesterol levels in the blood. It works by inhibiting HMG-CoA reductase, an enzyme that plays a key role in the production of cholesterol in the body. By reducing the amount of cholesterol produced by the liver, simvastatin helps to lower the levels of LDL (low-density lipoprotein) or "bad" cholesterol and triglycerides in the blood, while increasing HDL (high-density lipoprotein) or "good" cholesterol.

Simvastatin is used to prevent cardiovascular diseases such as heart attacks and strokes in individuals with high cholesterol levels, particularly those who have other risk factors such as diabetes, hypertension, or a history of smoking. It is available in various strengths and forms, and is typically taken orally once a day, usually in the evening.

Like all medications, simvastatin can cause side effects, ranging from mild to severe. Common side effects include headache, muscle pain, and gastrointestinal symptoms such as nausea, constipation, or diarrhea. Rare but serious side effects may include liver damage, muscle breakdown (rhabdomyolysis), and increased risk of diabetes. It is important to follow the dosage instructions carefully and inform your healthcare provider of any pre-existing medical conditions or medications you are taking, as these may affect the safety and efficacy of simvastatin.

... the features of which are attenuated by bezafibrate. Studies show that in patients with impaired glucose tolerance, bezafibrate ... Bezafibrate (marketed as Bezalip and various other brand names) is a fibrate drug used as a lipid-lowering agent to treat ... Like the other fibrates, bezafibrate is an agonist of PPARα; some studies suggest it may have some activity on PPARγ and PPARδ ... Bezafibrate has been shown to reduce tau protein hyperphosphorylation and other signs of tauopathy in transgenic mice having ...
The product, a combination of bezafibrate with chenodeoxycholic acid, was invented in 2001. Hepaconda is being developed as a ' ... fibrate combinations other than bezafibrate plus ursodoxycholic acid. Heliconda, a product for the treatment of drug-resistant ...
Another study of 48 patients with PBC found a combination of bezafibrate and UDCA showed a decrease of alkaline phosphatase in ... Reig A, Sesé P, Parés A (January 2018). "Effects of Bezafibrate on Outcome and Pruritus in Primary Biliary Cholangitis With ... 2017). "A 2-year multicenter, double-blind, randomized, placebo-controlled study of bezafibrate for the treatment of primary ... June 2008). "The efficacy of ursodeoxycholic acid and bezafibrate combination therapy for primary biliary cirrhosis: A ...
... company Giaconda has tested a treatment for Hepatitis C infection that combines chenodeoxycholic acid with bezafibrate. ...
Aluminium clofibrate Bezafibrate Ciprofibrate Choline fenofibrate Clinofibrate Clofibrate Clofibride Fenofibrate Gemfibrozil ...
They include fenofibrate, gemfibrozil, and bezafibrate and work to decrease triglycerides, increase HDL-C, and also decrease ...
... bezafibrate, and fenofibrate). They were originally indicated for dyslipidemia of cholesterol and more recently for disorders ...
... (INN) is an analogue of the cholesterol drug bezafibrate developed for the treatment of depression, traumatic brain ...
... bezafibrate MeSH D02.241.081.160.140.135.175 - clofenapate MeSH D02.241.081.160.140.135.193 - clofibrate MeSH D02.241.081.160. ... 225 - clofibric acid MeSH D02.241.081.160.225.133 - bezafibrate MeSH D02.241.081.160.225.187 - clofenapate MeSH D02.241.081.160 ...
C10AA05 Atorvastatin C10AA06 Cerivastatin C10AA07 Rosuvastatin C10AA08 Pitavastatin C10AB01 Clofibrate C10AB02 Bezafibrate ...
Among the fibrates, bezafibrate and fenofibrate, PPAR-alpha selective agonists, have been extensively studied as therapeutic ...
Bezafibrate (INN) Bezalip Bezitramide (INN) BG 9273 (Articles with short description, Short description is different from ...
... the features of which are attenuated by bezafibrate. Studies show that in patients with impaired glucose tolerance, bezafibrate ... Bezafibrate (marketed as Bezalip and various other brand names) is a fibrate drug used as a lipid-lowering agent to treat ... Like the other fibrates, bezafibrate is an agonist of PPARα; some studies suggest it may have some activity on PPARγ and PPARδ ... Bezafibrate has been shown to reduce tau protein hyperphosphorylation and other signs of tauopathy in transgenic mice having ...
Toxicity. Bezafibrate has high acute toxicity.. Risk. The use of bezafibrate, fenofibrate and gemfibrozil is not considered to ... Bezafibrate is not a persistent substance.. Bioaccumulation: In spite of a comparatively high log Kow of 4.25, bezafibrate ... Persistence. Bezafibrate is slowly degraded in the environment.. Bioaccumulation. All fibrates examined are fat soluble with a ... In surface waters, bezafibrate was shown to attenuate rapidly over a river stretch of 1 km, with unquantified adsorption to ...
Acids, Carbocyclic - Bezafibrate PubMed MeSh Term *Overview. Overview. subject area of * Identification of photocatalytic ... degradation products of bezafibrate in TiO2 aqueous suspensions by liquid and gas chromatography Journal Article ...
":"Bezafibrate","data":{"category":"Medicine","linkRef":"Bezafibrate"}},{"value":"Bezalip","data":{"category":"Medicine"," ...
Bezafibrate is a lipid-lowering agent, indicated for the treatment of hyperlipidemia.. Unipharms generic Bezafibrate Tablets ...
Bezafibrate: Uses, How It Works, How Its Done, Care, Pregnancy, and Lactation. by Dr. Cameron Troup MD in Pharmacology ... How does Bezafibrate work?. For the sake of simplicity, there are two types of cholesterol; a "bad" type called low-density ... How do I take Bezafibrate?. *One tablet should be taken once a day, either in the morning or night. Always try to take your ... The Bezafibrate functions primarily by stimulating the action of two enzymes that break down triglycerides. These are called ...
Bezafibrate. LDL decrease: 9.6-25% (400 mg). HDL increase: 15-24% (400 mg) ...
Using this medicine while you are pregnant can harm your unborn baby. Use an effective form of birth control to keep from getting pregnant. If you think you have become pregnant while using the medicine, tell your doctor right away. Do not use this medicine if you are also taking any of the following medicines: boceprevir (Victrelis®), cobicistat-containing products (Stribild®), cyclosporine (Gengraf®, Neoral®, Sandimmune®), danazol (Danocrine®), gemfibrozil (Lopid®), nefazodone (Serzone®), telaprevir (Incivek®), certain antibiotics (such as clarithromycin, erythromycin, itraconazole, ketoconazole, posaconazole, telithromycin, voriconazole, Nizoral®), or medicines to treat HIV/AIDS (such as atazanavir, indinavir, nelfinavir, ritonavir, saquinavir, tipranavir, Crixivan®, Kaletra®, Lexiva®, Norvir®, Prezista®, Reyataz®). Using these medicines together with sitagliptin and simvastatin combination may increase your risk of muscle injury and could result in kidney problems. Chinese ...
bezafibrate. *brimonidine. *bromocriptine. *fast acting bronchodilators (e.g., salbutamol, terbutaline). *long acting ...
pms-Rosuvastatin: Rosuvastatin belongs to the group of medications known as HMG CoA reductase inhibitors (statins). It is used, along with a healthy diet and exercise program, to improve cholesterol levels by lowering bad cholesterol and raising good cholesterol. It is also used to treat people who have certain inherited cholesterol disorders.
Bezafibrate Plus Ursodeoxycholic Acid for Treatment of Pruritus in Primary Biliary Cholangitis January 2018 ... Pares also describes the results of his study, which combines bezafibrate with ursodeoxycholic acid (UDCA) to treat severe ...
... fibrates such as bezafibrate, fenofibrate (Antara, Lipofen), and gemfibrozil (Lopid); medications for HIV or AIDS such as ...
Bezafibrate (Possibly safe. Probably compatible. Mild risk possible. Follow up recommended. Read the Comment.) ...
fibrates (e.g., bezafibrate, gemfibrozil, fenofibrate). *ginseng. *grapefruit juice. *hepatitis C antivirals (e.g., elbasvir, ...
Bezafibrate Bezafibrate is primarily a PPAR-alpha agonist, but also has some interaction with PPAR-beta (Peters et al 2003). ... The two studies most commonly referenced to with regards to Bezafibrate are The Bezafibrate Coronary Atherosclerosis ... The intervention of bezafibrate was shown to decrease plasma fibrinogen (involved in blood clotting) levels, reduce plasma ... Results showed that bezafibrate treatment reduced plasma triglycerides by 21% and increased HDL levels by 18%. The study ...
Bezafibrate 8. Simvastatin (Zocor) 9. Clofibrate 10. Insulin (Novolin) Related Therapies and Procedures. 1. Transplantation ( ...
Bezafibrate (Bezalip SR®). Fenofibrate (Lipidil EZ®, Lipidil Micro®, Lipidil Supra®). Gemfibrozil (Lopid®). *Lowers ...
... participated in the Bezafibrate Infarction Prevention trial underwent a neurovascular evaluation as part of the Bezafibrate ... Goldbourt U, Brunner D, Behar S, Reicher-Reiss H. Baseline characteristics of patients participating in the Bezafibrate ... Participants from 8 hospitals in central Israel were initially recruited for the Bezafibrate Infarction Prevention (BIP) ... Table 1. Baseline Characteristics of Participants in the Bezafibrate Infarction Prevention Neurocognitive Study, by Sarcopenia ...
Other drugs, such as blood lipid regulators (clofibric acid, bezafibrate), can inhibit lipolysis in adipose tissue. β Receptor ... Garcia-Ac, A.; Segura, P.A.; Gagnon, C.; Sauvé, S. Determination of bezafibrate, methotrexate, cyclophosphamide, orlistat and ...
Plasma concentrations of active lovastatin acid are markedly increased by gemfibrozil but not by bezafibrate. Clin Pharmacol ...
Q&A: Combination OCA-Bezafibrate for PBC, with Cynthia Levy, MD. November 23rd 2023. Article ...
Exposure to human pharmaceuticals carbamazepine, ibuprofen and bezafibrate causes molecular effects in Dreissena polymorpha. ... Exposure to human pharmaceuticals carbamazepine, ibuprofen and bezafibrate causes molecular effects in Dreissena polymorpha. ... Exposure to human pharmaceuticals carbamazepine, ibuprofen and bezafibrate causes molecular effects in Dreissena polymorpha. ... Exposure to human pharmaceuticals carbamazepine, ibuprofen and bezafibrate causes molecular effects in Dreissena polymorpha. ...
Bezafibrate for pruritus in fibrosing cholangiopathies. Take Quiz. Malignant colorectal polyps: Best practices. Take Quiz. ...
Fibrates (bezafibrate and fenofibrate) have also been evaluated in the treatment of patients with PBC who have an inadequate ...
Aktuelle API Auditberichte • GMP-Audits der Herstelung pharmazeutischer Ausgangs- und Wirkstoffe nach ICH Q7 / EU GMP Guide Part II • Diapharm
Bezafibrate Reduces Elevated Hepatic Fumarate in Insulin-Deficient Mice. Biomedicines, 10 (3). BASEL: MDPI. ISSN 2227-9059 ... Bezafibrate Improves Insulin Sensitivity and Metabolic Flexibility in STZ-Induced Diabetic Mice. Diabetes, 65 (9). S. 2540 - ...
However, only bezafibrate and enalapril were detected downstream in the treated waters leaving the plant. The results indicate ...
Intercept Pharmaceuticals Receives FDA Orphan Drug Designation for the Fixed-Dose Combination of OCA and Bezafibrate for the ... Intercept Presents New Data Showing Significant Impact of OCA-bezafibrate Combination on Normalization of Multiple Biomarkers ...
  • The use of bezafibrate, fenofibrate and gemfibrozil is not considered to pose an environmental risk. (janusinfo.se)
  • Comparative assessment of environmental risk when using the fibrates bezafibrate, fenofibrate and gemfibrozil from a Swedish perspective. (janusinfo.se)
  • Besides for lowering triglycerides, it is preferable to use a fibrate such as fenofibrate, bezafibrate etc. (ndtv.com)
  • For example bezafibrate is to be taken after meals, fenofibrate with food, gemfibrozil 30 minutes before meals etc. (ndtv.com)
  • Having previously fast-tracked this paper to publication in summary form, we now expand on why cimetidine/famotidine (histamine type-2 receptor antagonists), dipyridamole (antiplatelet agent), fenofibrate/bezafibrate (cholesterol/triglyceride-lowering agents), and sildenafil (phosphodiesterase-5 inhibitor) are worth considering for patients with COVID-19 based on their antiviral, anti-inflammatory, renoprotective, cardioprotective, and anticoagulation properties. (jmir.org)
  • Having recently published a short summary of our thesis [ 2 ], the current paper expands on why cimetidine or famotidine (histamine type-2 receptor antagonists), dipyridamole (antiplatelet agent), fenofibrate or bezafibrate (cholesterol/triglycerides-lowering agents), and sildenafil (phosphodiesterase-5 inhibitor) are worth considering for patients with COVID-19. (jmir.org)
  • Bezafibrate Infarction Prevention (BIP) study) (July 2000). (wikipedia.org)
  • A subset of 337 men (mean age at baseline 56.7 [SD, 6.5]) who previously (1990-1997) participated in the Bezafibrate Infarction Prevention trial underwent a neurovascular evaluation as part of the Bezafibrate Infarction Prevention Neurocognitive Study 15.0 (SD, 3.0) years after baseline and a sarcopenia evaluation 19.9 (SD, 1.0) years after baseline. (cdc.gov)
  • Secondary prevention by raising HDL cholesterol and reducing triglycerides in patients with coronary artery disease: the Bezafibrate Infarction Prevention (BIP) study. (medletter.com)
  • Bezafibrate improves markers of combined hyperlipidemia, effectively reducing LDL and triglycerides and improving HDL levels. (wikipedia.org)
  • Bezafibrate (marketed as Bezalip and various other brand names) is a fibrate drug used as a lipid-lowering agent to treat hyperlipidaemia. (wikipedia.org)
  • Further evidence that substantial bulk tolerance is available in the para position is given by the lipid lowering agent bezafibrate. (wikipedia.org)
  • Bezafibrate is a lipid-lowering agent, indicated for the treatment of hyperlipidemia. (unipharm.global)
  • People with decreased renal function (the dose of bezafibrate in Bezalip mono tablets is too high for people with kidney problems). (scopeheal.com)
  • Unipharm's generic Bezafibrate Tablets have been manufactured and marketed in Israel since 1990. (unipharm.global)
  • The combination of a cholesterol-lowering drug, bezafibrate, and a contraceptive steroid, medroxyprogesterone acetate, could be an effective, non-toxic treatment for a range of cancers, researchers at the University of Birmingham have found. (wikipedia.org)
  • In addition, Bezafibrate decreases the production of LDL cholesterol in the liver, which causes the liver cells to absorb excess LDL cholesterol from the blood. (scopeheal.com)
  • It is essential to follow a diet to lower cholesterol and exercise while consuming Bezafibrate. (scopeheal.com)
  • In the study, the researchers used tissue taken from the livers of rats dosed with bezafibrate, a drug commonly used to treat high cholesterol. (birmingham.ac.uk)
  • In surface waters, bezafibrate was shown to attenuate rapidly over a river stretch of 1 km, with unquantified adsorption to undissolved solids being noted. (janusinfo.se)
  • However, only bezafibrate and enalapril were detected downstream in the treated waters leaving the plant. (battlingforhealth.com)
  • In addition, a prospective observational study of dyslipidemic patients with diabetes or hyperglycemia showed that bezafibrate significantly reduces haemoglobin A1c (HbA1c) concentration as a function of baseline HbA1c levels, regardless of concurrent use of antidiabetic drugs. (wikipedia.org)
  • Bezafibrate Reduces Elevated Hepatic Fumarate in Insulin-Deficient Mice. (uni-koeln.de)
  • The Australian biotech company Giaconda combines bezafibrate with chenodeoxycholic acid in an anti-hepatitis C drug combination called Hepaconda. (wikipedia.org)
  • Risk of environmental impact of bezafibrate cannot be excluded, due to the lack of environmental toxicity data. (janusinfo.se)
  • Bezafibrate has been shown to reduce tau protein hyperphosphorylation and other signs of tauopathy in transgenic mice having human tau mutation. (wikipedia.org)
  • Bezafibrate has high acute toxicity. (janusinfo.se)
  • Bioaccumulation: 'In spite of a comparatively high log K ow of 4.25, bezafibrate has no significant bioaccumulation potential, with a calculated log D at pH 7 of 0.9. (janusinfo.se)
  • The main effect on cardiovascular morbidity is in patients with the metabolic syndrome, the features of which are attenuated by bezafibrate. (wikipedia.org)
  • We studied the effects of the pan-PPAR agonist bezafibrate on tau pathology, inflammation, lipid metabolism and behavior in transgenic mice with the P301S human tau mutation, which causes familial frontotemporal lobar degeneration. (nih.gov)
  • Sonal Kumar, MD, MPH, and David Victor III, MD, provide an overview of the emerging treatments in the primary biliary cholangitis landscape, highlighting PPAR agonists and combination OCA and bezafibrate. (consultantlive.com)
  • In case of administering a fibrate during breastfeeding it is advisable to choose those with a shorter half-life: Bezafibrate, Gemfibrozil. (e-lactancia.org)
  • Further evidence that substantial bulk tolerance is available in the para position is given by the lipid lowering agent bezafibrate. (wikipedia.org)
  • 14. Treatment of primary hypercholesterolemia: fluvastatin versus bezafibrate. (nih.gov)
  • Bezafibrate (BZF) and Fenofibric acid (FBA) act as PPARG agonists . (bvsalud.org)
  • In this multicentre, randomised clinical trial of 1-year duration, 138 patients with CHL under close dietary supervision received atorvastatin or bezafibrate as lipid-regulating agents. (medscape.com)
  • As expected from the mechanisms of action of these drugs, atorvastatin effectively lowered total cholesterol, LDL-C and apo B levels, whereas bezafibrate was most efficacious in lowering triglyceride-rich lipoproteins and raising HDL-C and apo A-I levels. (medscape.com)
  • However, even though bezafibrate was superior in this respect, atorvastatin significantly lowered triglycerides and raised the HDL-C and apo A-I levels as well. (medscape.com)
  • Finally, atorvastatin decreased the LDL-C/HDL-C ratio, an indicator of overall cardiovascular risk, nearly twice as much as bezafibrate. (medscape.com)
  • The Australian biotech company Giaconda combines bezafibrate with chenodeoxycholic acid in an anti-hepatitis C drug combination called Hepaconda. (wikipedia.org)
  • if this is not the case, cautious addition of a fibric acid derivative such as bezafibrate may be tried with a good chance of normalising the lipid profile. (medscape.com)
  • A Mendelian randomization study for drug repurposing reveals bezafibrate and fenofibric acid as potential osteoporosis treatments. (bvsalud.org)
  • There's a fixed-dose combination study that's ongoing with obeticholic acid and bezafibrate. (consultantlive.com)
  • I'm excited to see the combo with obeticholic acid and bezafibrate. (consultantlive.com)
  • Bezafibrate therefore exerts neuroprotective effects in a mouse model of tauopathy, as shown by decreased tau pathology and behavioral improvement. (nih.gov)
  • Since bezafibrate was given to the mice before tau pathology had developed, our data suggest that bezafibrate exerts a preventive effect on both tau pathology and its behavioral consequences. (nih.gov)
  • Bezafibrate treatment significantly decreased tau hyperphosphorylation using AT8 staining and the number of MC1-positive neurons. (nih.gov)
  • Bezafibrate improves markers of combined hyperlipidemia, effectively reducing LDL and triglycerides and improving HDL levels. (wikipedia.org)
  • Bezafibrate has been shown to reduce tau protein hyperphosphorylation and other signs of tauopathy in transgenic mice having human tau mutation. (wikipedia.org)
  • Bezafibrate is therefore a promising agent for the treatment of neurodegenerative diseases associated with tau pathology. (nih.gov)
  • Methods We evaluated all randomized controlled trials comparing the combination of UDCA and bezafibrate with UDCA monotherapy. (annalsgastro.gr)
  • Bezafibrate treatment also diminished microglial activation and expression of both inducible nitric oxide synthase and cyclooxygenase 2. (nih.gov)
  • Conclusion UDCA and bezafibrate combined treatment is superior to UDCA alone in UDCA non-responders with regard to decreasing liver biochemistry markers, without any significant increase in side effects in patients with PBC. (annalsgastro.gr)
  • Specific information on when to take Bezafibrate can be found in the Patient Information Leaflet that comes with this medicine or on the medicine label. (tajdearobpharma.com)
  • The main effect on cardiovascular morbidity is in patients with the metabolic syndrome, the features of which are attenuated by bezafibrate. (wikipedia.org)
  • On the other hand, bezafibrate had only a marginal effect on elevated LDL-C. Furthermore, both drugs lowered VLDL-C levels to a similar extent. (medscape.com)
  • Studies show that in patients with impaired glucose tolerance, bezafibrate may delay progress to diabetes, and in those with insulin resistance it slowed progress in the HOMA severity marker. (wikipedia.org)
  • Since some patients do not respond adequately to UDCA, other therapies, such as bezafibrate, have been developed. (annalsgastro.gr)
  • In this meta-analysis we evaluated the efficacy and safety of using both UDCA and bezafibrate in patients with an inadequate response to UDCA. (annalsgastro.gr)