Bezafibrate: An antilipemic agent that lowers CHOLESTEROL and TRIGLYCERIDES. It decreases LOW DENSITY LIPOPROTEINS and increases HIGH DENSITY LIPOPROTEINS.Hypolipidemic Agents: Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.Peroxisome Proliferator-Activated Receptors: 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.Clofibric Acid: An antilipemic agent that is the biologically active metabolite of CLOFIBRATE.Fibric Acids: Compounds that either share the structure of fibric acid in their molecular arrangement or are considered variants of the fibric acid structure.Gemfibrozil: A lipid-regulating agent that lowers elevated serum lipids primarily by decreasing serum triglycerides with a variable reduction in total cholesterol.Fenofibrate: An antilipemic agent which reduces both CHOLESTEROL and TRIGLYCERIDES in the blood.Hypertriglyceridemia: A condition of elevated levels of TRIGLYCERIDES in the blood.Acyl-CoA Dehydrogenase, Long-Chain: 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.Clofibrate: A fibric acid derivative used in the treatment of HYPERLIPOPROTEINEMIA TYPE III and severe HYPERTRIGLYCERIDEMIA. (From Martindale, The Extra Pharmacopoeia, 30th ed, p986)Hepatomegaly: Enlargement of the liver.Lipid Metabolism, Inborn Errors: Errors in the metabolism of LIPIDS resulting from inborn genetic MUTATIONS that are heritable.PPAR alpha: 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.Drug Information Services: Services providing pharmaceutic and therapeutic drug information and consultation.Universal Precautions: Prudent standard preventive measures to be taken by professional and other health personnel in contact with persons afflicted with a communicable disease, to avoid contracting the disease by contagion or infection. Precautions are especially applicable in the diagnosis and care of AIDS patients.Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.Hypoglycemic Agents: Substances which lower blood glucose levels.Alcoholic Beverages: Drinkable liquids containing ETHANOL.Diabetes Mellitus: A heterogeneous group of disorders characterized by HYPERGLYCEMIA and GLUCOSE INTOLERANCE.Diabetes Mellitus, Type 1: A subtype of DIABETES MELLITUS that is characterized by INSULIN deficiency. It is manifested by the sudden onset of severe HYPERGLYCEMIA, rapid progression to DIABETIC KETOACIDOSIS, and DEATH unless treated with insulin. The disease may occur at any age, but is most common in childhood or adolescence.Microcirculation: The circulation of the BLOOD through the MICROVASCULAR NETWORK.Pigment Epithelium of Eye: The layer of pigment-containing epithelial cells in the RETINA; the CILIARY BODY; and the IRIS in the eye.Retinal Vessels: The blood vessels which supply and drain the RETINA.Retinal Pigment Epithelium: The single layer of pigment-containing epithelial cells in the RETINA, situated closely to the tips (outer segments) of the RETINAL PHOTORECEPTOR CELLS. These epithelial cells are macroglia that perform essential functions for the photoreceptor cells, such as in nutrient transport, phagocytosis of the shed photoreceptor membranes, and ensuring retinal attachment.Electronic Mail: Messages between computer users via COMPUTER COMMUNICATION NETWORKS. This feature duplicates most of the features of paper mail, such as forwarding, multiple copies, and attachments of images and other file types, but with a speed advantage. The term also refers to an individual message sent in this way.Science: The study of natural phenomena by observation, measurement, and experimentation.Simvastatin: 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.Problem-Based Learning: Instructional use of examples or cases to teach using problem-solving skills and critical thinking.Curriculum: A course of study offered by an educational institution.Education, Dental: Use for articles concerning dental education in general.Ursodeoxycholic Acid: An epimer of chenodeoxycholic acid. It is a mammalian bile acid found first in the bear and is apparently either a precursor or a product of chenodeoxycholate. Its administration changes the composition of bile and may dissolve gallstones. It is used as a cholagogue and choleretic.Liver Cirrhosis, Biliary: FIBROSIS of the hepatic parenchyma due to obstruction of BILE flow (CHOLESTASIS) in the intrahepatic or extrahepatic bile ducts (BILE DUCTS, INTRAHEPATIC; BILE DUCTS, EXTRAHEPATIC). Primary biliary cirrhosis involves the destruction of small intra-hepatic bile ducts and bile secretion. Secondary biliary cirrhosis is produced by prolonged obstruction of large intrahepatic or extrahepatic bile ducts from a variety of causes.Cholagogues and Choleretics: Gastrointestinal agents that stimulate the flow of bile into the duodenum (cholagogues) or stimulate the production of bile by the liver (choleretic).Cholestasis, Intrahepatic: Impairment of bile flow due to injury to the HEPATOCYTES; BILE CANALICULI; or the intrahepatic bile ducts (BILE DUCTS, INTRAHEPATIC).Cholangitis, Sclerosing: Chronic inflammatory disease of the BILIARY TRACT. It is characterized by fibrosis and hardening of the intrahepatic and extrahepatic biliary ductal systems leading to bile duct strictures, CHOLESTASIS, and eventual BILIARY CIRRHOSIS.Cholestasis: Impairment of bile flow due to obstruction in small bile ducts (INTRAHEPATIC CHOLESTASIS) or obstruction in large bile ducts (EXTRAHEPATIC CHOLESTASIS).Fatty Acids: Organic, monobasic acids derived from hydrocarbons by the equivalent of oxidation of a methyl group to an alcohol, aldehyde, and then acid. Fatty acids are saturated and unsaturated (FATTY ACIDS, UNSATURATED). (Grant & Hackh's Chemical Dictionary, 5th ed)Cytokines: Non-antibody proteins secreted by inflammatory leukocytes and some non-leukocytic cells, that act as intercellular mediators. They differ from classical hormones in that they are produced by a number of tissue or cell types rather than by specialized glands. They generally act locally in a paracrine or autocrine rather than endocrine manner.Fatty Acids, Omega-3: A group of fatty acids, often of marine origin, which have the first unsaturated bond in the third position from the omega carbon. These fatty acids are believed to reduce serum triglycerides, prevent insulin resistance, improve lipid profile, prolong bleeding times, reduce platelet counts, and decrease platelet adhesiveness.Lymphocytes: White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each), or NATURAL KILLER CELLS.Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.Sarin: An organophosphorus ester compound that produces potent and irreversible inhibition of cholinesterase. It is toxic to the nervous system and is a chemical warfare agent.Education, Graduate: Studies beyond the bachelor's degree at an institution having graduate programs for the purpose of preparing for entrance into a specific field, and obtaining a higher degree.Sterol Regulatory Element Binding Protein 1: A sterol regulatory element binding protein that regulates expression of GENES involved in FATTY ACIDS metabolism and LIPOGENESIS. Two major isoforms of the protein exist due to ALTERNATIVE SPLICING.TriglyceridesUniversities: Educational institutions providing facilities for teaching and research and authorized to grant academic degrees.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.Sjogren-Larsson Syndrome: An autosomal recessive neurocutaneous disorder characterized by severe ichthyosis MENTAL RETARDATION; SPASTIC PARAPLEGIA; and congenital ICHTHYOSIS. It is caused by mutation of gene encoding microsomal fatty ALDEHYDE DEHYDROGENASE leading to defect in fatty alcohol metabolism.Aldehyde Oxidoreductases: Oxidoreductases that are specific for ALDEHYDES.Aldehyde Dehydrogenase: An enzyme that oxidizes an aldehyde in the presence of NAD+ and water to an acid and NADH. This enzyme was formerly classified as EC 126.96.36.199.Cerebral Palsy: A heterogeneous group of nonprogressive motor disorders caused by chronic brain injuries that originate in the prenatal period, perinatal period, or first few years of life. The four major subtypes are spastic, athetoid, ataxic, and mixed cerebral palsy, with spastic forms being the most common. The motor disorder may range from difficulties with fine motor control to severe spasticity (see MUSCLE SPASTICITY) in all limbs. Spastic diplegia (Little disease) is the most common subtype, and is characterized by spasticity that is more prominent in the legs than in the arms. Pathologically, this condition may be associated with LEUKOMALACIA, PERIVENTRICULAR. (From Dev Med Child Neurol 1998 Aug;40(8):520-7)Syndrome: A characteristic symptom complex.Aldehydes: Organic compounds containing a carbonyl group in the form -CHO.
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)
... was first introduced by Boehringer Mannheim in 1977. Like the other fibrates, bezafibrate is an agonist of PPARα; ... 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 ... Bezafibrate has been shown to reduce tau protein hyperphosphorylation and other signs of tauopathy in transgenic mice having ...
Bezafibrate Infarction Prevention Study Group (2003-10-27). "Current smoking, smoking cessation, and the risk of sudden cardiac ...
Giaconda (pharmaceutical company)
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 ...
... company Giaconda has tested a treatment for Hepatitis C infection that combines chenodeoxycholic acid with bezafibrate. As ...
Aluminium clofibrate Bezafibrate Ciprofibrate Choline fenofibrate Clinofibrate Clofibrate Clofibride Fenofibrate Gemfibrozil ...
... bezafibrate, and fenofibrate). They were originally indicated for cholesterol disorders and more recently for disorders that ...
... their salts Bacampicillin Benserazide Hydrochloride Betahistine Dihydrochloride Bethanidine Sulphate Bezafibrate Biclotymol ...
... (INN) is an analogue of the cholesterol drug bezafibrate developed for the treatment of depression, traumatic brain ...
List of MeSH codes (D02)
... 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 ...
ATC code C10
C10AA05 Atorvastatin C10AA06 Cerivastatin C10AA07 Rosuvastatin C10AA08 Pitavastatin C10AB01 Clofibrate C10AB02 Bezafibrate ...
List of drugs: Be
Bezafibrate (INN) Bezalip Bezitramide (INN) BG 9273. ...
Expression Profiling Identifies Bezafibrate as Potential Therapeutic Drug for Lung Adenocarcinoma. - Semantic Scholar
Drug-induced gene expression patterns that invert disease profiles have recently been illustrated to be a new strategy for drug-repositioning. In the present study, we validated this approach and focused on prediction of novel drugs for lung adenocarcinoma (AC), for which there is a pressing need to find novel therapeutic compounds. Firstly, connectivity map (CMap) analysis computationally predicted bezafibrate as a putative compound against lung AC. Then this hypothesis was verified by in vitro assays of anti-proliferation and cell cycle arrest. In silico docking evidence indicated that bezafibrate could target cyclin dependent kinase 2(CDK2), which regulates progression through the cell cycle. Furthermore, we found that bezafibrate can significantly down-regulate the expression of CDK2 mRNA and p-CDK2. Using a nude mice xenograft model, we also found that bezafibrate could inhibit tumor growth of lung AC in vivo. In conclusion, this study proposed bezafibrate as a potential therapeutic option for lung
This study provides strong evidence that bezafibrate has antidiabetic properties, supporting both in vitro data and earlier post hoc analyses suggesting that bezafibrate can prevent or delay the onset of type 2 diabetes (5-7). It further indicates that this effect is unique to bezafibrate among the fibrates. These findings have important implications for research. Our findings are bolstered by the similarity of subjects in exposure groups on clinically relevant characteristics, the fact that the finding of a protective effect is of a clinically relevant magnitude, statistically significant, and robust to sensitivity analyses including adjustment for BMI, and the monotonic duration-response relationship.. The results of the post hoc analysis are reassuring. It was reasonable to worry that fenofibrate was more likely to be prescribed to individuals with a high risk for diabetes or unrecorded diabetes, creating a falsely elevated hazard for development of diabetes during fenofibrate treatment ...
Molecules | Free Full-Text | Antihyperlipidemic Properties of Novel N-(Benzoylphenyl)-5-substituted-1H-indole-2-carboxamides in...
In the search for new potential antihyperlipidemic agents, the present study focuses on the synthesis of novel N-(benzoylphenyl)-5-substituted-1H-indole-2-carboxamides (compounds 8-12, 15, 16, 18) and investigating their antihyperlipidemic activity using Triton WR-1339-induced hyperlipidemic rats as an experimental model. Hyperlipidemia was developed by intraperitoneal injection of Triton WR-1339 (250 mg/kg body weight). The tested animals were divided into normal control (NCG), hyperlipidemic (HG), compound 8, 9, 15, 16, 18- and bezafibrate treated groups. At a dose of 15 mg/kg body weight, compounds 9, 16, 18 and bezafibrate (100 mg/kg) significantly (p | 0.0001) reduced elevated plasma triglycerides levels after 12 h compared to the hyperlipidemic control group. However, only the group treated with compounds 9, 16 and 18 showed an obviously significant (p | 0.001) reduction in plasma total cholesterol levels after 12 h compared to the hyperlipidemic control group. Moreover, high density lipoprotein
Bezafibrate(Abeita) generic is a fibrate drug, prescribed for high cholesterol in blood. It works mainly by stimulating the action of two enzymes.
SjÃ¶gren-Larsson syndrome presents with ichtyosis, spastic diplegia and cognitive deficits. It is caused by a deficiency of fatty aldehyde dehydrogenase. Treatments are limited to symptomatic therapies; for example, ziluteon (an inhibitor of 5-lipoxygenase) can reduce pruritus.. In a recent article, bezafibrate has been shown to induce the expression of the deficient protein in fibroblasts from some patients. This discovery could become of clinical importance ...
The IUPHAR/BPS Guide to Pharmacology. bezafibrate ligand page. Quantitative data and detailed annnotation of the targets of licensed and experimental drugs.
Human CYP2C enzymes metabolize ~30% of clinically prescribed drugs and various environmental chemicals. CYP2C8, an important member of this subfamily, metabolizes the anticancer drug paclitaxel, certain antidiabetic drugs, and endogenous substrates including arachidonic acid to physiologically active epoxyeicosatrienoic acids (EETs). Previous studies from our laboratory showed that microRNA 107 (miR107) and microRNA 103 down-regulate CYP2C8 post-transcriptionally. miR107 is located in intron 5 of the pantothenate kinase 1 (PANK1) gene. p53 has been reported to coregulate the induction of PANK1 and miR107. Here, we examine the possible down regulation of CYP2C8 by drugs capable of inducing miR107. Hypolipidemic drugs such as bezafibrate, known activators of the peroxisome proliferator-activated receptor α (PPARα), induce both the PANK1 gene and miR107 (≈2.5 fold) in primary human hepatocytes. Surprisingly, CYP2C8 mRNA and protein levels were induced by bezafibrate. CYP2C8 promoter activity ...
The effect of bezafibrate and omega-3 fatty acids on lymphocyte cytokine release and systemic inflammation in patients with...
The aim of this study was to compare the effects of fibrates and omega-3 fatty acids on lymphocyte secretory function and systemic inflammation in patients with isolated hypertriglyceridemia. The stud
Bezafibrate at Clinically Relevant Doses Decreases Serum/Liver Triglycerides via Down-Regulation of Sterol Regulatory Element...
Department of Metabolic Regulation, Institute on Aging and Adaptation, Shinshu University Graduate School of Medicine, Matsumoto, Japan (T.N., N.T., H.K., A.H., Y.K., X.Z., T.A.); Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan (N.T., Y.K.); and Laboratory of Metabolism, National Cancer Institute, Bethesda, Maryland (F.J.G ...
Bezafibrate and Simvastatin: An Effective and Safe Combination to Treat Mixed Hyperlipidaemia | Clinical Science
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Structure-Based Design, Synthesis, Molecular Docking, and Biological Activities of 2-(3-benzoylphenyl) Propanoic Acid...
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Phase 3 Study of Bezafibrate in Combination With Ursodeoxycholic Acid in Primary Biliary Cirrhosis - Full Text View -...
Primary biliary cirrhosis (PBC) is a chronic cholestatic liver disease that eventually leads to end-stage liver failure and death unless liver transplantation (LT) is performed. Ursodeoxycholic acid (UDCA) administered orally at the daily dose of 13-15 mg/kg is currently the only drug approved for the treatment of PBC. UDCA consistently improves biochemical liver tests, prolongs survival without LT, and delays histological progression as well as the occurrence of portal hypertension. However, a significant proportion (40%) of patients treated with UDCA shows an incomplete biochemical response and remains at high risk of death or LT. The development of new treatments in combination with UDCA is therefore needed. Several candidates exist among which is Bezafibrate. Bezafibrate belongs to the fibrates pharmacological class, which has been developed 4 decades ago for the treatment of mixed hyperlipidaemia. Bezafibrate is cheap, widely available and well tolerated. There is now a substantial body of ...
X-linked adrenoleukodystrophy is a devastating peroxisomal disorder with only limited options for treatment. Recent findings however have pointed towards fatty acid elongation as a possible target for therapeutic intervention of X-ALD. Chapter 2 describes how bezafibrate reduces VLCFA levels in X-ALD fibroblasts by inhibiting fatty acid chain elongation. Based on these results, an open-label pilot study was performed to evaluate the effect of bezafibrate on VLCFA accumulation in blood cells of AMN patients. Unfortunately, bezafibrate failed to lower VLCFA levels in blood cells of X-ALD patients. Most likely this is attributable to its inability to reach adequate drug levels in vivo. In chapter 3 the kinetic characteristics of ELOVL1 and further investigation of the effect of fibrates on fatty acid chain elongation are described. This revealed that bezafibrate had the strongest effect in intact cells while the CoA-ester of gemfibrozil was the strongest inhibitor of VLCFA elongation activity in ...
Purpose : Bezafibrate (BZF) is a fibrate drug used as a lipid-lowering agent to treat hyperlipidemia. The results of randomized clinical trial have shown the beneficial effects of systemic fenofibrate therapy in reducing the progression of diabetic retinopathy independently of serum lipid levels. BZF is a pan-agonist for all subtypes of peroxisome proliferator-activated receptor (PPAR) such as PPARα, PPARγ, and PPARβ/δ. It has been reported PPARs play a key role in microvascular inflammation or angiogenesis. However, the effects of BZF in retinal cells remain unclear. The purpose of this study is to investigate the effects of BZF on retinal microvascular inflammation. Methods : The primary human microvascular endothelial cells (HRMECs) and human RPE cell line (ARPE-19) were cultured. First, cytotoxicity and cell viability of BZF were assessed by CCK-8 assay and LDH activity assay. Next, we analyzed the effect of BZF(0,30,100μM) treatment on the expression of TNF-α-induced monocyte ...
Here, we describe an investigation, at the lipid, gene, and protein levels, of the effects of the antileukemia and antilymphoma therapy BaP (combined 0.5-mmol/L bezafibrate and 5-μmol/L MPA) on lipogenesis in AML and eBL cells. Our clearest observations on the effects of BaP treatment on lipogenesis in these two disease settings are the following: (i) phospholipid species with saturated and monounsaturated acyl chains were decreased, whereas phospholipids with polyunsaturated chains were increased, (ii) BaP treatment decreased the incorporation of 13C from 13C D-glucose into a variety of cellular lipids, especially into monounsaturated free fatty acids and phospholipids with monounsaturated acyl chains, (iii) BaP caused a decrease in the concentration, and probably the activity, of SCD1, and (iv) supplementation of BaP-treated cells with oleate (the product of SCD1 activity), but not with palmitate, protected AML and eBL cells from killing by BaP. Both bezafibrate and MPA appear to have ...
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Lipid-lowering drugs and risk of new-onset diabetes: a cohort study using Japanese healthcare data linked to clinical data for...
In this retrospective cohort study using data of claims, enrolment and health screening, we found that the use of LLDs (statins and fibrates) was associated with an increased risk of new-onset diabetes, compared with non-use. The adjusted HR of new-onset diabetes between two fibrates (bezafibrate and fenofibrate) was similar, while the HR in the high potency statins (atorvastatin, rosuvastatin and pitavastatin) was higher than that in the low potency statins (fluvastatin, pravastatin and simvastatin). The HR for new-onset diabetes was varied from 1.5 to 3.1 in the individual statins. As the incidence rate of new-onset diabetes was estimated as 22.6 per 1000 person-years during the period of non-use in our study, the absolute increase of the rate potentially due to the use of statins, corresponding to HR of 1.5 to 3.1, may be approximately 10 to 45 per 1000 person-years.. Previous studies on the association between the use of statins and new-onset diabetes have been inconclusive. In some of the ...
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice ...
This study demonstrates that variation in the PPARα gene influences the onset and progression of type 2 diabetes, in concurrence with the recent observation that bezafibrate reduces the incidence and delays the onset of type 2 diabetes (11). Allele and haplotype frequencies were not different between healthy middle-aged U.K. men and the type 2 diabetes sample, but haplotype frequency was different between subjects with age at diagnosis ≤45 years and both those with later age at diagnosis and with healthy middle-aged U.K. men without overt type 2 diabetes, indicating that PPARα predisposes to early-onset type 2 diabetes. PPARα gene variants influenced age at diagnosis in combination and in haplotype analysis. Carriers of the intron 1 and 7 rare C-alleles had a dramatically younger age at diagnosis, an effect confirmed in haplotype analysis, in which haplotypes 6 and 8, comprising the intron 1 C- and intron 7 C-alleles with the L162 or V162 alleles, respectively, were associated with an age ...
Looking for online definition of fibric acids in the Medical Dictionary? fibric acids explanation free. What is fibric acids? Meaning of fibric acids medical term. What does fibric acids mean?
Peroxisome Proliferator Receptor alpha Agonist drug class usage statistics for the United States (2004 - 2014). Statistics include a comparison of all drugs within the drug class of Peroxisome Proliferator Receptor alpha Agonist.
PPAR agonists are drugs which act upon the peroxisome proliferator-activated receptor. They are used for the treatment of symptoms of the metabolic syndrome, mainly for lowering triglycerides and blood sugar. PPAR-alpha and PPAR-gamma are the molecular targets of a number of marketed drugs. The main classes of PPAR agonists are: PPARα (alpha) is the main target of fibrate drugs, a class of amphipathic carboxylic acids (clofibrate, gemfibrozil, ciprofibrate, bezafibrate, and fenofibrate). They were originally indicated for cholesterol disorders and more recently for disorders that feature high triglycerides. PPARγ (gamma) is the main target of the drug class of thiazolidinediones (TZDs), used in diabetes mellitus and other diseases that feature insulin resistance. It is also mildly activated by certain NSAIDs (such as ibuprofen) and indoles, as well as from a number of natural compounds. Known inhibitors include the experimental agent GW-9662. They are also used in treating hyperlipidaemia in ...
Hydromorphone HCl extended-release tablets (Exalgo) are being studied in clinical trials for the management of moderate to severe pain in opioid-tolerant patients requiring continuous, around-the-clock opioid analgesia for extended lengths of time.7 The FDA has stated that the NDA in its current form is not sufficient for approval of this product. The manufacturers of this agent are in discussions to resolve the details related to the approval of this agent.. Pozen Inc. has begun phase III clinical trials for PA32540, a fixed combination of enteric-coated aspirin 325 mg and immediate-release omeprazole 40 mg.8 PA32540 is being studied for secondary stroke and myocardial infarction prevention in patients at risk for gastric ulcers.. Genentech had hoped to receive approval of rituximab for treating patients with earlier stages of rheumatoid arthritis (RA), but the FDA declined to support wider use of the agent due to the risk of the development of progressive multifocal ...
The Miller School study, published in Cell Metabolism, found that increasing the number of mitochondria in muscle was able to delay the onset and slow the progression of the disease in a mouse model of mitochondria myopathy created by Francisca Diaz, Ph.D., research assistant professor of neurology.. "Our findings showed that we can boost the function of even a defective mitochondrial enzyme by inducing the production of more mitochondria," says Carlos Moraes, Ph.D., professor of neurology, cell biology and anatomy, and senior author of the study. "Its a case of more is better-even a defective mitochondrial enzyme in large numbers is better than a small number.". The researchers were able to increase the mitochondrial levels through genetic overexpression of a master regulator of mitochondrial biogenesis (PGC-1alpha) or by using bezafibrate, a drug already used in humans with high cholesterol.. "The fact that we can induce mitochondrial biogenesis with drugs that are already in the marketplace ...
Huang Y, Powers C, Moore V, Schafer C, Ren M, Phoon CK, James JF, Glukhov AV, Javadov S, Vaz FM, Jefferies JL, Strauss AW, Khuchua Z. The PPAR pan-agonist bezafibrate ameliorates cardiomyopathy in a mouse model of Barth syndrome. Orphanet J Rare Dis. 2017 Mar 9;12(1):49. doi: 10.1186/s13023-017-0605-5. (PubMed - Open Access)*. Dudek J, Cheng IF, Chowdhury A, Wozny K, Balleininger M, Reinhold R, Grunau S, Callegari S, Toischer K, Wanders RJ, Hasenfuß G, Brügger B, Guan K, Rehling P. Cardiac-specific succinate dehydrogenase deficiency in Barth syndrome. EMBO Mol Med.2016 Feb 1;8(2):139-54. (PubMed - Open Access)▼. Angelini R, Lobasso S, Gorgoglione R, Bowron A, Steward CG, Corcelli A. Cardiolipin fingerprinting of leukocytes by MALDI-TOF/MS as screening tool for Barth syndrome. J Lipid Res. 2015 Sep;56(9):1787-94. doi: 10.1194/jlr.D059824. Epub 2015 Jul 5. (PubMed - Open Access)*▼. Cadalbert LC, Ghaffar FN, Stevenson D, Bryson S, Vaz FM, Gottlieb E, Strathdee D. Mouse tafazzin is required ...
Tricor is prescribed medicine to treat high cholesterol and high triglyceride levels. This medicine is also called as Fenofibrate. Tricor is connected with the set of drugs called fibric acid derivatives or cholesterol reducing drugs.
Tricor is prescribed medicine to treat high cholesterol and high triglyceride levels. This medicine is also called as Fenofibrate. Tricor is connected with the set of drugs called fibric acid derivatives or cholesterol reducing drugs.
fibrate class of lipid-regulating agents | XYZ ist die oberste Gruppe von Fibraten der lipidregulierenden Mittel
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Wirkungsweise systemischer Lipidsenker auf Lipoproteine, Apolipoproteine und Enzyme des Lipoproteinstoffwechsels | SpringerLink
Unter den systemischen Lipidsenkern nehmen die Fibrate einen hervorragenden Platz ein. Mit Clofibrat als Ausgangssubstanz ist diese Stoffgruppe seit gut 20 Jahren in die Therapie der Hyperlipidämien...
0174] In some embodiments, the second active is niacin, bezafibrate; ciprofibrate; clofibrate; gemfibrozil; fenofibrate; DF4 (Ac-D-W-F-K-A-F-Y-D-K-V-A-E-K-F-K-E-A-F-NH2); DFS; RVX-208 (Resverlogix); avasimibe; pactimibe sulfate (CS-505); CI-1011 (2,6-diisopropylphenyl[(2,4,6-triisopropylphenyl)acetyl]sulfamate); CI-976 (2,2-dimethyl-N-(2,4,6-trimethoxyphenyl)dodecanamide); VULM1457 (1-(2,6-diisopropyl-phenyl)-3-[4-(4-nitrophenylthio)phenyl]urea); CI-976 (2,2-dimethyl-N-(2,4,6-trimethoxyphenyl)dodecanamide); E-5324 (n-butyl-N-(2-(3-(5-ethyl-4-phenyl-1H-imidazol-1-yl)propoxy)-6-methylphe- nyl)urea); HL-004 (N-(2,6-diisopropylphenyl)tetradecylthioacetamide); KY-455 (N-(4,6-dimethyl-1-pentylindolin-7-yl)-2,2-dimethylpropanamide); FY-087 (N-[2-[N-pentyl-(6,6-dimethyl-2,4-heptadiynyl)amino]ethyl]-(2-met- hyl-1-naphthyl-thio)acetamide); MCC-147 (Mitsubishi Pharma); F 12511 ((S)-2,3,5-trimethyl-4-hydroxy-alpha-dodecylthioacetanilide); SMP-500 (Sumitomo Pharmaceuticals); CL 277082 ...
and the U.S. markets.. Tribute markets Cambia® (diclofenac potassium for oral solution), Bezalip® SR (bezafibrate), Soriatane® (acitretin), NeoVisc® (1.0% sodium hyaluronate solution) Uracyst® (sodium chondroitin sulfate solution 2%), Fiorinal®, Fiorinal® C, Visken®, Viskazide®, Collatamp® G, Durela®, Proferrin®, Iberogast®, MoviPrep®, Normacol®, Resultz®, Pegalax®, Balanse®, Balanse® Kids, Diaflor™, Mutaflor®, and Purfem® in the Canadian market. Additionally, NeoVisc® and Uracyst® are commercially available and are sold globally through various international partnerships. Tribute also has the U.S. rights to Fibricor® and its related authorized generic. In addition, it has the exclusive U.S. rights to develop and commercialize Bezalip® SR in the U.S. and has the exclusive right to sell bilastine, a product licensed from ...
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ACE inhibitors, alcohol, and fibrates are among the substances that can negatively interact with Levemir. This eMedTV Web article outlines other medicines that may cause Levemir drug interactions and describes the potential problems that may occur.
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Clofibric Acid, A Peroxisome Proliferator-Activated Receptor Alpha Agonist, forms a Ternary Complex with the Ferric Iron
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TY - JOUR. T1 - Role of ozone for reducing fouling due to pharmaceuticals in MF (microfiltration) process. AU - Oh, Byung Soo. AU - Jang, Ha Young. AU - Hwang, Tae Mun. AU - Kang, Joonwun. PY - 2007/2/15. Y1 - 2007/2/15. N2 - The aim of this study was to evaluate the potential use of ozone integrated with a microfiltration (MF) process, focusing on the role of ozone in reducing the membrane fouling caused by dissolved organic matter. In this study, several pharmaceuticals, including Ibuprofen (IB), Bezafibrate (BZ), Amoxicillin (AM) and Sulfamethoxazole (SMX), were tested as model foulants. The mechanism of fouling of these compounds in the tested MF was found to be adequately predicted by the adsorptive fouling model rather than any other of the classical fouling models. In the ozone-MF hybrid experiments, the pre-ozonation was able to reduce the membrane fouling due to: (1) the preventive effect of the ozone destruction of the pharmaceuticals in the aqueous phase prior to foulant accumulation ...
Hypertriglyceridemia Medication: Fibric Acid Agents, Omega-3 Acids, Lipid-Lowering Agents, Other, Lipid-Lowering Agents, Statins
Hypertriglyceridemia, a condition in which triglyceride levels are elevated, is a common disorder in the United States (see the following image). It is often caused or exacerbated by uncontrolled diabetes mellitus, obesity, and sedentary habits, all of which are more prevalent in industrialized societies than in developing nations.
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Riva-Fenofibrate Micro: Fenofibrate belongs to the class of medications known as fibrates. It is used in addition to diet and exercise to treat people with abnormal cholesterol levels.
Teva-Fenofibrate Micro: Fenofibrate belongs to the class of medications known as fibrates. It is used in addition to diet and exercise to treat people with abnormal cholesterol levels.
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Identification of Novel Peroxisome Proliferator-Activated Receptor Alpha Transcriptional Targets in the Retina | IOVS | ARVO...
Purpose : The peroxisome proliferator-activated receptor alpha agonist fenofibrate prevents progression of diabetic retinopathy, yet its mechanism of protective action is not known. Here, we tested the hypothesis that peroxisome proliferator-activated receptor alpha agonists promote retinal health in the setting of diabetes by inducing a unique transcriptional signature in the eye. Methods : First, we induced peroxisome proliferator-activated receptor alpha activity in the retina using systemically- or locally-introduced agonists and measured changes in canonical transcriptional targets. Second, we investigated retinal peroxisome proliferator-activated receptor responsiveness using a transgenic reporter system. Third, we performed a microarray analysis of transcript changes in whole retina after intravitreous delivery of several peroxisome proliferator-activated receptor alpha agonists and validated putative targets. Results : Canonical genes involved in lipid metabolism and beta-oxidation are ...
Fibrates induce mdr2 gene expression and biliary phospholipid secretion in the mouse | Biochemical Journal | Portland Press
Disruption of the murine mdr2 gene leads to the complete absence of biliary phospholipids. We tested the hypothesis that the increase in biliary phospholipid output induced by fibrates is mediated via induction of the hepatic mdr2 gene and its encoded product, the P-glycoprotein canalicular flippase. Increased levels of mdr2 mRNA were observed in the liver of mice treated with different fibrates: ciprofibrate, 660±155% (as compared with control group); clofibrate, 611±77%; bezafibrate, 410±47%; fenofibrate, 310±52%; gemfibrozil, 190±25% (P , 0.05 compared with control group). Induction of expression of the mdr gene family was specific to the mdr2 gene. Two- to three-fold increases in P-glycoprotein immunodetection were evident on the canalicular plasma-membrane domain of clofibrate- and ciprofibrate-treated mice. Biliary phospholipid output increased from 4.2±1.2 nmol/min per g of liver in the control group to 8.5±0.6, 7.1±2.9 and 5.8±2.5 in ciprofibrate-, clofibrate- and ...
What treatments for elevated triglycerides?. , Dietary advice is essential, and these are the first to apply, with the recommendations of lifestyle hygiene (increase in physical activity).. , You should also know that fish oils have a beneficial effect on triglyceride levels. We are no longer at the time of cod liver oil, all this is now in the form of capsules (dietary supplements).. , Medications are very effective. They are usually indicated when dietary recommendations are insufficient. These are fibrates, derivatives of fibric acid. They are lipid-lowering drugs (drugs that lower the level of lipids in the blood). They lower cholesterol and triglyceride levels, and are prescribed by a doctor.. By reducing the level of triglycerides, fibrates help reduce LDL cholesterol - called bad cholesterol. But in studies, fibrates have not always prevented myocardial infarction ... ...
Fibrates are intended to increase levels of HDL, or good cholesterol, while lowering triglycerides, a potentially harmful type of fat that can accumulate in the arteries. While the Western University of Health Services researchers who are behind the current study say that the class of medication is effective at lowering triglycerides, evidence is lacking in their ability to improve HDL levels ...
Chipscreen Biosciences in China was developing peroxisome proliferator-activated receptor (PPAR) alpha agonists for the treatment of cardiovascular disease and
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Reducing cholesterol is one of the primary uses for choline fenofibrate. This eMedTV segment features more details on what this fibrate drug is used for and also includes information on how it works and who can take it.
GW 590735, a peroxisome proliferator activated receptor (PPAR) alpha agonist, was in development with GlaxoSmithKline and Ligand Pharmaceuticals for the
... ! Lopid is an effective medication which helps to fight with high levels of serum triglycerides. Lopid acts by reducing the production of triglycerides in the liver. It is fibrates.
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Patent US5147901 - Propionphenone derivatives as photoinitiators for photopolymerization - Google Patents
Propiophenones of the formula I ##STR1## in which R1 is hydrogen or C1 -C4 -alkyl, --Si(CH3)3, allyl or benzyl, R2 is hydrogen, C1 -C8 -alkyl, C1 -C4 -alkyl which is substituted by C1 -C4 -alkoxy or --OH, --(CH2 --CH2 --O)n --R5 where n is 2 to 20 and R5 is H or C1 -C4 -alkyl, --Si(CH3)3, benzyl, C3 -C6 -alkenyl, C3 -C4 -alkynyl or 2-tetrahydrofuranyl, or R1 and R2 together are a C1 -C6 -alkylidene radical or a C2 -C6 -alkylidene radical which is substituted by hydroxyl, C1 -C4 -alkoxy or phenyl, a linear or branched C2 -C6 -alkanediyl radical, a benzylidene, cyclopentylidene or cyclohexylidene radical or a 2,2,2-trichloroethylidene, 2-furylmethylidene or dimethylsilylidene radical, R3 is phenyl which is unsubstituted or substituted by one or more --Cl, C1 -C4 -alkyl, C1 -C4 -alkoxy or C1 -C4 -alkylthio radicals, and is also benzoylphenyl, phenoxyphenol or phenylthiophenyl, R4 is C1 -C4 -alkyl, or phenyl which is unsubstituted or substituted by one or more --Cl, C1 -C4 -alkyl or C1 -C4 -alkoxy radicals,
BACKGROUND: Fibrates are effective for modifying atherogenic dyslipidaemia, and particularly for lowering serum triglycerides. However, evidence that fibrates reduce mortality and morbidity associated with cardiovascular disease (CVD), or overall mortality and morbidity, in the primary prevention of CVD is lacking. OBJECTIVES: This Cochrane Review and meta-analysis aimed to evaluate the clinical benefits and harms of fibrates versus placebo or usual care or fibrates plus other lipid-modifying drugs versus other lipid-modifying drugs alone for the primary prevention of cardiovascular disease (CVD) morbidity and mortality. SEARCH METHODS: We searched the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE (Ovid), Embase (Ovid), CINAHL (EBSCO), and Web of Science (all from inception to 19 May 2016). We searched four clinical trial registers (last searched on 3 August 2016) with the help of an experienced professional librarian. We searched the databases to identify randomised ...
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This study showed that fenofibrate was very effective in lowering total, LDL, non-HDL cholesterol significantly in female diabetic patients compared to mal
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Selective induction of rat hepatic CYP1 and CYP4 proteins and of peroxisomal proliferation by green tea. - PubMed - NCBI
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June 30, 2012 Health Care, Medicine Comments Off A population-based study has shown an association between new fibrate use in older patients and nephrologist consultations and hospital admissions for a rise in creatinine level .. Though the rise may prompt clinical concern but it is uncertain that the changes in creatinine reflect renal injury. The results of FIELD trial has shown that the increase in serum creatinine with fenofibrate was reversible on discontinuation, and at the end of the trial fenofibrate treatment appeared to have slowed loss of renal function and reduced proteinuria .. References. 1. Zhao YY, Weir MA, Manno M, et al. New fibrate use and acute renal outcomes in elderly adults: a population-based study. Ann Intern Med 2012;156:560 ...
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Hyperlipidemia continues to be a common problem in individuals with HIV, particularly those receiving HIV protease inhibitors (PIs) or the nucleoside reverse transcriptase inhibitor, stavudine. PI-treated patients have been noted to have increases in low-density lipoprotein (LDL), triglycerides (TG), and total cholesterol compared to PI-treatment naive individuals. The prevalence of lipid abnormalities in patients receiving PI-containing therapy has been estimated at 27-57 percent; moreover, cardiovascular complications have begun to be revealed. Triglyceride elevations, in particular, are not only an independent risk factor for the development of coronary artery disease, but may also lead to pancreatitis. Despite treatment with fibric acid derivatives, such as gemfibrozil, TGs typically remain elevated above the upper limit of normal in HIV-infected subjects. One possible reason for persistently elevated TGs in these patients is reduced efficacy of their fibric acid therapy, which may result ...
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Mylan-Gemfibrozil: Gemfibrozil belongs to the class of medications known as fibrates. It is used to treat high cholesterol. It works by blocking the production of certain types of cholesterol, especially the type known as triglycerides.
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The effect of bezafibrate and omega-3 fatty acids on lymphocyte cytokine release and systemic inflammation in patients with...
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Bezafibrate at Clinically Relevant Doses Decreases Serum/Liver Triglycerides via Down-Regulation of Sterol Regulatory Element...
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- A post hoc analysis was used to examine the effect of bezafibrate on progression to use of oral antidiabetic medications or insulin in individuals with diabetes at baseline. (diabetesjournals.org)
- The effect of bezafibrate on cardiac function was evaluated by echocardiography in TazKD mice with or without beta-adrenergic stress. (biomedcentral.com)
- Bezalip tablets contain the active ingredient bezafibrate, which is a type of medicine known as a fibrate. (netdoctor.co.uk)
- Bezalip mono modified-release tablets contain the active ingredient bezafibrate, which is a type of medicine known as a fibrate. (netdoctor.co.uk)
- Bezafibrate (marketed as Bezalip and various other brand names) is a fibrate drug used as a lipid-lowering agent to treat hyperlipidaemia. (wikipedia.org)
- OBJECTIVE The purpose of this study was to test the hypothesis that bezafibrate, an approved fibrate, can prevent or delay type 2 diabetes. (diabetesjournals.org)
- In response to efforts to develop these agents, at least one observer has pointed out that the fibrate bezafibrate actually is a pan-PPAR agonist and affects insulin resistance ( 5 ). (diabetesjournals.org)
- Bezafibrate (BZF) is a fibrate drug used as a lipid-lowering agent to treat hyperlipidemia. (arvojournals.org)
- Bezalip Retard SR (Bezafibrate) should not be used by patients who are pregnant, breastfeeding, lactose intolerant, children, allergic to other fibrate medications, or who have gall bladder disease, nephrotic syndrome, or reduced kidney function. (4nrx-uk.md)
- Bezafibrate is a fibrate class anti-hyperlipidaemia drug. (guidetopharmacology.org)
- Bezafibrate is the second generation of fibrate groups used as the drug of choice in the treatment of hyperlipidemia. (innovareacademics.in)
- Further evidence that substantial bulk tolerance is available in the para position is given by the lipid lowering agent bezafibrate. (wikipedia.org)
- What is Bezalip Retard SR (Bezafibrate) used for? (4nrx-uk.md)
- Bezalip Retard SR (Bezafibrate) is an oral medication prescribed along with a balanced diet and regular exercise to treat patients with high cholesterol or triglyceride levels in the blood. (4nrx-uk.md)
- How should I use Bezalip Retard SR (Bezafibrate)? (4nrx-uk.md)
- Bezalip Retard SR (Bezafibrate) should always be used strictly according to your doctor`s instructions to get the safest and most effective results from treatment. (4nrx-uk.md)
- Strictly use Bezalip Retard SR (Bezafibrate) as prescribed and follow all instructions provided by your doctor. (4nrx-uk.md)
- Bezalip Retard SR (Bezafibrate) may not be safe or suitable for all patients. (4nrx-uk.md)
- Hence, it is reasonable to hypothesize that the status of bezafibrate as a pan-PPAR agonist may give it antidiabetic properties unique among fibrates. (diabetesjournals.org)
- The aim was to evaluate the efficacy of the pan-PPAR agonist, bezafibrate, in tafazzin knockdown mice (TazKD), a mouse model of Barth syndrome that exhibits age-dependent dilated cardiomyopathy with left ventricular (LV) dysfunction. (biomedcentral.com)
- The mechanism of decreasing lipid levels by bezafibrate is by increasing the release of triglycerides, cholesterol, low-density lipoprotein and raising the amount of high-density lipoprotein, bezafibrate works as a peroxisome proliferation activated receptor agonist (PPARs) . (innovareacademics.in)
- Bezafibrate increased mitochondrial biogenesis, however also promoted oxidative stress in cardiomyocytes. (biomedcentral.com)
- Bezafibrate Upregulates Mitochondrial Biogenesis and Influence Neural Differentiation of Human-Induced Pluripotent Stem Cells. (pan.pl)
- Bezafibrate (BZ) regulates mitochondrial biogenesis by activation of PPAR's receptors and enhancing the level of PGC-1α coactivator. (pan.pl)
- Bezafibrate is used to lower the levels of fats (lipids) called cholesterol and triglycerides in the blood. (netdoctor.co.uk)
- Bezafibrate works mainly by stimulating the action of two enzymes that breakdown triglycerides. (netdoctor.co.uk)
- Bezafibrate also decreases the production of triglycerides by the liver. (netdoctor.co.uk)
- As a result of both these actions, bezafibrate lowers the levels of triglycerides in the blood. (netdoctor.co.uk)
- Bezafibrate improves markers of combined hyperlipidemia, effectively reducing LDL and triglycerides and improving HDL levels. (wikipedia.org)
- Whereas bezafibrate is used to lower triglycerides and some studies have shown a slight decrease in progression to diabetes. (healthtap.com)
- These clinical end point data were supported by biochemical evidence showing that bezafibrate slowed progression of insulin resistance ( 7 ). (diabetesjournals.org)
- Long-term use of bezafibrate slows the progression of coronary atheromas and coronary events in young male survivors of acute myocardial infarction. (thefreedictionary.com)
- In silico docking evidence indicated that bezafibrate could target cyclin dependent kinase 2(CDK2), which regulates progression through the cell cycle. (semanticscholar.org)
- We evaluated the efficacy and safety of bezafibrate for the treatment of hypertriglyceridemia in HIV-infected individuals on HAART. (scielo.br)
- Therefore, bezafibrate seems to be safe and effective for the reduction of hypertriglyceridemia in HIV-infected patients on HAART. (scielo.br)
- The study included 107 patients with isolated hypertriglyceridemia who received bezafibrate (200 mg twice daily), omega-3 fatty acids (1 g twice daily) or placebo for 12 weeks. (springer.com)
- A trial assessing the ability of a lipid-altering agent, bezafibrate, to retard the development of coronary lesions. (thefreedictionary.com)
- At baseline and after 7 months of cholesterol-lowering therapy with bezafibrate (400 mg/day) in the therapy group, coronary vasomotor response to dynamic exercise (percent change in cross-sectional vascular area at maximal exercise vs. rest [100%]) in normal and stenotic, previously dilated vessels was assessed by quantitative coronary angiography. (onlinejacc.org)
- 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)
- Randomized controlled trials should be considered to assess the utility of bezafibrate in treating patients with diabetes or in preventing diabetes in high-risk patients. (diabetesjournals.org)
- Post hoc analyses of a placebo-controlled randomized trial showed that bezafibrate may postpone or prevent type 2 diabetes ( 5 , 6 ). (diabetesjournals.org)
- In addition, the effects of 6 weeks of bezafibrate therapy were assessed in a double-blind, placebo-controlled, crossover trial. (ahajournals.org)
- Thus, we demonstrate that bezafibrate has a potent therapeutic effect on preventing cardiac dysfunction in a mouse model of Barth syndrome with obvious implications for treating the human disease. (biomedcentral.com)
- Expression Profiling Identifies Bezafibrate as Potential Therapeutic Drug for Lung Adenocarcinoma. (semanticscholar.org)
- The purpose of this study is to obtained a validated method for analyzing bezafibrate in urine using solid phase extraction (SPE)-High performance liquid chromatography (HPLC). (innovareacademics.in)
- Solid phase extraction (SPE) using hydrophilic-lipophilic balance (HLB) cartridge was performed for bezafibrate extraction from urine, afterward, a validation of analysis method using high-performance liquid chromatography (HPLC)-(UV) detection was conducted to parameters, including: selectivity (Rs), linearity (r), accuracy, precision, limit of detection (LOD) and limit of quantification (LOQ). (innovareacademics.in)
- Furthermore, we found that bezafibrate can significantly down-regulate the expression of CDK2 mRNA and p-CDK2. (semanticscholar.org)
- Bezafibrate additionally decreased total and low-density lipoprotein-cholesterol levels and the HOMA and insignificantly decreased post-glucose load plasma glucose, as well as increased high-density lipoprotein-cholesterol. (springer.com)
- CONCLUSIONS Bezafibrate appears to have clinically important antidiabetic properties. (diabetesjournals.org)
- Bezafibrate treatment was associated with a reduction in lymphocyte release of interleukin-2, interferon-γ and tumor necrosis factor-α, which was accompanied by a reduction in plasma hsCRP levels. (springer.com)
- Prolonged treatment with suprapharmacological dose of bezafibrate (0.5% in rodent diet) over a 4-month period effectively prevented LV dilation in mice isoproterenol treatment. (biomedcentral.com)
- Surprisingly, improvement of systolic function in bezafibrate-treated mice was accompanied with simultaneous reduction of cardiolipin content and increase of monolysocardiolipin levels in cardiac muscle. (biomedcentral.com)
- Using a nude mice xenograft model, we also found that bezafibrate could inhibit tumor growth of lung AC in vivo. (semanticscholar.org)
- In addition, the effects of triglyceride-lowering therapy by bezafibrate were studied. (ahajournals.org)
- The result of recovery extraction using SPE and validation of method exhibited the values that fulfilled the requirements and can be used for analysis bezafibrate in the urine. (innovareacademics.in)
- Until now has not been reported an analysis of bezafibrate in biological fluids with SPE by UV detector. (innovareacademics.in)
- Firstly, connectivity map (CMap) analysis computationally predicted bezafibrate as a putative compound against lung AC. (semanticscholar.org)
- Bezafibrate intake over 2 months substantially ameliorates the development of LV systolic dysfunction in isoproterenol-stressed TazKD mice. (biomedcentral.com)
- Bezafibrate has been shown to reduce tau protein hyperphosphorylation and other signs of tauopathy in transgenic mice having human tau mutation. (wikipedia.org)
- In a recent article, bezafibrate has been shown to induce the expression of the deficient protein in fibroblasts from some patients. (ommbidblog.com)