Ciprofibrate 100Mg Tablets
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Partial Agreement in the Social and Public Health Field
COUNCIL OF EUROPE COMMITTEE OF MINISTERS (PARTIAL AGREEMENT IN THE SOCIAL AND PUBLIC HEALTH FIELD) RESOLUTION AP (88) 2 ON THE CLASSIFICATION OF MEDICINES WHICH ARE OBTAINABLE ONLY ON MEDICAL PRESCRIPTION (Adopted by the Committee of Ministers on 22 September 1988 at the 419th meeting of the Ministers' Deputies, and superseding Resolution AP (82) 2) AND APPENDIX I Alphabetical list of medicines adopted by the Public Health Committee (Partial Agreement) updated to 1 July 1988 APPENDIX II Pharmaco-therapeutic classification of medicines appearing in the alphabetical list in Appendix I updated to 1 July 1988 RESOLUTION AP (88) 2 ON THE CLASSIFICATION OF MEDICINES WHICH ARE OBTAINABLE ONLY ON MEDICAL PRESCRIPTION (superseding Resolution AP (82) 2) (Adopted by the Committee of Ministers on 22 September 1988 at the 419th meeting of the Ministers' Deputies) The Representatives on the Committee of Ministers of Belgium, France, the Federal Republic of Germany, Italy, Luxembourg, the Netherlands and the United Kingdom of Great Britain and Northern Ireland, these states being parties to the Partial Agreement in the social and public health field, and the Representatives of Austria, Denmark, Ireland, Spain and Switzerland, states which have participated in the public health activities carried out within the above-mentioned Partial Agreement since 1 October 1974, 2 April 1968, 23 September 1969, 21 April 1988 and 5 May 1964, respectively, Considering that the aim of the Council of Europe is to achieve greater unity between its members and that this -
Clofibrate Causes an Upregulation of PPAR- Target Genes but Does Not
tapraid4/zh6-areg/zh6-areg/zh600707/zh65828d07a xppws S� 1 4/20/07 9: 48 MS: R-00603-2006 Ini: 07/rgh/dh A " #h!si$l %egul Integr &$ ' #h!si$l 2%&' R000 (R000) 200!$ 3. Originalarbeiten *irst publis#ed "arc# + 5) 200! doi' + 0$ + + 52,a-pregu$ 0060&$ 2006$ Clofibrate causes an upregulation of PPAR-� target genes but does not alter AQ: 1 expression of SREBP target genes in liver and adipose tissue of pigs Sebastian Luci, Beatrice Giemsa, Holger Kluge, and Klaus Eder Institut fu¨r Agrar- und Erna¨hrungswissenschaften, Martin-Luther-Universita¨t Halle-Wittenberg, Halle (Saale), Ger an! Submitted 25 August 2006 accepted in final form ! "arc# 200! AQ: 2 Luci S, Giemsa B, Kluge H, Eder K. Clofibrate causes an usuall0 increased 3#en baseline concentrations are lo3 1?62$ upregulation of PPAR-� target genes but does not alter expression of Effects of PPAR-� activation #ave been mostl0 studied in SREBP target genes in liver and adipose tissue of pigs$ A " #h!si$l rodents) 3#ic# ex#ibit a strong expression of PPAR-� in liver %egul Integr &$ ' #h!si$l 2%&' R000 (R000) 200!$ *irst publis#ed and s#o3 peroxisome proliferation in t#e liver in response to "arc# + 5) 200! doi' + 0$ + + 52,a-pregu$ 0060&$ 2006$ ./#is stud0 inves- PPAR-� activation 1&62$ Expression of PPAR-� and sensitivit0 tigated t#e effect of clofibrate treatment on expression of target genes of peroxisome proliferator-activated receptor 1PPAR2-� and various to peroxisomal induction b0 PPAR-� agonists) #o3ever) var0 genes of t#e lipid metabolism in liver and adipose tissue of pigs$ An greatl0 -
Joint Assessment Report Was Discussed by the Phvwp at Its Meeting in July 2007 and Finalised in September 2007
ASSESSMENT REPORT on the benefit:risk of fibrates EXECUTIVE SUMMARY 1. BACKGROUND In the light of the established role of statins in the primary and secondary prevention of cardiovascular disease (CVD) and safety concerns arising from the use of fibrates, the CHMP Pharmacovigilance Working Party (PhVWP) agreed to undertake a benefit:risk assessment of this class of medicines. The objective was to establish the current place of fibrates in the treatment of cardiovascular and dyslipidaemic diseases, and in diabetes mellitus; also to provide recommendations regarding amendments of the Summary of Product Characteristics (SPC), as necessary. Fibrates exert their effects mainly by activating the peroxisome proliferator-activated receptor-alpha (PPAR-alpha). Unique in this class, bezafibrate is an agonist for all three PPAR isoforms alpha, gamma, and delta. Fibrates have been shown to reduce plasma triglycerides by 30% to 50% and raise the level of high density lipoprotein cholesterol (HDL- C) by 2% to 20%. Their effect on low density lipoprotein cholesterol (LDL-C) is variable, ranging from no effect to a small decrease of the order of 10%. Today there are four licensed fibrates: bezafibrate, fenofibrate, gemfibrozil and ciprofibrate. Their currently approved indications are quite broad and in many cases still use the old Fredrickson classification for dyslipidaemias. 2. METHODOLOGY In February 2006 a List of Questions was agreed by the PhVWP for the Marketing Authorisation Holders (MAHs) of medicinal products containing one of the four currently licensed fibrates (Annex 1). Other clofibrate-containing medicinal products (e.g. etofibrate, etofyllinclofibrate) were excluded from this class review, since these are available only in a few member states via national marketing authorizations. -
Pharmaceuticals Appendix
)&f1y3X PHARMACEUTICAL APPENDIX TO THE HARMONIZED TARIFF SCHEDULE )&f1y3X PHARMACEUTICAL APPENDIX TO THE TARIFF SCHEDULE 3 Table 1. This table enumerates products described by International Non-proprietary Names (INN) which shall be entered free of duty under general note 13 to the tariff schedule. The Chemical Abstracts Service (CAS) registry numbers also set forth in this table are included to assist in the identification of the products concerned. For purposes of the tariff schedule, any references to a product enumerated in this table includes such product by whatever name known. Product CAS No. Product CAS No. ABAMECTIN 65195-55-3 ADAPALENE 106685-40-9 ABANOQUIL 90402-40-7 ADAPROLOL 101479-70-3 ABECARNIL 111841-85-1 ADEMETIONINE 17176-17-9 ABLUKAST 96566-25-5 ADENOSINE PHOSPHATE 61-19-8 ABUNIDAZOLE 91017-58-2 ADIBENDAN 100510-33-6 ACADESINE 2627-69-2 ADICILLIN 525-94-0 ACAMPROSATE 77337-76-9 ADIMOLOL 78459-19-5 ACAPRAZINE 55485-20-6 ADINAZOLAM 37115-32-5 ACARBOSE 56180-94-0 ADIPHENINE 64-95-9 ACEBROCHOL 514-50-1 ADIPIODONE 606-17-7 ACEBURIC ACID 26976-72-7 ADITEREN 56066-19-4 ACEBUTOLOL 37517-30-9 ADITOPRIME 56066-63-8 ACECAINIDE 32795-44-1 ADOSOPINE 88124-26-9 ACECARBROMAL 77-66-7 ADOZELESIN 110314-48-2 ACECLIDINE 827-61-2 ADRAFINIL 63547-13-7 ACECLOFENAC 89796-99-6 ADRENALONE 99-45-6 ACEDAPSONE 77-46-3 AFALANINE 2901-75-9 ACEDIASULFONE SODIUM 127-60-6 AFLOQUALONE 56287-74-2 ACEDOBEN 556-08-1 AFUROLOL 65776-67-2 ACEFLURANOL 80595-73-9 AGANODINE 86696-87-9 ACEFURTIAMINE 10072-48-7 AKLOMIDE 3011-89-0 ACEFYLLINE CLOFIBROL 70788-27-1 -
Colesevelam Hydrochloride (Cholestagel) a New, Potent Bile Acid Sequestrant Associated with a Low Incidence of Gastrointestinal Side Effects
ORIGINAL INVESTIGATION Colesevelam Hydrochloride (Cholestagel) A New, Potent Bile Acid Sequestrant Associated With a Low Incidence of Gastrointestinal Side Effects Michael H. Davidson, MD; Maureen A. Dillon; Bruce Gordon, MD; Peter Jones, MD; Julie Samuels, MD; Stuart Weiss, MD; Jonathon Isaacsohn, MD; Phillip Toth, MD; Steven K. Burke, MD Objectives: To compare colesevelam hydrochloride mg/dL) (19.1%) in the 3.75-g/d colesevelam treatment (Cholestagel), a nonabsorbed hydrogel with bile acid– group. Low-density lipoprotein cholesterol concentra- sequestering properties, with placebo for its lipid- tions at the end of treatment were significantly reduced lowering efficacy, its effects on laboratory and clinical from baseline levels in the 3.0- and 3.75-g/d colesevelam safety parameters, and the incidence of adverse events. treatment groups (P = .01 and P,.001, respectively). To- tal cholesterol levels demonstrated a similar response to Methods: Following diet and placebo lead-in periods, colesevelam treatment, with an 8.1% decrease from base- placebo or colesevelam was administered at 4 dosages (1.5, line in the 3.75-g/d treatment group (P<.001). High- 2.25, 3.0, or 3.75 g/d) for 6 weeks with morning and density lipoprotein cholesterol levels rose significantly evening meals to men and women with hypercholester- in the 3.0- and 3.75-g/d colesevelam treatment groups, olemia (low-density lipoprotein cholesterol level .4.14 by 11.2% (P = .006) and 8.1% (P = .02), respectively. mmol/L [.160 mg/dL]). Patients returned to the clinic Median triglyceride levels did not change from baseline, every 2 weeks throughout the treatment period for lipid nor were there any significant differences between parameter measurements and adverse event assess- treatment groups. -
Download Product Insert (PDF)
PRODUCT INFORMATION Etofibrate Item No. 21022 CAS Registry No.: 31637-97-5 Formal Name: 3-pyridinecarboxylic acid, Cl 2-[2-(4-chlorophenoxy)-2-methyl- O 1-oxopropoxy]ethyl ester O Synonym: Nicotinic Acid O O N MF: C18H18ClNO5 O FW: 363.8 Purity: ≥98% UV/Vis.: λmax: 222, 263 nm Supplied as: A crystalline solid Storage: -20°C Stability: ≥2 years Information represents the product specifications. Batch specific analytical results are provided on each certificate of analysis. Laboratory Procedures Etofibrate is supplied as a crystalline solid. A stock solution may be made by dissolving the etofibrate in the solvent of choice. Etofibrate is soluble in organic solvents such as ethanol, DMSO, and dimethyl formamide (DMF), which should be purged with an inert gas. The solubility of etofibrate in ethanol and DMSO is approximately 80 mg/ml and approximately 50 mg/ml in DMF. Etofibrate is sparingly soluble in aqueous buffers. For maximum solubility in aqueous buffers, etofibrate should first be dissolved in ethanol and then diluted with the aqueous buffer of choice. Etofibrate has a solubility of approximately 0.1 mg/ml in a 1:5 solution of ethanol:PBS (pH 7.2) using this method. We do not recommend storing the aqueous solution for more than one day. Description Etofibrate is a combination of niacin and clofibrate (Item No. 10956) that acts as a hypolipidemic agent.1 In vivo, etofibrate decreases plasma cholesterol and triglyceride concentrations and increases bile cholesterol content in rats.1,2 It also decreases thromboxane formation, platelet aggregation, and plasma viscosity and inhibits neointima formation in a carotid artery balloon injury rat model.3 Formulations containing etofibrate have been used to treat hyperlipidemia. -
Rosuvastatin
Rosuvastatin Rosuvastatin Systematic (IUPAC) name (3R,5S,6E)-7-[4-(4-fluorophenyl)-2-(N-methylmethanesulfonamido)-6-(propan- 2-yl)pyrimidin-5-yl]-3,5-dihydroxyhept-6-enoic acid Clinical data Trade names Crestor AHFS/Drugs.com monograph MedlinePlus a603033 Pregnancy AU: D category US: X (Contraindicated) Legal status AU: Prescription Only (S4) UK: Prescription-only (POM) US: ℞-only Routes of oral administration Pharmacokinetic data Bioavailability 20%[1] Protein binding 88%[1] Metabolism Liver (CYP2C9(major) andCYP2C19-mediated; only minimally (~10%) metabolised)[1] Biological half-life 19 hours[1] Excretion Faeces (90%)[1] Identifiers CAS Registry 287714-41-4 Number ATC code C10AA07 PubChem CID: 446157 IUPHAR/BPS 2954 DrugBank DB01098 UNII 413KH5ZJ73 KEGG D01915 ChEBI CHEBI:38545 ChEMBL CHEMBL1496 PDB ligand ID FBI (PDBe, RCSB PDB) Chemical data Formula C22H28FN3O6S Molecular mass 481.539 SMILES[show] InChI[show] (what is this?) (verify) Rosuvastatin (marketed by AstraZenecaas Crestor) 10 mg tablets Rosuvastatin, marketed as Crestor, is a member of the drug class of statins, used in combination with exercise, diet, and weight-loss to treat high cholesterol and related conditions, and to prevent cardiovascular disease. It was developed by Shionogi. Crestor is the fourth- highest selling drug in the United States, accounting for approx. $5.2 billion in sales in 2013.[2] Contents [hide] 1Medical uses 2Side effects and contraindications 3Drug interactions 4Structure 5Mechanism of action 6Pharmacokinetics 7Indications and regulation -
Pharmacological Targeting of the Atherogenic Dyslipidemia Complex: the Next Frontier in CVD Prevention Beyond Lowering LDL Cholesterol
Diabetes Volume 65, July 2016 1767 Changting Xiao,1 Satya Dash,1 Cecilia Morgantini,1 Robert A. Hegele,2 and Gary F. Lewis1 Pharmacological Targeting of the Atherogenic Dyslipidemia Complex: The Next Frontier in CVD Prevention Beyond Lowering LDL Cholesterol Diabetes 2016;65:1767–1778 | DOI: 10.2337/db16-0046 Notwithstanding the effectiveness of lowering LDL cho- has been the primary goal of dyslipidemia management, lesterol, residual CVD risk remains in high-risk popula- with statins as the treatment of choice for CVD prevention. tions, including patients with diabetes, likely contributed Large-scale, randomized, clinical trials of LDL-lowering PERSPECTIVES IN DIABETES to by non-LDL lipid abnormalities. In this Perspectives therapies have demonstrated significant reduction in CVD in Diabetes article, we emphasize that changing demo- events over a wide range of baseline LDL-C levels (2,3). graphics and lifestyles over the past few decades have However, even with LDL-C levels lowered substantially or “ resulted in an epidemic of the atherogenic dyslipidemia at treatment goals with statin therapy, CVD risks are not ” complex, the main features of which include hypertrigly- eliminated and there remains significant “residual risk.” In- ceridemia, low HDL cholesterol levels, qualitative changes tensifying statin therapy may provide additional benefits in LDL particles, accumulation of remnant lipoproteins, (4,5); this approach, however, has limited potential, owing and postprandial hyperlipidemia. We brieflyreviewthe to tolerability, side effects, and finite efficacy. Further LDL-C underlying pathophysiology of this form of dyslipidemia, lowering may also be achieved with the use of nonstatin in particular its association with insulin resistance, obe- sity, and type 2 diabetes, and the marked atherogenicity agents, such as cholesterol absorption inhibitors and PCSK9 of this condition. -
PI Changes for Fibrates
Changes to Product Information as approved by the CHMP on 21 October 2010, pending endorsement by the European Commission 1 BEZAFIBRATE ANNEX I -SUMMARY OF PRODUCT CHARACTERISTICS 4.1 Therapeutic indications (to replace current text) [Product name] is indicated as an adjunct to diet and other non-pharmacological treatment (e.g. exercise, weight reduction) for the following: - Treatment of severe hypertriglyceridaemia with or without low HDL cholesterol. - Mixed hyperlipidaemia when a statin is contraindicated or not tolerated. 5.1 Pharmacodynamic properties (Additional text) There is evidence that treatment with fibrates may reduce coronary heart disease events but they have not been shown to decrease all cause mortality in the primary or secondary prevention of cardiovascular disease ANNEX III -LABELLING AND PACKAGE LEAFLET What [Product name] is and what it is used for [Product name] belongs to a group of medicines, commonly known as fibrates. These medicines are used to lower the level of fats (lipids) in the blood. For example the fats known as triglycerides. [Product name] is used, alongside a low fat diet and other non-medical treatments such as exercise and weight loss, to lower levels of fats in the blood. 2 CIPROFIBRATE ANNEX I -SUMMARY OF PRODUCT CHARACTERISTICS 4.1 Therapeutic indications (to replace current text) [Product name] is indicated as an adjunct to diet and other non-pharmacological treatment (e.g. exercise, weight reduction) for the following: - Treatment of severe hypertriglyceridaemia with or without low HDL cholesterol. - Mixed hyperlipidaemia when a statin is contraindicated or not tolerated. 5.1 Pharmacodynamic properties (Additional text) There is evidence that treatment with fibrates may reduce coronary heart disease events but they have not been shown to decrease all cause mortality in the primary or secondary prevention of cardiovascular disease ANNEX III -LABELLING AND PACKAGE LEAFLET What [Product name] is and what it is used for [Product name] belongs to a group of medicines, commonly known as fibrates. -
NCEP Drug Treatment
NCEP Drug Treatment The information contained in this document is taken directly from the National Cholesterol Education Program, Adult Treatment Panel III (NCEP, ATP III) that is published by the National Institutes of Health – National Heart, Lung and Blood Institute. Major Classes of Drugs Available Affecting Lipoprotein Metabolism HMG CoA reductase inhibitors—lovastatin, pravastatin, simvastatin, fluvastatin, atorvastatin Bile acid sequestrants—cholestyramine, colestipol, colesevelam Nicotinic acid—crystalline, timed-release preparations, Niaspan® Fibric acid derivatives (fibrates)—gemfibrozil, fenofibrate, clofibrate Estrogen replacement Omega-3 fatty acids Major Uses and Lipid/ Lipoprotien Effects of Each Drug Class Drug Class Major Use Lipid/ Lipoprotein Effects LDL ↓ 18-55% HMG CoA reductase To lower LDL cholesterol HDL ↑ 5-15% inhibitors (statins) TG ↓ 7-30% LDL ↓ 15-30% Bile acid sequestrants To lower LDL cholesterol HDL ↑ 3-5% TG No effect or increase LDL ↓ 5-25% Useful in most lipid and Nicotinic acid HDL ↑ 15-35% lipoprotein abnormalities TG ↓ 20-50% LDL ↓ 5-20% (in nonhypertriglyceridemic persons); Hypertriglyceridemia; may be increased in hypertriglyceridemic persons Fibric acids Atherogenic dyslipidemia HDL ↑ 10-35% (more in severe hypertriglyceridemia) TG ↓ 20-50% NCEP Drug Treatment The information contained in this document is taken directly from the National Cholesterol Education Program, Adult Treatment Panel III (NCEP, ATP III) that is published by the National Institutes of Health – National Heart, Lung and -
Fenofibrate, Bezafibrate, Ciprofibrate and Gemfibrozil Procedure Number
28 February 2011 EMA/CHMP/580013/2012 Assessment report for fenofibrate, bezafibrate, ciprofibrate, and gemfibrozil containing medicinal products pursuant to Article 31 of Directive 2001/83/EC, as amended INN: fenofibrate, bezafibrate, ciprofibrate and gemfibrozil Procedure number: EMEA/H/A-1238 Assessment Report as adopted by the CHMP with all information of a commercially confidential nature deleted. 7 Westferry Circus ● Canary Wharf ● London E14 4HB ● United Kingdom Telephone +44 (0)20 7418 8400 Facsimile +44 (0)20 7523 7051 E -mail [email protected] Website www.ema.europa.eu An agency of the European Union © European Medicines Agency, 2013. Reproduction is authorised provided the source is acknowledged. Table of contents 1. Background information on the procedure .............................................. 3 1.1. Referral of the matter to the CHMP ......................................................................... 3 2. Scientific discussion ................................................................................ 3 2.1. Introduction......................................................................................................... 3 2.2. Clinical aspects .................................................................................................... 4 2.2.1. PhVWP recommendation ..................................................................................... 4 2.2.2. CHMP review ..................................................................................................... 7 2.2.3. Discussion ..................................................................................................... -
Lipid Lowering Drugs Prescription and the Risk of Peripheral Neuropathy
1047 J Epidemiol Community Health: first published as 10.1136/jech.2003.013409 on 16 November 2004. Downloaded from RESEARCH REPORT Lipid lowering drugs prescription and the risk of peripheral neuropathy: an exploratory case-control study using automated databases Giovanni Corrao, Antonella Zambon, Lorenza Bertu`, Edoardo Botteri, Olivia Leoni, Paolo Contiero ............................................................................................................................... J Epidemiol Community Health 2004;58:1047–1051. doi: 10.1136/jech.2003.013409 Study objective: Although lipid lowering drugs are effective in preventing morbidity and mortality from cardiovascular events, the extent of their adverse effects is not clear. This study explored the association between prescription of lipid lowering drugs and the risk of peripheral neuropathy. Design: A population based case-control study was carried out by linkage of several automated databases. Setting: Resident population of a northern Italian Province aged 40 years or more. Participants: Cases were patients discharged for peripheral neuropathy in 1998–1999. For each case up See end of article for authors’ affiliations to 20 controls were randomly selected among those eligible. Altogether 2040 case patients and 36 041 ....................... controls were included in the study. Exposure ascertainment: Prescription drug database was used to assess exposure to lipid lowering drugs Correspondence to: Professor G Corrao, at any time in the one year period preceding the index date.