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Effects of Pitavastatin, Atorvastatin, and Rosuvastatin on the Risk Of
biomedicines Article Effects of Pitavastatin, Atorvastatin, and Rosuvastatin on the Risk of New-Onset Diabetes Mellitus: A Single-Center Cohort Study Wei-Ting Liu 1, Chin Lin 2,3,4, Min-Chien Tsai 5, Cheng-Chung Cheng 6, Sy-Jou Chen 7,8, Jun-Ting Liou 6 , Wei-Shiang Lin 6, Shu-Meng Cheng 6, Chin-Sheng Lin 6,* and Tien-Ping Tsao 6,9,* 1 Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei 11490, Taiwan; [email protected] 2 School of Public Health, National Defense Medical Center, Taipei 11490, Taiwan; [email protected] 3 School of Medicine, National Defense Medical Center, Taipei 11490, Taiwan 4 Graduate Institute of Life Sciences, National Defense Medical Center, Taipei 11490, Taiwan, 5 Department of Physiology and Biophysics, Graduate Institute of Physiology, National Defense Medical Center, Taipei 11490, Taiwan; [email protected] 6 Division of Cardiology, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei 11490, Taiwan; [email protected] (C.-C.C.); [email protected] (J.-T.L.); [email protected] (W.-S.L.); [email protected] (S.-M.C.) 7 Department of Emergency Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei 11490, Taiwan; [email protected] 8 Graduate Institute of Injury Prevention and Control, College of Public Health and Nutrition, Taipei Medical University, Taipei 11031, Taiwan 9 Division of Cardiology, Cheng Hsin General Hospital, Taipei 11220, Taiwan * Correspondence: [email protected] (C.-S.L.); [email protected] (T.-P.T.); Tel.: +886-2-6601-2656 (C.-S.L.); +886-2-2826-4400 (T.-P.T.) Received: 25 October 2020; Accepted: 11 November 2020; Published: 13 November 2020 Abstract: Statins constitute the mainstay treatment for atherosclerotic cardiovascular disease, which is associated with the risk of new-onset diabetes mellitus (NODM). -
Nustendi, INN-Bempedoic Acid, Ezetimibe
Summary of risk management plan for Nustendi (Bempedoic acid/Ezetimibe) This is a summary of the risk management plan (RMP) for Nustendi. The RMP details important risks of Nustendi, how these risks can be minimized, and how more information will be obtained about Nustendi's risks and uncertainties (missing information). Nustendi's summary of product characteristics (SmPC) and its package leaflet give essential information to healthcare professionals and patients on how Nustendi should be used. This summary of the RMP for Nustendi should be read in the context of all this information, including the assessment report of the evaluation and its plain-language summary, all which is part of the European Public Assessment Report (EPAR). Important new concerns or changes to the current ones will be included in updates of Nustendi's RMP. I. The Medicine and What It Is Used For Nustendi is authorized for treatment of primary hypercholesterolemia in adults, as an adjunct to diet (see SmPC for the full indication). It contains bempedoic acid as the active substance and it is given by mouth. Further information about the evaluation of Nustendi’s benefits can be found in Nustendi’s EPAR, including in its plain-language summary, available on the EMA website, under the medicine’s webpage https://www.ema.europa.eu/en/medicines/human/EPAR/nustendi II. Risks Associated With the Medicine and Activities to Minimize or Further Characterize the Risks Important risks of Nustendi, together with measures to minimize such risks and the proposed studies for learning -
Zetia® (Ezetimibe) Tablets
29480958T REV 14 ZETIA® (EZETIMIBE) TABLETS DESCRIPTION ZETIA (ezetimibe) is in a class of lipid-lowering compounds that selectively inhibits the intestinal absorption of cholesterol and related phytosterols. The chemical name of ezetimibe is 1-(4-fluorophenyl)- 3(R)-[3-(4-fluorophenyl)-3(S)-hydroxypropyl]-4(S)-(4-hydroxyphenyl)-2-azetidinone. The empirical formula is C24H21F2NO3. Its molecular weight is 409.4 and its structural formula is: OH OH S SR N F F O Ezetimibe is a white, crystalline powder that is freely to very soluble in ethanol, methanol, and acetone and practically insoluble in water. Ezetimibe has a melting point of about 163°C and is stable at ambient temperature. ZETIA is available as a tablet for oral administration containing 10 mg of ezetimibe and the following inactive ingredients: croscarmellose sodium NF, lactose monohydrate NF, magnesium stearate NF, microcrystalline cellulose NF, povidone USP, and sodium lauryl sulfate NF. CLINICAL PHARMACOLOGY Background Clinical studies have demonstrated that elevated levels of total cholesterol (total-C), low density lipoprotein cholesterol (LDL-C) and apolipoprotein B (Apo B), the major protein constituent of LDL, promote human atherosclerosis. In addition, decreased levels of high density lipoprotein cholesterol (HDL-C) are associated with the development of atherosclerosis. Epidemiologic studies have established that cardiovascular morbidity and mortality vary directly with the level of total-C and LDL-C and inversely with the level of HDL-C. Like LDL, cholesterol-enriched triglyceride-rich lipoproteins, including very-low- density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), and remnants, can also promote atherosclerosis. The independent effect of raising HDL-C or lowering triglycerides (TG) on the risk of coronary and cardiovascular morbidity and mortality has not been determined. -
Bempedoic Acid) Tablets, for Oral Use Most Common (Incidence ≥ 2% and Greater Than Placebo) Adverse Reactions Initial U.S
HIGHLIGHTS OF PRESCRIBING INFORMATION • Tendon Rupture: Tendon rupture has occurred. Discontinue NEXLETOL These highlights do not include all the information needed to use at the first sign of tendon rupture. Avoid NEXLETOL in patients who NEXLETOL™ safely and effectively. See full prescribing information have a history of tendon disorders or tendon rupture. (5.2) for NEXLETOL. --------------------------------ADVERSE REACTIONS---------------------------- NEXLETOL (bempedoic acid) tablets, for oral use Most common (incidence ≥ 2% and greater than placebo) adverse reactions Initial U.S. Approval: 2020 are upper respiratory tract infection, muscle spasms, hyperuricemia, back pain, abdominal pain or discomfort, bronchitis, pain in extremity, anemia, ----------------------------INDICATIONS AND USAGE-------------------------- and elevated liver enzymes. (6.1) NEXLETOL is an adenosine triphosphate-citrate lyase (ACL) inhibitor indicated as an adjunct to diet and maximally tolerated statin therapy for the To report SUSPECTED ADVERSE REACTIONS, contact Esperion at treatment of adults with heterozygous familial hypercholesterolemia or 833-377-7633 (833 ESPRMED) or FDA at 1-800-FDA-1088 or established atherosclerotic cardiovascular disease who require additional www.fda.gov/medwatch. lowering of LDL-C. (1) --------------------------------DRUG INTERACTIONS---------------------------- Limitations of Use: The effect of NEXLETOL on cardiovascular morbidity • Simvastatin: Avoid concomitant use of NEXLETOL with simvastatin and mortality has not been -
Statins: Mechanism of Action and Effects
J.Cell.Mol.Med. Vol 5, No 4, 2001 pp. 378-387 Review Statins: mechanism of action and effects Camelia Stancu, Anca Sima * "Nicolae Simionescu" Institute of Cellular Biology and Pathology, Bucharest, Romania Received: November 12, 2001; Accepted: December 5, 2001 • Introduction • Effects on • Classification of statins - cholesterol esterification and - How they are obtained its accumulation in macrophages - Liver metabolism - endothelial cell function - Physico-chemical properties - inflammatory process - Specific activity - proliferation, migration and • Mechanisms for the action of statins apoptosis of arterial smooth muscle cells - Mechanisms involving lipids - stability of the atherosclerotic plaque - Mechanisms involving intracellular - platelets activation signaling pathways - coagulation process • Beneficial effects of statins • Adverse effects of statins therapy • Conclusions Abstract The beneficial effects of statins are the result of their capacity to reduce cholesterol biosyntesis, mainly in the liver, where they are selectively distributed, as well as to the modulation of lipid metabolism, derived from their effect of inhibition upon HMG-CoA reductase. Statins have antiatherosclerotic effects, that positively correlate with the percent decrease in LDL cholesterol. In addition, they can exert antiatherosclerotic effects independently of their hypolipidemic action. Because the mevalonate metabolism generates a series of isoprenoids vital for different cellular functions, from cholesterol synthesis to the control of cell growth and differentiation, HMG-CoA reductase inhibition has beneficial pleiotropic effects. Consequently, statins reduce significantly the incidence of coronary events, both in primary and secondary prevention, being the most efficient hypolipidemic compounds that have reduced the rate of mortality in coronary patients. Independent of their hypolipidemic properties, statins interfere with events involved in bone formation and impede tumor cell growth. -
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 -
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. -
Bempedoic Acid and Inclisiran for Patients with Heterozygous Familial Hypercholesterolemia and for Secondary Prevention of ASCVD: Effectiveness and Value
Bempedoic Acid and Inclisiran for Patients with Heterozygous Familial Hypercholesterolemia and for Secondary Prevention of ASCVD: Effectiveness and Value Draft Evidence Report November 12, 2020 Prepared for ©Institute for Clinical and Economic Review, 2020 ICER Staff and Consultants Modeling Team Grace A. Lin, MD, MAS Dhruv S. Kazi, MD, MSc, MS Associate Professor of Medicine and Health Policy Associate Director, Smith Center for Outcomes University of California, San Francisco Research in Cardiology Director, Cardiac Critical Care Unit Jane Jih, MD, MPH Beth Israel Deaconess Medical Center Assistant Professor, Division of General Internal Associate Professor, Harvard Medical School Medicine University of California, San Francisco Foluso Agboola, MBBS, MPH Director, Evidence Synthesis Dr. Kazi was responsible for the development of the ICER cost-effectiveness model, interpretation of results, and drafting of the economic sections of this report; the Rick Chapman, PhD, MS resulting ICER reports do not necessarily represent the Director of Health Economics views of Beth Israel Deaconess Medical Center or ICER Harvard Medical School. Steven D. Pearson, MD, MSc President ICER DATE OF PUBLICATION: November 12, 2020 How to cite this document: Lin GA, Kazi DS, Jih J, Agboola F, Chapman R, Pearson SD. Inclisiran and Bempedoic Acid for Patients with Heterozygous Familial Hypercholesterolemia and for Secondary Prevention of ASCVD: Effectiveness and Value; Draft Evidence Report. Institute for Clinical and Economic Review, November 12, 2020. https://icer-review.org/material/high-cholesterol-update- draft-evidence-report/ Grace Lin served as the lead author for the report and wrote the background, other benefits, and contextual considerations sections of the report, with Jane Jih serving as a co-author. -
Lipobay, INN-Cerivastatin
ANNEX I LIST OF THE NAMES, PHARMACEUTICAL FORM, STRENGTHS OF THE MEDICINAL PRODUCTS, ROUTE OF ADMINISTRATION, MARKETING AUTHORISATION HOLDERS, PACKAGING AND PACKAGE SIZES IN THE MEMBER STATES EMEA 2002 Reproduction and/or distribution of this document is authorised for non commercial purposes only provided the EMEA is acknowledged ANNEX I Marketing Authorisation Route of Member State Invented name Strength Pharmaceutical Form Packaging Package-size Holder administration Austria Bayer Austria Gesellschaft Lipobay 0.1 mg Film-coated tablet Oral use Blister 14, 20, 28, 30, G.m.b.H. 50, 98, 100 and Lerchenfelder Guertel 9-11 160 tablets A-1164 Wien Austria Bayer Austria Gesellschaft Lipobay 0.2 mg Film-coated tablet Oral use Blister 14, 20, 28, 30, G.m.b.H. 50, 98, 100 and Lerchenfelder Guertel 9-11 160 tablets A-1164 Wien Austria Bayer Austria Gesellschaft Lipobay 0.3 mg Film-coated tablet Oral use Blister 30 tablets G.m.b.H. Lerchenfelder Guertel 9-11 A-1164 Wien Austria Bayer Austria Gesellschaft Lipobay 0.4 mg Film-coated tablet Oral use Blister 30 tablets G.m.b.H. Lerchenfelder Guertel 9-11 A-1164 Wien Austria Bayer Austria Gesellschaft Liposterol 0.4 mg Film-coated tablet Oral use Blister 30 tablets G.m.b.H. Lerchenfelder Guertel 9-11 A-1164 Wien CPMP/811/02 1 EMEA 2002 Belgium Bayer NV Lipobay 0.1 mg Film-coated tablet Oral use Blister 14, 20, 28, 30, Louizalaan 143 50, 98, 100 and B-1050 Brussel 160 tablets Belgium Belgium Bayer NV Lipobay 0.2 mg Film-coated tablet Oral use Blister 14, 20, 28, 30, Louizalaan 143 50, 98, 100 and B-1050 Brussel 160 tablets Belgium Belgium Bayer NV Lipobay 0.3 mg Film-coated tablet Oral use Blister 14, 20, 28, 30, Louizalaan 143 50, 98, 100 and B-1050 Brussel 160 tablets Belgium Belgium Bayer NV Lipobay 0.4 mg Film-coated tablet Oral use Blister 14, 20, 28, 30, Louizalaan 143 50, 98, 100 and B-1050 Brussel 160 tablets Belgium Belgium Fournier Pharma S.A. -
Pitavastatin (Livalo) Have Not Been Shown to Decrease LDL-C More Doses of Other Statins and No Data Are Available on Clinical Outcomes with Pitavastatin
Livalo (Pitavastatin) Thomas Dayspring MD, FACP, FNLA 1) LIVALO DISCUSSION: Although new to the US pitavastatin has been used in Japan for many years with great safety (in a population fairly sensitive to statins). Because it binds much more completely with HMG CoA reductase than other statins, it takes a much less concentration compared to other statins to inhibit cholesterol synthesis (thus it is marketed at 1, 2 and 4 mg rather than the usual 10, 20, and 40 mg). The best and most current review of it I have seen is from Clin. Lipidol. (2010) 5(3), 309–323 where all statins are compared on all clinically important pharmacokinetic and pharmacodynamic parameters. The author concludes: "Pitavastatin is a novel statin that induces plaque regression (IVUS Study) and is non- inferior to atorvastatin and, on some measures, superior to simvastatin and to pravastatin in the elderly. Pitavastatin addresses non-LDL-C risk factors, including producing sustained increases in HDL-C levels. Both the pitavastatin molecule and the lactone metabolite undergo very little metabolism by CYP3A4 and, therefore, unlike some other statins, does not interact with CYP3A4 substrates. It is the least lipophilic statin and thus requires like rosuvastatin various ABC transporters and solute carriers like organic anion transporters to get in and out of cells and thus there are potential interactions (as with most other statins) with erythromycin, cyclosporine, gemfibrozil, ritonavir/lopinavir etc. It's LDL-C lowering ability is in the Lipitor 20-40 mg range with a 30-40% range (depending on the dose used) and is somewhat more effective at raising HDL-C and apoA-I than other statins: the mechanism is it stimulates apoA-I production and ABCA1 upregulation (Biochemical and Biophysical Research Communications 324 (2004) 835–839).