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Drug Class Review Beta Adrenergic Blockers
Drug Class Review Beta Adrenergic Blockers Final Report Update 4 July 2009 Update 3: September 2007 Update 2: May 2005 Update 1: September 2004 Original Report: September 2003 The literature on this topic is scanned periodically. The purpose of this report is to make available information regarding the comparative effectiveness and safety profiles of different drugs within pharmaceutical classes. Reports are not usage guidelines, nor should they be read as an endorsement of, or recommendation for, any particular drug, use, or approach. Oregon Health & Science University does not recommend or endorse any guideline or recommendation developed by users of these reports. Mark Helfand, MD, MPH Kim Peterson, MS Vivian Christensen, PhD Tracy Dana, MLS Sujata Thakurta, MPA:HA Drug Effectiveness Review Project Marian McDonagh, PharmD, Principal Investigator Oregon Evidence-based Practice Center Mark Helfand, MD, MPH, Director Oregon Health & Science University Copyright © 2009 by Oregon Health & Science University Portland, Oregon 97239. All rights reserved. Final Report Update 4 Drug Effectiveness Review Project TABLE OF CONTENTS INTRODUCTION .......................................................................................................................... 6 Purpose and Limitations of Evidence Reports........................................................................................ 8 Scope and Key Questions .................................................................................................................... 10 METHODS................................................................................................................................. -
Advice for Primary Care Regarding Beta Blockers in Heart Failure and Qof
Advice for Primary Care Regarding Beta-Blockers in Heart Failure and QOF ADVICE FOR PRIMARY CARE REGARDING BETA BLOCKERS IN HEART FAILURE AND QOF Author(s): Trudi Phillips, Lead Nurse, SEWCN / Heart Failure Specialist Nurse, Cwm Taf HB Date: 20 th May 2010 Version: 4: Status Final Pathway: Heart Failure Intended Audience: Cardiac Network, GPs and Primary Care Staff Purpose and Summary of Document: To advise GPs and primary care on the initiation of Beta Blockers for patients with heart failure and changing Beta Blocker medication. Publication / Distribution: • Cardiac Network primary care distribution list • Cardiac Network GPs via email • Network website ( http://www.sewcn.wales.nhs.uk ; http://nww.sewcn.wales.nhs.uk ) • Highlight in next e-Newsletter and Heart Matters Date of Issue: 21 st May 2010 Review Date: May 2011 Date published on Network Website: 10 th May 2010 South East Wales Cardiac Network Advice for Primary Care Regarding Beta-Blockers in Heart Failure and QOF Author: Trudi Phillips. SEWCN and Cwm Taf Date: 7th May 2010 Status: Final HB Intended Audience: Page: 1 of 3 Cardiac Network GPs Primary Care Staff Advice for primary care regarding Beta-blockers in Heart Failure and QOF Carvedilol, Bisoprolol and Nebivolol (in the elderly) are the only three beta-blockers currently licensed for use in heart failure in the UK. Beta-blockade therapy for heart failure should be introduced in a ‘ start low, go slow ’ manner, with assessment of heart rate, blood pressure, and clinical status after each titration. Beta blocker Starting dose Maximum target dose Bisoprolol 1.25 mg od 10 mg od Carvedilol 3.125 mg bd 25mg bd Nebivolol (in the elderly) 1.25 mg od 10 mg od For patients with mild to moderate heart failure maximum dose of Carvedilol is 50 mg twice daily if weight more than 85 kg How to use: • Start with a low dose (see above). -
Zonegran, INN-Zonisamide
SCIENTIFIC DISCUSSION 1. Introduction Many patients (30 to 40% of the overall population with epilepsy) continue to have seizures in spite of receiving antiepileptic drug (AED) treatment. The prevalence of active epilepsy, 5-10/1000, is one of the highest among serious neurological disorders with more than 50 million people affected worldwide. Two peaks of incidence are observed, in early childhood and among elderly people. Some patients will have life-long epilepsy. International classifications, such as the International League Against Epilepsy (ILAE) classification recognise many epileptic diseases or syndromes and each of them can be expressed clinically by one or several seizure groupings. Partial epilepsies (localisation related) are the more frequent, accounting for more than 60% of the epilepsies, and they include most of the difficult-to-treat patients. In terms of seizure types, partial epilepsies include simple partial seizures (without impairment of consciousness), complex partial seizures (with impairment of consciousness and often more disabling) and secondarily generalized tonic-clonic seizures. The symptoms are a function of the localisation of the site of seizure onset in the brain (epileptogenic zone) and of the propagation pathways of the abnormal discharge. Therapeutic management usually follows a staged approach with newly diagnosed patients starting prophylactic treatment with a single drug, and several alternative drugs may be tried in the event of lack of efficacy or poor tolerability. For patients not responding to several attempts of monotherapy, combinations of antiepileptic drugs are generally employed early in the management process. Uncontrolled epilepsy is associated with cognitive deterioration, psychosocial dysfunction, dependent behaviour, restricted lifestyle, poor quality of life and excess mortality, in particular from sudden unexpected death in epilepsy patients (SUDEP). -
DRUGS REQUIRING PRIOR AUTHORIZATION in the MEDICAL BENEFIT Page 1
Effective Date: 08/01/2021 DRUGS REQUIRING PRIOR AUTHORIZATION IN THE MEDICAL BENEFIT Page 1 Therapeutic Category Drug Class Trade Name Generic Name HCPCS Procedure Code HCPCS Procedure Code Description Anti-infectives Antiretrovirals, HIV CABENUVA cabotegravir-rilpivirine C9077 Injection, cabotegravir and rilpivirine, 2mg/3mg Antithrombotic Agents von Willebrand Factor-Directed Antibody CABLIVI caplacizumab-yhdp C9047 Injection, caplacizumab-yhdp, 1 mg Cardiology Antilipemic EVKEEZA evinacumab-dgnb C9079 Injection, evinacumab-dgnb, 5 mg Cardiology Hemostatic Agent BERINERT c1 esterase J0597 Injection, C1 esterase inhibitor (human), Berinert, 10 units Cardiology Hemostatic Agent CINRYZE c1 esterase J0598 Injection, C1 esterase inhibitor (human), Cinryze, 10 units Cardiology Hemostatic Agent FIRAZYR icatibant J1744 Injection, icatibant, 1 mg Cardiology Hemostatic Agent HAEGARDA c1 esterase J0599 Injection, C1 esterase inhibitor (human), (Haegarda), 10 units Cardiology Hemostatic Agent ICATIBANT (generic) icatibant J1744 Injection, icatibant, 1 mg Cardiology Hemostatic Agent KALBITOR ecallantide J1290 Injection, ecallantide, 1 mg Cardiology Hemostatic Agent RUCONEST c1 esterase J0596 Injection, C1 esterase inhibitor (recombinant), Ruconest, 10 units Injection, lanadelumab-flyo, 1 mg (code may be used for Medicare when drug administered under Cardiology Hemostatic Agent TAKHZYRO lanadelumab-flyo J0593 direct supervision of a physician, not for use when drug is self-administered) Cardiology Pulmonary Arterial Hypertension EPOPROSTENOL (generic) -
Summary of Product Characteristics
Health Products Regulatory Authority Summary of Product Characteristics 1 NAME OF THE VETERINARY MEDICINAL PRODUCT Cardisure 3.5 mg/ml Oral Solution for Dogs 2 QUALITATIVE AND QUANTITATIVE COMPOSITION Each ml contains Active substance: Pimobendan 3.5 mg Excipients: Benzyl alcohol (E1519) 1.0 mg For the full list of excipients, see section 6.1. 3 PHARMACEUTICAL FORM Oral Solution. Clear, colourless, semi-viscous liquid. 4 CLINICAL PARTICULARS 4.1 Target Species Dogs. 4.2 Indications for use, specifying the target species For the treatment of canine congestive heart failure originating from valvular insufficiency (mitral and/or tricuspid regurgitation) or dilated cardiomyopathy. 4.3 Contraindications Do not use in cases of hypertrophic cardiomyopathies or clinical conditions where an augmentation of cardiac output is not possible for functional or anatomical reasons (e.g. aortic stenosis). Do not use in dogs with severe impairment of liver function, as pimobendan is metabolised mainly via the liver. Do not use in cases of known hypersensitivity to the active substance or to any of the excipients. 4.4 Special warnings for each target species None known. 4.5 Special precautions for use Special precautions for use in animals The blood glucose should be tested regularly during treatment in dogs with existing diabetes mellitus. Monitoring of cardiac function and morphology is recommended in animals treated with pimobendan (See also section 4.6). Special precautions to be taken by the person administering the veterinary medicinal product to animals Accidental ingestion, especially by a child, may lead to the occurrence of tachycardia, orthostatic hypotension, flushing of the face and headaches. -
SPECIALTY MEDICATIONS Available Through Accredo Health Group, Inc., Medco’S Specialty Pharmacy Call Toll-Free (800) 803-2523, 8:00 A.M
SPECIALTY MEDICATIONS available through Accredo Health Group, Inc., Medco’s specialty pharmacy Call toll-free (800) 803-2523, 8:00 a.m. to 8:00 p.m., eastern time, Monday through Friday, to confirm that your medication is covered. Effective as of July 1, 2011 Abraxane® (paclitaxel protein-bound particles) Berinert® (C 1 esterase inhibitor [human])* (PA) (QD) Actemra ™ (tocilizumab) (PA) Betaseron® (interferon beta-1b) (PA) Actimmune® (interferon gamma-1b) (PA) Botox® (botulinum toxin type A) (PA) Adagen® (pegademase bovine) Carbaglu ™ (carglumic acid) Adcirca® (tadalafil) (ST) (QD) Carimune® NF (immune globulin intravenous [human]) (PA) Advate® (antihemophilic factor [recombinant]) (CPA) Cerezyme® (imiglucerase) (CPA) (ST) Afinitor® (everolimus) (PA) (QD) Cimzia® (certolizumab pegol) (ST) Aldurazyme® (laronidase) (CPA) Copaxone® (glatiramer acetate) (PA) Alphanate® (antihemophilic factor [human]) (CPA) Copegus® (ribavirin) (ST) AlphaNine® SD (coagulation factor IX [human]) (CPA) Corifact® (factor XIII [human]) (CPA) Amevive® (alefacept) (PA) Cystadane® (betaine) Ampyra ™ (dalfampridine) (PA) CytoGam® (cytomegalovirus immune globulin Apokyn® (apomorphine hydrochloride) (PA) (QD) intravenous [human])* (CPA) Aralast® (alpha[1]-proteinase inhibitor [human]) Cytovene® IV (ganciclovir sodium)* Aranesp® (darbepoetin alfa) (PA) Dacogen® (decitabine) Arcalyst® (rilonacept) (PA) (QD) Dysport® (abobotulinumtoxinA) (PA) Arixtra® (fondaparinux sodium)* Egrifta ™ (tesamorelin) (PA) Arranon® (nelarabine) Elaprase® (idursulfase) (CPA) Arzerra® (ofatumumab) -
Mechanisms of Action of Antiepileptic Drugs
Review Mechanisms of action of antiepileptic drugs Epilepsy affects up to 1% of the general population and causes substantial disability. The management of seizures in patients with epilepsy relies heavily on antiepileptic drugs (AEDs). Phenobarbital, phenytoin, carbamazepine and valproic acid have been the primary medications used to treat epilepsy for several decades. Since 1993 several AEDs have been approved by the US FDA for use in epilepsy. The choice of the AED is based primarily on the seizure type, spectrum of clinical activity, side effect profile and patient characteristics such as age, comorbidities and concurrent medical treatments. Those AEDs with broad- spectrum activity are often found to exert an action at more than one molecular target. This article will review the proposed mechanisms of action of marketed AEDs in the US and discuss the future of AEDs in development. 1 KEYWORDS: AEDs anticonvulsant drugs antiepileptic drugs epilepsy Aaron M Cook mechanism of action seizures & Meriem K Bensalem-Owen† The therapeutic armamentarium for the treat- patients with refractory seizures. The aim of this 1UK HealthCare, 800 Rose St. H-109, ment of seizures has broadened significantly article is to discuss the past, present and future of Lexington, KY 40536-0293, USA †Author for correspondence: over the past decade [1]. Many of the newer AED pharmacology and mechanisms of action. College of Medicine, Department of anti epileptic drugs (AEDs) have clinical advan- Neurology, University of Kentucky, 800 Rose Street, Room L-455, tages over older, so-called ‘first-generation’ First-generation AEDs Lexington, KY 40536, USA AEDs in that they are more predictable in their Broadly, the mechanisms of action of AEDs can Tel.: +1 859 323 0229 Fax: +1 859 323 5943 dose–response profile and typically are associ- be categorized by their effects on the neuronal [email protected] ated with less drug–drug interactions. -
Chapter 25 Mechanisms of Action of Antiepileptic Drugs
Chapter 25 Mechanisms of action of antiepileptic drugs GRAEME J. SILLS Department of Molecular and Clinical Pharmacology, University of Liverpool _________________________________________________________________________ Introduction The serendipitous discovery of the anticonvulsant properties of phenobarbital in 1912 marked the foundation of the modern pharmacotherapy of epilepsy. The subsequent 70 years saw the introduction of phenytoin, ethosuximide, carbamazepine, sodium valproate and a range of benzodiazepines. Collectively, these compounds have come to be regarded as the ‘established’ antiepileptic drugs (AEDs). A concerted period of development of drugs for epilepsy throughout the 1980s and 1990s has resulted (to date) in 16 new agents being licensed as add-on treatment for difficult-to-control adult and/or paediatric epilepsy, with some becoming available as monotherapy for newly diagnosed patients. Together, these have become known as the ‘modern’ AEDs. Throughout this period of unprecedented drug development, there have also been considerable advances in our understanding of how antiepileptic agents exert their effects at the cellular level. AEDs are neither preventive nor curative and are employed solely as a means of controlling symptoms (i.e. suppression of seizures). Recurrent seizure activity is the manifestation of an intermittent and excessive hyperexcitability of the nervous system and, while the pharmacological minutiae of currently marketed AEDs remain to be completely unravelled, these agents essentially redress the balance between neuronal excitation and inhibition. Three major classes of mechanism are recognised: modulation of voltage-gated ion channels; enhancement of gamma-aminobutyric acid (GABA)-mediated inhibitory neurotransmission; and attenuation of glutamate-mediated excitatory neurotransmission. The principal pharmacological targets of currently available AEDs are highlighted in Table 1 and discussed further below. -
Different Beta-Blocking Effects of Carvedilol and Bisoprolol in Humans
Journal of Clinical and Basic Cardiology An Independent International Scientific Journal Journal of Clinical and Basic Cardiology 2001; 4 (1), 53-56 Different beta-blocking effects of carvedilol and bisoprolol in humans Koshucharova G, Klein W, Lercher P, Maier R, Stepan V Stoschitzky K, Zweiker R Homepage: www.kup.at/jcbc Online Data Base Search for Authors and Keywords Indexed in Chemical Abstracts EMBASE/Excerpta Medica Krause & Pachernegg GmbH · VERLAG für MEDIZIN und WIRTSCHAFT · A-3003 Gablitz/Austria ORIGINAL PAPERS, CLINICAL CARDIOLOGY Different Beta-Blocking Effects of Carvedilol and Bisoprolol J Clin Basic Cardiol 2001; 4: 53 Different Beta-Blocking Effects of Carvedilol and Bisoprolol in Humans G. Koshucharova, R. Zweiker, R. Maier, P. Lercher, V. Stepan, W. Klein, K. Stoschitzky Bisoprolol is a beta1-selective beta-adrenergic antagonist while carvedilol is a non-selective beta-blocker with additional blockade of alpha1-adrenoceptors. Administration of bisoprolol has been shown to cause up-regulation of β-adrenoceptor density and to decrease nocturnal melatonin release, whereas carvedilol lacks these typical effects of beta-blocking drugs. The objective of the present study was to investigate beta-blocking effects of bisoprolol and carvedilol in healthy subjects. We compared the effects of single oral doses of clinically recommended amounts of bisoprolol (2.5, 5 and 10 mg) and carvedilol (25, 50 and 100 mg) to those of placebo in a randomised, double-blind, cross-over study in 12 healthy male volun- teers. Three hours after oral administration of the drugs heart rate and blood pressure were measured at rest, after 10 min. of exercise, and after 15 min. -
Dynamic Analysis of Cardiovascular Drugs Data
Available online www.jocpr.com Journal of Chemical and Pharmaceutical Research, 2014, 6(5):1517-1520 ISSN : 0975-7384 Research Article CODEN(USA) : JCPRC5 Dynamic analysis of cardiovascular drugs data Humei Yang and SunShi The Affiliated Hospital of Qingdao University Medical College , China _____________________________________________________________________________________________ ABSTRACT Cardiovascular disease is an important disease which is a serious hazard to human health, not only that, but the cause is still quite complicated. Therefore, it is very important to carry out research work of cardiovascular drugs in the medical profession. In this article, the money amount sequence method and DDD number sequence method were used to statistically analyze the data of cardiovascular drugs which were purchased by patients in a hospital in Shanghai in 2010-2013 year. The data of cardiovascular drugs second-class hospitals and upper-class hospitals in Shanghai included the drug varieties, prescription medication, the amount of money, which were statistically analyzed in order to provide recommendations for future cardiovascular medication guide. Through this research, we have come to the result that the money of cardiovascular drugs accounts greater of the amount of all of the drugs in the second-class hospitals than that in the upper-class hospitals, and cardiovascular medication amounts, prescriptions, etc of the second-class hospitals and upper-class hospitals had increased than before. Calcium antagonists and angiotensin ⅱ receptor antagonist drugs led occupation, as well as a small amount of varieties of drugs had gone into the top 10 amounts .As for cardiovascular drugs, foreign markets occupy a major market. That is to say that between different levels of hospitals there is some difference in cardiovascular drug use, but the drugs with good effects are already the first choice. -
Supporting Information a Analysed Substances
Electronic Supplementary Material (ESI) for Analyst. This journal is © The Royal Society of Chemistry 2020 List of contents: Tab. A1 Detailed list and classification of analysed substances. Tab. A2 List of selected MS/MS parameters for the analytes. Tab. A1 Detailed list and classification of analysed substances. drug of therapeutic doping agent analytical standard substance abuse drug (WADA class)* supplier (+\-)-amphetamine ✓ ✓ S6 stimulants LGC (+\-)-methamphetamine ✓ S6 stimulants LGC (+\-)-3,4-methylenedioxymethamphetamine (MDMA) ✓ S6 stimulants LGC methylhexanamine (4-methylhexan-2-amine, DMAA) S6 stimulants Sigma cocaine ✓ ✓ S6 stimulants LGC methylphenidate ✓ ✓ S6 stimulants LGC nikethamide (N,N-diethylnicotinamide) ✓ S6 stimulants Aldrich strychnine S6 stimulants Sigma (-)-Δ9-tetrahydrocannabinol (THC) ✓ ✓ S8 cannabinoids LGC (-)-11-nor-9-carboxy-Δ9-tetrahydrocannabinol (THC-COOH) S8 cannabinoids LGC morphine ✓ ✓ S7 narcotics LGC heroin (diacetylmorphine) ✓ ✓ S7 narcotics LGC hydrocodone ✓ ✓ Cerillant® oxycodone ✓ ✓ S7 narcotics LGC (+\-)-methadone ✓ ✓ S7 narcotics Cerillant® buprenorphine ✓ ✓ S7 narcotics Cerillant® fentanyl ✓ ✓ S7 narcotics LGC ketamine ✓ ✓ LGC phencyclidine (PCP) ✓ S0 non-approved substances LGC lysergic acid diethylamide (LSD) ✓ S0 non-approved substances LGC psilocybin ✓ S0 non-approved substances Cerillant® alprazolam ✓ ✓ LGC clonazepam ✓ ✓ Cerillant® flunitrazepam ✓ ✓ LGC zolpidem ✓ ✓ LGC VETRANAL™ boldenone (Δ1-testosterone / 1-dehydrotestosterone) ✓ S1 anabolic agents (Sigma-Aldrich) -
Somatropin Adult Mcp004d
Subject: Recombinant Human Growth Hormone Original Effective Date: 7/5/2007 (somatropin)_ADULT Growth Hormone Deficiency ° GHD ° HIV/AIDS-associated wasting and cachexia ° Short Bowel Syndrome (SBS) Policy Number: Revision Date(s): 4/28/2010, 4/27/2011, MCP-004-D 3/14/2017 Review Dates: 4/28/2010, 4/27/2011, 3/14/2017, 7/10/2018 DISCLAIMER This Molina Clinical Policy (MCP) is intended to facilitate the Utilization Management process. It expresses Molina's determination as to whether certain services or supplies are medically necessary, experimental, investigational, or cosmetic for purposes of determining appropriateness of payment. The conclusion that a particular service or supply is medically necessary does not constitute a representation or warranty that this service or supply is covered (i.e., will be paid for by Molina) for a particular member. The member's benefit plan determines coverage. Each benefit plan defines which services are covered, which are excluded, and which are subject to dollar caps or other limits. Members and their providers will need to consult the member's benefit plan to determine if there are any exclusion(s) or other benefit limitations applicable to this service or supply. If there is a discrepancy between this policy and a member's plan of benefits, the benefits plan will govern. In addition, coverage may be mandated by applicable legal requirements of a State, the Federal government or CMS for Medicare and Medicaid members. CMS's Coverage Database can be found on the CMS website. The coverage directive(s) and criteria from an existing National Coverage Determination (NCD) or Local Coverage Determination (LCD) will supersede the contents of this MCP document and provide the directive for all Medicare members.