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Pharmacy Prior Authorization Non-Formulary and Prior
Pharmacy Prior Authorization Non-Formulary and Prior Authorization Guidelines Scroll down to see PA Criteria by drug class, or Ctrl+F to search document by drug name PA Guideline Requirements Duration of Approval if Requirements Are Met Non-Formulary Requests for Non-Formulary Medications that do not have specific Prior Authorization Initial Approval: Medication Guidelines will be reviewed based on the following: • Minimum of 3 months, Guideline • An appropriate diagnosis/indication for the requested medication, depending on the • An appropriate dose of medication based on age and indication, diagnosis, to determine • Documented trial of 2 formulary agents for an adequate duration have not been effective or adherence, efficacy and tolerated patient safety monitoring OR • All other formulary medications are contraindicated based on the patient’s diagnosis, other Renewal: medical conditions or other medication therapy, • Minimum of 6 months OR • Maintenance medications • There are no other medications available on the formulary to treat the patient’s condition may be approved Indefinite Maryland Physicians Care determines patient medication trials and adherence by a review of pharmacy claims data over the preceding twelve months. Additional information may be requested on a case-by-case basis to allow for proper review. Medications Requests for Medications requiring Prior Authorization (PA) will be reviewed based on the PA As documented in the requiring Prior Guidelines/Criteria for that medication. Scroll down to view the PA Guidelines for specific individual guideline Authorization medications. Medications that do not have a specific PA guideline will follow the Non-Formulary Medication Guideline. Additional information may be required on a case-by-case basis to allow for adequate review. -
NO-1886 Decreases Ectopic Lipid Deposition and Protects Pancreatic Cells in Diet-Induced Diabetic Swine
399 NO-1886 decreases ectopic lipid deposition and protects pancreatic cells in diet-induced diabetic swine W Yin*,1,2,5, D Liao*,1,2, M Kusunoki6,SXi1, K Tsutsumi3, Z Wang1, X Lian1, T Koike4, J Fan4, Y Yang5 and C Tang5 1Department of Biochemistry and Biotechnology, Nanhua University School of Life Sciences and Technology, Hengyang, Hunan 421001, China 2Department of Pathophysiology, Central South University Xiangya Medical College, Changsha, Hunan, China 3Research and Development, Otsuka Pharmaceutical Factory Inc., Tokushima, Japan 4Laboratory of Cardiovascular Disease, Department of Pathology, Institute of Basic Medical Sciences, University of Tsukuba, Tsukuba 305-8575, Japan 5Institute of Cardiovascular Research, Nanhua University Medical School, Hengyang, Hunan 421001, China 6Department of Internal Medicine, Faculty of Medicine, Aichi Medical University, Nagakute-cho, Aichigunte, Aichi 480-11, Japan (Requests for offprints should be addressed to W Yin, Department of Biochemistry and Molecular Biology, Nanhua University School of Life Sciences and Technology, Hengyang, Hunan 421001, China; Email: [email protected]) *W Yin and D Liao contributed equally to this paper Abstract The synthetic compound NO-1886 (ibrolipim) is a lipo- skeletal muscle, liver and pancreas, and also caused pan- protein lipase activator that has been proven to be highly creatic cell damage. However, supplementing 1% NO- effective in lowering plasma triglycerides. Recently, we 1886 (200 mg/kg per day) into the high-fat/high-sucrose found that NO-1886 also reduced plasma free fatty acids diet decreased ectopic lipid deposition, improved insulin and glucose in high-fat/high-sucrose diet-induced dia- resistance, and alleviated the cell damage. These results betic rabbits. -
Pharmacological Agents Currently in Clinical Trials for Disorders in Neurogastroenterology
Pharmacological agents currently in clinical trials for disorders in neurogastroenterology Michael Camilleri J Clin Invest. 2013;123(10):4111-4120. https://doi.org/10.1172/JCI70837. Clinical Review Esophageal, gastrointestinal, and colonic diseases resulting from disorders of the motor and sensory functions represent almost half the patients presenting to gastroenterologists. There have been significant advances in understanding the mechanisms of these disorders, through basic and translational research, and in targeting the receptors or mediators involved, through clinical trials involving biomarkers and patient responses. These advances have led to relief of patients’ symptoms and improved quality of life, although there are still significant unmet needs. This article reviews the pipeline of medications in development for esophageal sensorimotor disorders, gastroparesis, chronic diarrhea, chronic constipation (including opioid-induced constipation), and visceral pain. Find the latest version: https://jci.me/70837/pdf Review Pharmacological agents currently in clinical trials for disorders in neurogastroenterology Michael Camilleri Clinical Enteric Neuroscience Translational and Epidemiological Research (CENTER), Mayo Clinic, Rochester, Minnesota, USA. Esophageal, gastrointestinal, and colonic diseases resulting from disorders of the motor and sensory functions represent almost half the patients presenting to gastroenterologists. There have been significant advances in under- standing the mechanisms of these disorders, through basic and translational research, and in targeting the recep- tors or mediators involved, through clinical trials involving biomarkers and patient responses. These advances have led to relief of patients’ symptoms and improved quality of life, although there are still significant unmet needs. This article reviews the pipeline of medications in development for esophageal sensorimotor disorders, gastropa- resis, chronic diarrhea, chronic constipation (including opioid-induced constipation), and visceral pain. -
Does Your Patient Have Bile Acid Malabsorption?
NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #198 NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #198 Carol Rees Parrish, MS, RDN, Series Editor Does Your Patient Have Bile Acid Malabsorption? John K. DiBaise Bile acid malabsorption is a common but underrecognized cause of chronic watery diarrhea, resulting in an incorrect diagnosis in many patients and interfering and delaying proper treatment. In this review, the synthesis, enterohepatic circulation, and function of bile acids are briefly reviewed followed by a discussion of bile acid malabsorption. Diagnostic and treatment options are also provided. INTRODUCTION n 1967, diarrhea caused by bile acids was We will first describe bile acid synthesis and first recognized and described as cholerhetic enterohepatic circulation, followed by a discussion (‘promoting bile secretion by the liver’) of disorders causing bile acid malabsorption I 1 enteropathy. Despite more than 50 years since (BAM) including their diagnosis and treatment. the initial report, bile acid diarrhea remains an underrecognized and underappreciated cause of Bile Acid Synthesis chronic diarrhea. One report found that only 6% Bile acids are produced in the liver as end products of of British gastroenterologists investigate for bile cholesterol metabolism. Bile acid synthesis occurs acid malabsorption (BAM) as part of the first-line by two pathways: the classical (neutral) pathway testing in patients with chronic diarrhea, while 61% via microsomal cholesterol 7α-hydroxylase consider the diagnosis only in selected patients (CYP7A1), or the alternative (acidic) pathway via or not at all.2 As a consequence, many patients mitochondrial sterol 27-hydroxylase (CYP27A1). are diagnosed with other causes of diarrhea or The classical pathway, which is responsible for are considered to have irritable bowel syndrome 90-95% of bile acid synthesis in humans, begins (IBS) or functional diarrhea by exclusion, thereby with 7α-hydroxylation of cholesterol catalyzed interfering with and delaying proper treatment. -
Drugs That Require Prior Authorization
Drugs That Require Prior Authorization (PA) Before Being Approved for Coverage You will need authorization by your HMSA Akamai Advantage (PPO) plan before filling prescriptions for the drugs shown in the chart below. The HMSA Akamai Advantage plan will only provide coverage after it determines that the drug is being prescribed according to the criteria specified in the chart. You, your appointed representative, or your prescriber can request prior authorization by calling HMSA at 1 (855) 479-3659, 24 hours a day, 7 days a week. Customer service is available in English and other languages. TTY/TDD users should call 711. PA Criteria Prior Authorization Group ACITRETIN Drug Names ACITRETIN, SORIATANE Covered Uses All FDA-approved indications not otherwise excluded from Part D, prevention of non-melanoma skin cancers in high risk individuals. Exclusion Criteria Required Medical Information Age Restrictions Prescriber Restrictions Coverage Duration Plan Year Other Criteria Prior Authorization Group ACTEMRA Drug Names ACTEMRA Covered Uses All FDA-approved indications not otherwise excluded from Part D, unicentric Castleman's disease, multicentric Castleman's disease. Exclusion Criteria Required Medical Information For moderately to severely active rheumatoid arthritis (new starts only): Inadequate response, intolerance or contraindication to a self-injectable tumor necrosis factor (TNF) inhibitor (e.g., adalimumab) or a targeted synthetic disease-modifying antirheumatic drug (DMARD) (e.g., tofacitinib). For active polyarticular juvenile idiopathic arthritis (new starts only): Inadequate response, intolerance or contraindication to a TNF inhibitor (e.g., adalimumab). For active systemic juvenile idiopathic arthritis (new starts only): Inadequate response to a corticosteroid monotherapy, methotrexate or leflunomide. Age Restrictions Prescriber Restrictions Coverage Duration Plan Year Other Criteria Prior Authorization Group ACTHAR HP Drug Names H.P. -
Stems for Nonproprietary Drug Names
USAN STEM LIST STEM DEFINITION EXAMPLES -abine (see -arabine, -citabine) -ac anti-inflammatory agents (acetic acid derivatives) bromfenac dexpemedolac -acetam (see -racetam) -adol or analgesics (mixed opiate receptor agonists/ tazadolene -adol- antagonists) spiradolene levonantradol -adox antibacterials (quinoline dioxide derivatives) carbadox -afenone antiarrhythmics (propafenone derivatives) alprafenone diprafenonex -afil PDE5 inhibitors tadalafil -aj- antiarrhythmics (ajmaline derivatives) lorajmine -aldrate antacid aluminum salts magaldrate -algron alpha1 - and alpha2 - adrenoreceptor agonists dabuzalgron -alol combined alpha and beta blockers labetalol medroxalol -amidis antimyloidotics tafamidis -amivir (see -vir) -ampa ionotropic non-NMDA glutamate receptors (AMPA and/or KA receptors) subgroup: -ampanel antagonists becampanel -ampator modulators forampator -anib angiogenesis inhibitors pegaptanib cediranib 1 subgroup: -siranib siRNA bevasiranib -andr- androgens nandrolone -anserin serotonin 5-HT2 receptor antagonists altanserin tropanserin adatanserin -antel anthelmintics (undefined group) carbantel subgroup: -quantel 2-deoxoparaherquamide A derivatives derquantel -antrone antineoplastics; anthraquinone derivatives pixantrone -apsel P-selectin antagonists torapsel -arabine antineoplastics (arabinofuranosyl derivatives) fazarabine fludarabine aril-, -aril, -aril- antiviral (arildone derivatives) pleconaril arildone fosarilate -arit antirheumatics (lobenzarit type) lobenzarit clobuzarit -arol anticoagulants (dicumarol type) dicumarol -
Lipoprotein Lipase As an Attractive Target for Correcting Dyslipidemia and Reduction of Cvd Residual Risk
ISSN 2311-715X УКРАЇНСЬКИЙ БІОФАРМАЦЕВТИЧНИЙ ЖУРНАЛ, № 4 (45) 2016 UDC 577.125.8:616.005 National University of Pharmacy D. A. Dorovsky, A. L. Zagayko LIPOPROTEIN LIPASE AS AN ATTRACTIVE TARGET FOR CORRECTING DYSLIPIDEMIA AND REDUCTION OF CVD RESIDUAL RISK Lipoprotein lipase has long been known to hydrolyse triglycerides from triglycerides-rich lipoproteins. It also the ability to promote the binding of lipoproteins to the wide variation of lipoprotein receptors. There are some studies that suggest the possible atherogenic role of lipoprotein lipase. In theory, lipoprotein lipase deficiency should help to clarify this question. However, the rarity of this condition means that it has not been possible to conduct epidemiological studies. During the last decade it became obvious that elevated plasma TG and low HDL-cholesterol are part of CVD residual risk. Thus LPL is an attractive target for correcting dyslipidemia and reduction of CVD residual risk. Key words: Lipoprotein lipase; atherosclerosis; lipoproteins INTRODUCTION differences in M expression of LPL contributed to diffe- Lipoprotein lipase (LPL) is synthesized and secreted rences in the development of atherosclerotic plaque for- in several tissues, such as skeletal muscle, adipose tissue, mation. Concentrations of LPL protein, activity and mRNA cardiac muscle and macrophages (M), binding to the in atherosclerosis-prone mice were found to be seve- vascular endothelial cell surface of the capillary through- ral-fold higher than in atherosclerosis-resistant counter- heparan sulphate. parts. Ichikawa et al. compared atherosclerotic lesions in Lipoprotein lipase (LPL) plays a central role in lipo wild-type strains with lesions in rabbits with over-exp- protein metabolism by catalyzing hydrolysis of triglyce- ressed M-specific human lipoprotein lipase, after giving rides (TG) in very low-density lipoprotein (VLDL) partic- both groups food containing 0.3 % cholesterol. -
(12) United States Patent (10) Patent No.: US 8,486,621 B2 Luo Et Al
USOO8486.621B2 (12) United States Patent (10) Patent No.: US 8,486,621 B2 Luo et al. (45) Date of Patent: Jul. 16, 2013 (54) NUCLEICACID-BASED MATRIXES 2005. O130180 A1 6/2005 Luo et al. 2006/0084607 A1 4/2006 Spirio et al. (75) Inventors: ity, N. (US); Soong Ho 2007/01482462007/0048759 A1 3/20076/2007 Luo et al. m, Ithaca, NY (US) 2008.0167454 A1 7, 2008 Luo et al. 2010, O136614 A1 6, 2010 Luo et al. (73) Assignee: Cornell Research Foundation, Inc., 2012/0022244 A1 1, 2012 Yin Ithaca, NY (US) FOREIGN PATENT DOCUMENTS (*) Notice: Subject to any disclaimer, the term of this WO WO 2004/057023 A1 T 2004 patent is extended or adjusted under 35 U.S.C. 154(b) by 808 days. OTHER PUBLICATIONS Lin et al. (J Biomech Eng. Feb. 2004;126(1):104-10).* (21) Appl. No.: 11/464,184 Li et al. (Nat Mater. Jan. 2004:3(1):38-42. Epub Dec. 21, 2003).* Ma et al. (Nucleic Acids Res. Dec. 22, 1986;14(24):9745-53).* (22) Filed: Aug. 11, 2006 Matsuura, et al. Nucleo-nanocages: designed ternary oligodeoxyribonucleotides spontaneously form nanosized DNA (65) Prior Publication Data cages. Chem Commun (Camb). 2003; (3):376-7. Li, et al. Multiplexed detection of pathogen DNA with DNA-based US 2007/01 17177 A1 May 24, 2007 fluorescence nanobarcodes. Nat Biotechnol. 2005; 23(7): 885-9. Lund, et al. Self-assembling a molecular pegboard. JAm ChemSoc. Related U.S. Application Data 2005; 127(50): 17606-7. (60) Provisional application No. 60/722,032, filed on Sep. -
Major Products
Data Section Major Products Innovative Pharmaceuticals Business Innovative Pharmaceuticals Business Brand Name (Generic Name) Efficacy Launched Remarks Brand Name (Generic Name) Efficacy Launched Remarks Japan [Daiichi Sankyo Co., Ltd.] US [Daiichi Sankyo Inc.] A first combination drug of the DPP-4 inhibitor teneligliptin and the SGLT2 inhibitor Opioid-induced First once-daily oral product approved by the FDA for the treatment of opioid-induced (teneligliptin / Type 2 diabetes mellitus MOVANTIK (naloxegol) 2015 CANALIA 2017 canagliflozin approved in Japan, which demonstrates blood glucose-lowering activity constipation treatment constipation (OIC) for adults with chronic non-cancer pain. canagliflozin) treatment through a complementary pharmacological effect. Orally active Factor Xa inhibitor. It is an anticoagulant that specifically, reversibly and directly inhibits the enzyme, Factor Xa, a clotting factor in the blood. Approved for indications to Sodium channel blocker. Suppresses the excessive excitation of nerves in the brain, and VIMPAT (lacosamide) Anti-epileptic agent 2016 SAVAYSA (edoxaban) Anticoagulant 2015 reduce the risk of stroke and systemic embolism (SE) in patients with non-valvular atrial reduces the occurrence of epileptic seizures. fibrillation (NVAF) and for the treatment of venous thromboembolism (VTE) (deep vein ADP receptor inhibitor. Inhibits platelet aggregation and reduces the incidence of artery thrombosis (DVT) and pulmonary embolism (PE)). Efient (prasugrel) Antiplatelet agent 2014 stenosis and occlusion due to thrombosis. Effient (prasugrel) Antiplatelet agent 2009 Inhibits platelet aggregation and reduces the incidence of artery stenosis and occlusion. Treatment for Benicar 2002 Benicar: Olmesartan osteoporosis / inhibitor Human monoclonal anti-RANKL antibody. Subcutaneous formulation which controls Benicar HCT 2003 Benicar HCT: A combination drug of olmesartan medoxomil and hydrochlorothiazide (diuretic) PRALIA (denosumab) for rheumatoid arthritis- 2013 bone resorption and bone destruction by specifically inhibiting RANKL. -
WO 2013/037390 Al R
(12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date WO 2013/037390 Al 21 March 2013 (21.03.2013) P O P C T (51) International Patent Classification: (74) Agent: WINGEFELD, Renate; c/o Sanofi-Aventis C07D 471/04 (2006.01) A61P 9/00 (2006.01) Deutschland GmbH, Patents Germany, Industriepark A61K 31/437 (2006.01) A61P 25/00 (2006.01) Hochst, Geb. K 801, 65926 Frankfurt (DE). A61P 3/10 (2006.01) A61P 35/00 (2006.01) (81) Designated States (unless otherwise indicated, for every (21) International Application Number: kind of national protection available): AE, AG, AL, AM, PCT/EP201 1/065715 AO, AT, AU, AZ, BA, BB, BG, BH, BR, BW, BY, BZ, CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, DO, (22) International Filing Date: DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, HN, 12 September 201 1 (12.09.201 1) HR, HU, ID, IL, IN, IS, JP, KE, KG, KM, KN, KP, KR, (25) Filing Language: English KZ, LA, LC, LK, LR, LS, LT, LU, LY, MA, MD, ME, MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, (26) Publication Language: English OM, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SC, SD, (71) Applicant (for all designated States except US): SANOFI SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, TN, TR, [FR/FR]; 54, rue de la Boetie, F-75008 Paris (FR). TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW. -
Research Article Hepatic Gene Expression Profiles Are Altered by Dietary Unsalted Korean Fermented Soybean
Hindawi Publishing Corporation Journal of Nutrition and Metabolism Volume 2011, Article ID 260214, 10 pages doi:10.1155/2011/260214 Research Article Hepatic Gene Expression Profiles Are Altered by Dietary Unsalted Korean Fermented Soybean (Chongkukjang) Consumption in Mice with Diet-Induced Obesity JuRyoun Soh,1 Dae Young Kwon,2 and Youn-Soo Cha1 1 Department of Food Science and Human Nutrition, and Research Institute of Human Ecology, Chonbuk National University, 664-14 Dukjin-Dong 1-Ga, Jeonju 561-756, Republic of Korea 2 Food Functional Research Division, Korean Food Research Institutes, San 46-1, Baekhyun-dong, Bundang-gu, Sungnam-si, Gyeonggi-do 463-746, Republic of Korea Correspondence should be addressed to Youn-Soo Cha, [email protected] Received 30 August 2010; Revised 1 December 2010; Accepted 3 January 2011 Academic Editor: Phillip B. Hylemon Copyright © 2011 JuRyoun Soh et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. We found that Chongkukjang, traditional unsalted fermented soybean, has an antiobesity effect in mice with diet-induced obesity and examined the changes in hepatic transcriptional profiles using cDNA microarray. High-fat diet-induced obese C57BL/6J mice were divided into three groups: normal-diet control group (NDcon, 10% of total energy from fat), high-fat diet control group (HDcon, 45% of total energy from fat), and HDcon plus 40% Chongkukjang (HDC) and were fed for 9 weeks. The HDC group mice were pair-fed (isocalorie) with mice in the HDcon group. -
Statin Intolerance— Facing Adversity
Official Publication of the National Lipid Association LipidSpin Theme: Statin Intolerance— Facing Adversity Also in this issue: Evidence-Based Approach to the Use of CoQ10 to Deal with Statin Intolerance Vitamin D Deficiency and Statin Intolerance This issue sponsored by the Southeast Lipid Association Volume 11 Issue 4 Fall 2013 visit www.lipid.org Elsvier MauiAd.Full Page8.13:Maui Ad 8/30/13 9:08 AM Page 1 MORETHANA MEETING IN MAUI Join us for the opening session of the 2014 Clinical Lipid Update Meeting as world renowned thought leaders discuss Lipid Management and Metabolic Syndrome in various populations from around the world. W.Virgil Brown,MD,FNLA Cesare R. Sirtori,MD,PhD Yuji Matsuzawa,MD,PhD GeraldWatts,DSc,MB,BS,PhD This meeting features evidence-based sessions that include: A debate from John Brunzell,MD and Sekar Kathiresan,MD How Close are we to Personalizing CVD Prevention with Genetics? Other key sessions include: HDL Analytics & Functionality Debate: Is it time to Stop using Benjamin Ansell, MD, FNLA Fibrates Combined with Statins? Jocelyne R. Benatar, MD, MBChB Cardiovascular Risk inAsians Eliot Brinton, MD, FNLA and Pacific Islanders Beatriz Rodriguez, MD, PhD Dietary Issues and Supplements Keawe’aimoku Kaholokula, PhD Kathleen Wyne, MD, PhD, FNLA Nathan Wong, PhD Terry Jacobson, MD, FNLA Latha Palaniappan, MD, MPH Forrest Batz, PharmD Geeta Sikand, RD, FNLA See you in Maui! Visit www.lipid.org/springclu to register now. To book your room, call 800-888-6100 and ask for the National Lipid Association room rate. Get the NLA room rate starting at $235/night plus tax if you book your room by February 11, 2014.