Psychiatry Pharmacogenetic Genotyping Panel

Total Page:16

File Type:pdf, Size:1020Kb

Psychiatry Pharmacogenetic Genotyping Panel PSYCHIATRY PHARMACOGENETIC GENOTYPING PANEL Table of Contents PSYCHIATRY PHARMACOGENETIC GENOTYPING PANEL Table of Contents ............................................................................................................................................. 2 About the Test ....................................................................................................................................................... 4 Indications ............................................................................................................................................................... 4 Testing Methods, Sensitivity, and Limitations ................................................................................................. 4 Turnaround Time ................................................................................................................................................... 4 Specimen and Shipping Requirements ............................................................................................................ 5 Customer Services and Genetic Counseling ................................................................................................... 5 Disclaimer ............................................................................................................................................................... 5 References.............................................................................................................................................................. 6 MEDICATION LIST ................................................................................................................................................. 7 Amitriptyline ....................................................................................................................................................... 7 Amphetamine .................................................................................................................................................... 7 Amoxapine ......................................................................................................................................................... 7 Aripiprazole ........................................................................................................................................................ 7 Atomoxetine ....................................................................................................................................................... 8 Brexpiprazole ..................................................................................................................................................... 8 Brivaracetam ...................................................................................................................................................... 8 Bupropion ........................................................................................................................................................... 9 Chlorpromazine ................................................................................................................................................. 9 Citalopram .......................................................................................................................................................... 9 Clobazam .......................................................................................................................................................... 10 Clomipramine .................................................................................................................................................. 10 Clonidine ........................................................................................................................................................... 10 Clozapine .......................................................................................................................................................... 11 Desipramine ..................................................................................................................................................... 11 Desvenlafaxine ................................................................................................................................................ 11 Deutetrabenazine ........................................................................................................................................... 12 Dextroamphetamine ...................................................................................................................................... 12 Dextromethorphan-Quinidine ...................................................................................................................... 12 Diazepam .......................................................................................................................................................... 13 Donepezil .......................................................................................................................................................... 13 Doxepin ............................................................................................................................................................. 13 Duloxetine ........................................................................................................................................................ 13 Escitalopram .................................................................................................................................................... 14 Flibanserin ........................................................................................................................................................ 14 Fluoxetine ......................................................................................................................................................... 14 Fluphenazine ................................................................................................................................................... 15 Fluvoxamine ..................................................................................................................................................... 15 Fosphenytoin ................................................................................................................................................... 15 Galantamine ..................................................................................................................................................... 15 Haloperidol ....................................................................................................................................................... 16 Iloperidone ....................................................................................................................................................... 16 Imipramine ........................................................................................................................................................ 16 Lisdexamfetamine .......................................................................................................................................... 17 Lorazepam ....................................................................................................................................................... 17 Maprotiline ........................................................................................................................................................ 17 Methadone ....................................................................................................................................................... 17 Mirtazapine ....................................................................................................................................................... 17 Nortriptyline ..................................................................................................................................................... 18 Olanzapine ........................................................................................................................................................ 18 Oxazepam ......................................................................................................................................................... 18 Paliperidone ..................................................................................................................................................... 19 Paroxetine ......................................................................................................................................................... 19 Perphenazine ................................................................................................................................................... 19 Phenobarbital ................................................................................................................................................... 19 Phenytoin .......................................................................................................................................................... 20 Pimozide ........................................................................................................................................................... 20 Primidone.........................................................................................................................................................
Recommended publications
  • Pindolol of the Activation of Postsynaptic 5-HT1A Receptors
    Potentiation by (-)Pindolol of the Activation of Postsynaptic 5-HT1A Receptors Induced by Venlafaxine Jean-Claude Béïque, Ph.D., Pierre Blier, M.D., Ph.D., Claude de Montigny, M.D., Ph.D., and Guy Debonnel, M.D. The increase of extracellular 5-HT in brain terminal regions antagonist WAY 100635 (100 ␮g/kg, i.v.). A short-term produced by the acute administration of 5-HT reuptake treatment with VLX (20 mg/kg/day ϫ 2 days) resulted in a inhibitors (SSRI’s) is hampered by the activation of ca. 90% suppression of the firing activity of 5-HT neurons somatodendritic 5-HT1A autoreceptors in the raphe nuclei. in the dorsal raphe nucleus. This was prevented by the The present in vivo electrophysiological studies were coadministration of (-)pindolol (15 mg/kg/day ϫ 2 days). undertaken, in the rat, to assess the effects of the Taken together, these results indicate that (-)pindolol coadministration of venlafaxine, a dual 5-HT/NE reuptake potentiated the activation of postsynaptic 5-HT1A receptors inhibitor, and (-)pindolol on pre- and postsynaptic 5-HT1A resulting from 5-HT reuptake inhibition probably by receptor function. The acute administration of venlafaxine blocking the somatodendritic 5-HT1A autoreceptor, but not and of the SSRI paroxetine (5 mg/kg, i.v.) induced a its postsynaptic congener. These results support and extend suppression of the firing activity of dorsal hippocampus CA3 previous findings providing a biological substratum for the pyramidal neurons. This effect of venlafaxine was markedly efficacy of pindolol as an accelerating strategy in major potentiated by a pretreatment with (-)pindolol (15 mg/kg, depression.
    [Show full text]
  • ZHONG-THESIS-2016.Pdf
    ANTIDEPRESSANTMINING AZ AMAZ DESIGNING A WEBBASED ALGORITHM AND VISUAL LANGUAGE FOR ANTIDEPRESSANT DRUG SELECTION TO EDUCATE PRIMARY CARE PRACTITIONERS By Amy Zhong A thesis submitted to Johns Hopkins University in conformity with the requirements for the degree of Master of Arts Baltimore, Maryland March, 2016 © 2016 Amy Zhong All Rights Reserved ABSTRACT Depression is a common mental disorder that affects approximately 14.8 million American adults each year. In addition to being a debilitating condition, depression often occurs in tandem with other medical conditions such as diabetes, heart disease, and cancer. While psychiatric professionals are essential for the management of mental health, majority of patients seek care from their primary care practitioners. This phenomenon is of great concern because diagnosis of depression within primary care settings has only been accurate 25-50% of the time. The antidepressant drug selection algorithm utilizes a unique formula to integrate patient and family medical histories, patient symptoms, and patient preferences to make optimal treatment selections. The development of a visual language explores the use of graphic elements to improve understanding of major pharmacological mechanisms, knowledge essential to making rational DQWLGHSUHVVDQWGUXJVHOHFWLRQV,QFUHDWLQJWKLVPRELOHZHEEDVHGDSSOLFDWLRQZHKRSHWR¿OOD void in resources available to primary care practitioners, and improve management of mental health within the primary care setting. By Amy Zhong Chairpersons of the Supervisory Committee Adam I. Kaplin, M.D., Ph.D., esis Preceptor Assistant Professor, Departments of Psychiatry and Neurology e Johns Hopkins University School of Medicine Kristen Rahn Hollinger, Ph.D., esis Preceptor Instructor, Departments of Psychiatry and Neurology e Johns Hopkins University School of Medicine Jennifer E.
    [Show full text]
  • Therapeutic Potential of Nicotinamide Adenine Dinucleotide (NAD) T ∗ Marta Arenas-Jala,B, , J.M
    European Journal of Pharmacology 879 (2020) 173158 Contents lists available at ScienceDirect European Journal of Pharmacology journal homepage: www.elsevier.com/locate/ejphar Therapeutic potential of nicotinamide adenine dinucleotide (NAD) T ∗ Marta Arenas-Jala,b, , J.M. Suñé-Negrea, Encarna García-Montoyaa a Pharmacy and Pharmaceutical Technology Department (Faculty of Pharmacy and Food Sciences), University of Barcelona, Barcelona, Spain b ICN2 – Catalan Institute of Nanoscience and Nanotechnology (Autonomous University of Barcelona), Bellaterra (Barcelona), Spain ARTICLE INFO ABSTRACT Keywords: Nicotinamide adenine nucleotide (NAD) is a small ubiquitous hydrophilic cofactor that participates in several NAD aspects of cellular metabolism. As a coenzyme it has an essential role in the regulation of energetic metabolism, Metabolism but it is also a cosubstrate for enzymes that regulate fundamental biological processes such as transcriptional Therapeutic potential regulation, signaling and DNA repairing among others. The fluctuation and oxidative state of NAD levels reg- Drug discovery ulate the activity of these enzymes, which is translated into marked effects on cellular function. While alterations Supplementation in NAD homeostasis are a common feature of different conditions and age-associated diseases, in general, in- creased NAD levels have been associated with beneficial health effects. Due to its therapeutic potential, the interest in this molecule has been renewed, and the regulation of NAD metabolism has become an attractive target for drug discovery. In fact, different approaches to replenish or increase NAD levels have been tested, including enhancement of biosynthesis and inhibition of NAD breakdown. Despite further research is needed, this review provides an overview and update on NAD metabolism, including the therapeutic potential of its regulation, as well as pharmacokinetics, safety, precautions and formulation challenges of NAD supplementa- tion.
    [Show full text]
  • Create a Healing Environment for Patients with Pseudobulbar Affect by Maude Mcgill, Phd, RN-BC, and Marzell Mcgill, BA, LPN
    Strictly Clinical Create a healing environment for patients with pseudobulbar affect By Maude McGill, PhD, RN-BC, and Marzell McGill, BA, LPN tact their provider for prompt appropriate treatment. • Signs and symptoms include: Teach patients how to manage PBA • emotional responses (such as crying or laughing) for optimal quality of life. that don’t fit the situation • emotional episodes lasting longer than expected • sudden emotional outbursts (these outbursts can I just don’t understand why Mom is crying. When I include frustration, anger, laughter, or crying) walked in the room, she was happy and calm. Then, • moments of intense emotions that are out of the when I asked her about her day, her smile turned into patient’s control a frown and she started crying uncontrollably. I’ve nev - • facial expressions that don’t match the emotional er seen her cry like that. I’m concerned. response. EMOTIONS ARE NATURAL . We’ve all heard the cliché, “Emotions make us human.” People cry when they’re hurt and laugh when things are funny. However, mil - lions of people find that controlling their emotions is hard because of pseudobul - bar affect (PBA). PBA refers to inappropriate, involun - tary, or uncontrollable laughing or crying caused by the residual effects of a nervous system disorder. Al - though PBA is closely asso - ciated with post-stroke pa - tients, it can occur with any nervous system condition, including Alzheimer’s dis - ease, traumatic brain injury, and multiple sclerosis. Sci - entists have labeled PBA a disorder of emotional incon - tinence (patients can’t control their emotional respons - Navigating the new normal of PBA es).
    [Show full text]
  • Metabolic-Hydroxy and Carboxy Functionalization of Alkyl Moieties in Drug Molecules: Prediction of Structure Influence and Pharmacologic Activity
    molecules Review Metabolic-Hydroxy and Carboxy Functionalization of Alkyl Moieties in Drug Molecules: Prediction of Structure Influence and Pharmacologic Activity Babiker M. El-Haj 1,* and Samrein B.M. Ahmed 2 1 Department of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, University of Science and Technology of Fujairah, Fufairah 00971, UAE 2 College of Medicine, Sharjah Institute for Medical Research, University of Sharjah, Sharjah 00971, UAE; [email protected] * Correspondence: [email protected] Received: 6 February 2020; Accepted: 7 April 2020; Published: 22 April 2020 Abstract: Alkyl moieties—open chain or cyclic, linear, or branched—are common in drug molecules. The hydrophobicity of alkyl moieties in drug molecules is modified by metabolic hydroxy functionalization via free-radical intermediates to give primary, secondary, or tertiary alcohols depending on the class of the substrate carbon. The hydroxymethyl groups resulting from the functionalization of methyl groups are mostly oxidized further to carboxyl groups to give carboxy metabolites. As observed from the surveyed cases in this review, hydroxy functionalization leads to loss, attenuation, or retention of pharmacologic activity with respect to the parent drug. On the other hand, carboxy functionalization leads to a loss of activity with the exception of only a few cases in which activity is retained. The exceptions are those groups in which the carboxy functionalization occurs at a position distant from a well-defined primary pharmacophore. Some hydroxy metabolites, which are equiactive with their parent drugs, have been developed into ester prodrugs while carboxy metabolites, which are equiactive to their parent drugs, have been developed into drugs as per se.
    [Show full text]
  • Treatment of Psychosis: 30 Years of Progress
    Journal of Clinical Pharmacy and Therapeutics (2006) 31, 523–534 REVIEW ARTICLE Treatment of psychosis: 30 years of progress I. R. De Oliveira* MD PhD andM.F.Juruena MD *Department of Neuropsychiatry, School of Medicine, Federal University of Bahia, Salvador, BA, Brazil and Department of Psychological Medicine, Institute of Psychiatry, King’s College, University of London, London, UK phrenia. Thirty years ago, psychiatrists had few SUMMARY neuroleptics available to them. These were all Background: Thirty years ago, psychiatrists had compounds, today known as conventional anti- only a few choices of old neuroleptics available to psychotics, and all were liable to cause severe extra them, currently defined as conventional or typical pyramidal side-effects (EPS). Nowadays, new antipsychotics, as a result schizophrenics had to treatments are more ambitious, aiming not only to suffer the severe extra pyramidal side effects. improve psychotic symptoms, but also quality of Nowadays, new treatments are more ambitious, life and social reinsertion. We briefly but critically aiming not only to improve psychotic symptoms, outline the advances in diagnosis and treatment but also quality of life and social reinsertion. Our of schizophrenia, from the mid 1970s up to the objective is to briefly but critically review the present. advances in the treatment of schizophrenia with antipsychotics in the past 30 years. We conclude DIAGNOSIS OF SCHIZOPHRENIA that conventional antipsychotics still have a place when just the cost of treatment, a key factor in Up until the early 1970s, schizophrenia diagnoses poor regions, is considered. The atypical anti- remained debatable. The lack of uniform diagnostic psychotic drugs are a class of agents that have criteria led to relative rates of schizophrenia being become the most widely used to treat a variety of very different, for example, in New York and psychoses because of their superiority with London, as demonstrated in an important study regard to extra pyramidal symptoms.
    [Show full text]
  • Strategies for Managing Sexual Dysfunction Induced by Antidepressant Medication
    King’s Research Portal DOI: 10.1002/14651858.CD003382.pub3 Document Version Publisher's PDF, also known as Version of record Link to publication record in King's Research Portal Citation for published version (APA): Taylor, M. J., Rudkin, L., Bullemor-Day, P., Lubin, J., Chukwujekwu, C., & Hawton, K. (2013). Strategies for managing sexual dysfunction induced by antidepressant medication. Cochrane Database of Systematic Reviews, (5). https://doi.org/10.1002/14651858.CD003382.pub3 Citing this paper Please note that where the full-text provided on King's Research Portal is the Author Accepted Manuscript or Post-Print version this may differ from the final Published version. If citing, it is advised that you check and use the publisher's definitive version for pagination, volume/issue, and date of publication details. And where the final published version is provided on the Research Portal, if citing you are again advised to check the publisher's website for any subsequent corrections. General rights Copyright and moral rights for the publications made accessible in the Research Portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognize and abide by the legal requirements associated with these rights. •Users may download and print one copy of any publication from the Research Portal for the purpose of private study or research. •You may not further distribute the material or use it for any profit-making activity or commercial gain •You may freely distribute the URL identifying the publication in the Research Portal Take down policy If you believe that this document breaches copyright please contact [email protected] providing details, and we will remove access to the work immediately and investigate your claim.
    [Show full text]
  • Evidence for the Involvement of Spinal Cord 1 Adrenoceptors in Nitrous
    Anesthesiology 2002; 97:1458–65 © 2002 American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc. Evidence for the Involvement of Spinal Cord ␣ 1 Adrenoceptors in Nitrous Oxide–induced Antinociceptive Effects in Fischer Rats Ryo Orii, M.D., D.M.Sc.,* Yoko Ohashi, M.D.,* Tianzhi Guo, M.D.,† Laura E. Nelson, B.A.,‡ Toshikazu Hashimoto, M.D.,* Mervyn Maze, M.B., Ch.B.,§ Masahiko Fujinaga, M.D.ʈ Background: In a previous study, the authors found that ni- opioid peptide release in the brain stem, leading to the trous oxide (N O) exposure induces c-Fos (an immunohisto- 2 activation of the descending noradrenergic inhibitory chemical marker of neuronal activation) in spinal cord ␥-ami- nobutyric acid–mediated (GABAergic) neurons in Fischer rats. neurons, which results in modulation of the pain–noci- 1 In this study, the authors sought evidence for the involvement ceptive processing in the spinal cord. Available evi- Downloaded from http://pubs.asahq.org/anesthesiology/article-pdf/97/6/1458/337059/0000542-200212000-00018.pdf by guest on 01 October 2021 ␣ of 1 adrenoceptors in the antinociceptive effect of N2O and in dence suggests that at the level of the spinal cord, there activation of GABAergic neurons in the spinal cord. appear to be at least two neuronal systems that are Methods: Adult male Fischer rats were injected intraperitone- involved (fig. 1). In one of the pathways, activation of ally with ␣ adrenoceptor antagonist, ␣ adrenoceptor antago- 1 2 ␣ nist, opioid receptor antagonist, or serotonin receptor antago- the 2 adrenoceptors produces either direct presynaptic nist and, 15 min later, were exposed to either air (control) or inhibition of neurotransmitter release from primary af- 75% N2O.
    [Show full text]
  • Ondansetron Does Not Attenuate the Analgesic Efficacy of Nefopam Kai-Zhi Lu 1*, Hong Shen 2*, Yan Chen 1, Min-Guang Li 1, Guo-Pin Tian 1, Jie Chen 1
    Int. J. Med. Sci. 2013, Vol. 10 1790 Ivyspring International Publisher International Journal of Medical Sciences 2013; 10(12):1790-1794. doi: 10.7150/ijms.5386 Research Paper Ondansetron Does Not Attenuate the Analgesic Efficacy of Nefopam Kai-zhi Lu 1*, Hong Shen 2*, Yan Chen 1, Min-guang Li 1, Guo-pin Tian 1, Jie Chen 1 1. Department of Anaesthesiology, Southwest Hospital, Third Military Medical University, Chongqing 400038, China; 2. Department of Radiology, Chongqing Fifth Hospital, Chongqing.400062, China. * These authors contributed equally to this work. Corresponding author: Dr. Jie Chen: Department of Anaesthesiology, Southwest Hospital, Third Military Medical University, Gaotanyan 19 Street, Shapingba, Chongqing 400038, China. Tel: 0086-23-68754197. Fax: 0086-23-65463285. E-mail: [email protected] © Ivyspring International Publisher. This is an open-access article distributed under the terms of the Creative Commons License (http://creativecommons.org/ licenses/by-nc-nd/3.0/). Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited. Received: 2012.10.15; Accepted: 2013.10.17; Published: 2013.10.29 Abstract Objectives: The aim of this study was to investigate if there is any interaction between ondansetron and nefopam when they are continuously co-administrated during patient-controlled intravenous analgesia (PCIA). Methods: The study was a prospective, randomized, controlled, non-inferiority clinical trial com- paring nefopam-plus-ondansetron to nefopam alone. A total of 230 postoperative patients using nefopam for PCIA, were randomly assigned either to a group receiving continuous infusion of ondansetron (Group O) or to the other group receiving the same volume of normal saline con- tinuously (Group N).
    [Show full text]
  • 2D6 Substrates 2D6 Inhibitors 2D6 Inducers
    Physician Guidelines: Drugs Metabolized by Cytochrome P450’s 1 2D6 Substrates Acetaminophen Captopril Dextroamphetamine Fluphenazine Methoxyphenamine Paroxetine Tacrine Ajmaline Carteolol Dextromethorphan Fluvoxamine Metoclopramide Perhexiline Tamoxifen Alprenolol Carvedilol Diazinon Galantamine Metoprolol Perphenazine Tamsulosin Amiflamine Cevimeline Dihydrocodeine Guanoxan Mexiletine Phenacetin Thioridazine Amitriptyline Chloropromazine Diltiazem Haloperidol Mianserin Phenformin Timolol Amphetamine Chlorpheniramine Diprafenone Hydrocodone Minaprine Procainamide Tolterodine Amprenavir Chlorpyrifos Dolasetron Ibogaine Mirtazapine Promethazine Tradodone Aprindine Cinnarizine Donepezil Iloperidone Nefazodone Propafenone Tramadol Aripiprazole Citalopram Doxepin Imipramine Nifedipine Propranolol Trimipramine Atomoxetine Clomipramine Encainide Indoramin Nisoldipine Quanoxan Tropisetron Benztropine Clozapine Ethylmorphine Lidocaine Norcodeine Quetiapine Venlafaxine Bisoprolol Codeine Ezlopitant Loratidine Nortriptyline Ranitidine Verapamil Brofaramine Debrisoquine Flecainide Maprotline olanzapine Remoxipride Zotepine Bufuralol Delavirdine Flunarizine Mequitazine Ondansetron Risperidone Zuclopenthixol Bunitrolol Desipramine Fluoxetine Methadone Oxycodone Sertraline Butylamphetamine Dexfenfluramine Fluperlapine Methamphetamine Parathion Sparteine 2D6 Inhibitors Ajmaline Chlorpromazine Diphenhydramine Indinavir Mibefradil Pimozide Terfenadine Amiodarone Cimetidine Doxorubicin Lasoprazole Moclobemide Quinidine Thioridazine Amitriptyline Cisapride
    [Show full text]
  • Schizophrenia Care Guide
    August 2015 CCHCS/DHCS Care Guide: Schizophrenia SUMMARY DECISION SUPPORT PATIENT EDUCATION/SELF MANAGEMENT GOALS ALERTS Minimize frequency and severity of psychotic episodes Suicidal ideation or gestures Encourage medication adherence Abnormal movements Manage medication side effects Delusions Monitor as clinically appropriate Neuroleptic Malignant Syndrome Danger to self or others DIAGNOSTIC CRITERIA/EVALUATION (PER DSM V) 1. Rule out delirium or other medical illnesses mimicking schizophrenia (see page 5), medications or drugs of abuse causing psychosis (see page 6), other mental illness causes of psychosis, e.g., Bipolar Mania or Depression, Major Depression, PTSD, borderline personality disorder (see page 4). Ideas in patients (even odd ideas) that we disagree with can be learned and are therefore not necessarily signs of schizophrenia. Schizophrenia is a world-wide phenomenon that can occur in cultures with widely differing ideas. 2. Diagnosis is made based on the following: (Criteria A and B must be met) A. Two of the following symptoms/signs must be present over much of at least one month (unless treated), with a significant impact on social or occupational functioning, over at least a 6-month period of time: Delusions, Hallucinations, Disorganized Speech, Negative symptoms (social withdrawal, poverty of thought, etc.), severely disorganized or catatonic behavior. B. At least one of the symptoms/signs should be Delusions, Hallucinations, or Disorganized Speech. TREATMENT OPTIONS MEDICATIONS Informed consent for psychotropic
    [Show full text]
  • CDPHP Medicare Advantage 2021 Part D Prior Authorization Criteria
    CDPHP Medicare Advantage 2021 Part D Prior Authorization Criteria The following guidelines outline the Part D drugs that require prior authorization through the CDPHP pharmacy department. Please be aware that these guidelines do not reflect those instances in which it is the member’s responsibility to seek prior authorization. Coverage for a service is subject to the member’s eligibility, specific contract benefits, and CDPHP policy. Requests for a service that does not meet criteria outlined in the CDPHP Medicare Advantage pharmacy policies or for an extension beyond what has been approved by CDPHP should be directed to the pharmacy department at (518) 641-3784. POLICIES Policy Reference/Type of Service Requiring Prior Authorization Effective Date: September 1, 2021 abiraterone (ZYTIGA) Covered indications: All Medically-Accepted Indications (FDA approved and 1350/20.000278 compendia-supported). Exclusions: None PA applies to new starts only Approvals: 12 months. ACNE 1350/20.000118 Covered indications: All Medically-Accepted Indications (FDA approved and • avita cream/gel compendia-supported). • tretinoin cream/gel Criteria: Enrollee has tried or prescriber has considered using one of the accepted therapies noted in national guidelines, including, but not limited to topical benzoyl peroxide, topical antibiotics, systemic antibiotics but deemed one or all of them inappropriate for the enrollee. Exclusions: Cosmetic Use. Approvals: 12 months. ACTIMMUNE (Interferon-Gamma 1B) Covered indications: All Medically-Accepted Indications (FDA approved and 1350/20.000278 compendia-supported). Exclusions: None PA applies to new starts only Approvals: 12 months. ADEMPAS (riociguat) Covered indications: All FDA-approved indications not otherwise excluded 1350/20.000278 from Part D.
    [Show full text]