Therapeutic Class Overview Sedative Hypnotics
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Journal of Pharmacology and Experimental Therapeutics
Journal of Pharmacology and Experimental Therapeutics Molecular Determinants of Ligand Selectivity for the Human Multidrug And Toxin Extrusion Proteins, MATE1 and MATE-2K Bethzaida Astorga, Sean Ekins, Mark Morales and Stephen H Wright Department of Physiology, University of Arizona, Tucson, AZ 85724, USA (B.A., M.M., and S.H.W.) Collaborations in Chemistry, 5616 Hilltop Needmore Road, Fuquay-Varina NC 27526, USA (S.E.) Supplemental Table 1. Compounds selected by the common features pharmacophore after searching a database of 2690 FDA approved compounds (www.collaborativedrug.com). FitValue Common Name Indication 3.93897 PYRIMETHAMINE Antimalarial 3.3167 naloxone Antidote Naloxone Hydrochloride 3.27622 DEXMEDETOMIDINE Anxiolytic 3.2407 Chlordantoin Antifungal 3.1776 NALORPHINE Antidote Nalorphine Hydrochloride 3.15108 Perfosfamide Antineoplastic 3.11759 Cinchonidine Sulfate Antimalarial Cinchonidine 3.10352 Cinchonine Sulfate Antimalarial Cinchonine 3.07469 METHOHEXITAL Anesthetic 3.06799 PROGUANIL Antimalarial PROGUANIL HYDROCHLORIDE 100MG 3.05018 TOPIRAMATE Anticonvulsant 3.04366 MIDODRINE Antihypotensive Midodrine Hydrochloride 2.98558 Chlorbetamide Antiamebic 2.98463 TRIMETHOPRIM Antibiotic Antibacterial 2.98457 ZILEUTON Antiinflammatory 2.94205 AMINOMETRADINE Diuretic 2.89284 SCOPOLAMINE Antispasmodic ScopolamineHydrobromide 2.88791 ARTICAINE Anesthetic 2.84534 RITODRINE Tocolytic 2.82357 MITOBRONITOL Antineoplastic Mitolactol 2.81033 LORAZEPAM Anxiolytic 2.74943 ETHOHEXADIOL Insecticide 2.64902 METHOXAMINE Antihypotensive Methoxamine -
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. -
Gabitril® (Tiagabine)
Gabitril (Tiagabine) What is Gabitril (Tiagabine)? Gabitril is an anti-epileptic drug that has been used to treat patients with epilepsy since 1997. It is helpful in the treatment of partial seizures. Starting the Medicine: We usually gradually increase the dose, until your body gets adjusted to the medication. Since each patient is unique in that he/she breaks down the medication differently or may need a higher or lower dosage to control their seizures, there is no standard dose that is appropriate for all patients. What dosages does the pill come in and what does it look like? 4 mg round, yellow tablet 12 mg oval, green tablet 16 mg oval, blue tablet 20 mg oval, pink tablet What Side Effects Can Be Caused By Gabitril? Side effects can be dose related (common) or idiosyncratic (rare): Common Dose - Related Side Effects: Dizziness, drowsiness, difficulty concentrating, or nausea may occur. If you have these side effects, your doctor may: • spread out the dose more frequently during the day • slow the rate of dose increase Comprehensive Epilepsy Center (734) 936-9020 - 1 - • instruct you to take the pills with food since this will slow the rate at which the medicine gets into the blood, but will not affect the total amount that is absorbed. Rare Side Effects: Rare side effects may include: difficulty sleeping, nervousness, or balance problems. Skin Rash: An allergic reaction, or rash, may occur with Gabitril. If this occurs, notify your doctor immediately. Pregnancy: Currently, no information is available about the effects of Gabitril during pregnancy. Any woman taking Gabitril should discuss this issue with her doctor BEFORE becoming pregnant. -
Resolution of Refractory Pruritus with Aprepitant in a Patient With
Case Report Resolution of refractory pruritus with aprepitant in a patient with microcystic adnexal carcinoma Johanna S Song, MD,ab Hannah Song, BA,a Nicole G Chau, MD,ac Jeffrey F Krane, MD, PhD,ad Nicole R LeBoeuf, MD, MPHabe aHarvard Medical School; bDepartment of Dermatology, Brigham and Women’s Hospital; cCenter for Head and Neck Oncology, Dana-Farber Cancer Institute; dHead and Neck Pathology Service, Brigham and Women’s Hospital; and eCenter for Cutaneous Oncology, Dana-Farber Cancer Institute, all in Boston, Massachusetts ubstance P is an important neurotransmit- biopsied, and the patient was diagnosed with MAC ter implicated in itch pathways.1 After bind- with gross nodal involvement. Laboratory findings ing to its receptor, neurokinin-1 (NK-1), including serum chemistries, blood urea nitrogen, substance P induces release of factors including complete blood cell count, thyroid, and liver func- S 2 histamine, which may cause pruritus. Recent lit- tion were normal. Positron emission tomography- erature has reported successful use of aprepitant, an computed tomography (PET-CT) imaging was NK-1 antagonist that has been approved by the US negative for distant metastases. Food and Drug Administration for the treatment Treatment was initiated with oral aprepitant – of chemotherapy-induced nausea and vomiting, for 125 mg on day 1, 80 mg on day 2, and 80 mg on treatment of pruritus. We report here the case of a day 3 –with concomitant weekly carboplatin (AUC patient with microcystic adnexal carcinoma (MAC) 1.5) and paclitaxel (30 mg/m2) as well as radiation. who presented with refractory pruritus and who had Within hours after the first dose of aprepitant, the rapid and complete resolution of itch after adminis- patient reported a notable cessation in his pruri- tration of aprepitant. -
Drug Class Review Newer Drugs for Insomnia
Drug Class Review Newer Drugs for Insomnia Final Update 2 Report October 2008 The Agency for Healthcare Research and Quality has not yet seen or approved this report. The purpose of Drug Effectiveness Review Project reports is to make available information regarding the comparative clinical effectiveness and harms of different drugs. 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. Update 1: July 2006 Original: December 2005 Susan Carson, MPH Marian S. McDonagh, PharmD Sujata Thakurta, MPA:HA Po-Yin Yen, MS Drug Effectiveness Review Project Marian McDonagh, PharmD, Principal Investigator Oregon Evidence-based Practice Center Mark Helfand, MD, MPH, Director Copyright © 2008 by Oregon Health & Science University Portland, Oregon 97239. All rights reserved. Final Report Update 2 Drug Effectiveness Review Project The medical literature relating to the topic is scanned periodically (see http://www.ohsu.edu/xd/research/centers-institutes/evidence-based-policy- center/derp/documents/methods.cfm for scanning process description). Upon review of the last scan, the Drug Effectiveness Review Project governance group elected not to proceed with another full update of this report based on the information contained in the scan. Some portions of the report may not be up to date. Prior versions of this report can be accessed at the DERP website. Insomnia Page 2 of 87 Final Report Update 2 Drug Effectiveness Review Project TABLE OF CONTENTS INTRODUCTION ............................................................................................................. 6 Scope and Key Questions ...................................................................................................................... -
GABA Receptors
D Reviews • BIOTREND Reviews • BIOTREND Reviews • BIOTREND Reviews • BIOTREND Reviews Review No.7 / 1-2011 GABA receptors Wolfgang Froestl , CNS & Chemistry Expert, AC Immune SA, PSE Building B - EPFL, CH-1015 Lausanne, Phone: +41 21 693 91 43, FAX: +41 21 693 91 20, E-mail: [email protected] GABA Activation of the GABA A receptor leads to an influx of chloride GABA ( -aminobutyric acid; Figure 1) is the most important and ions and to a hyperpolarization of the membrane. 16 subunits with γ most abundant inhibitory neurotransmitter in the mammalian molecular weights between 50 and 65 kD have been identified brain 1,2 , where it was first discovered in 1950 3-5 . It is a small achiral so far, 6 subunits, 3 subunits, 3 subunits, and the , , α β γ δ ε θ molecule with molecular weight of 103 g/mol and high water solu - and subunits 8,9 . π bility. At 25°C one gram of water can dissolve 1.3 grams of GABA. 2 Such a hydrophilic molecule (log P = -2.13, PSA = 63.3 Å ) cannot In the meantime all GABA A receptor binding sites have been eluci - cross the blood brain barrier. It is produced in the brain by decarb- dated in great detail. The GABA site is located at the interface oxylation of L-glutamic acid by the enzyme glutamic acid decarb- between and subunits. Benzodiazepines interact with subunit α β oxylase (GAD, EC 4.1.1.15). It is a neutral amino acid with pK = combinations ( ) ( ) , which is the most abundant combi - 1 α1 2 β2 2 γ2 4.23 and pK = 10.43. -
Tiagabine Synergistically Interacts with Gabapentin in the Electroconvulsive Threshold Test in Mice
Neuropsychopharmacology (2003) 28, 1817–1830 & 2003 Nature Publishing Group All rights reserved 0893-133X/03 $25.00 www.neuropsychopharmacology.org Tiagabine Synergistically Interacts with Gabapentin in the Electroconvulsive Threshold Test in Mice 1,5 2 3 ,1,4 Jarogniew J Łuszczki , Mariusz S´ wia˛der , Jolanta Parada-Turska and Stanisław J Czuczwar* 1 2 Department of Pathophysiology, Medical University, Lublin, Poland; Department of Pharmacology and Toxicology, Medical University, Lublin, 3 4 Poland; Department of Rheumatology, Medical University, Lublin, Poland; Isotope Laboratory, Institute of Agricultural Medicine, Lublin, Poland Polytherapy, based on the rational combining of antiepileptic drugs (AEDs), is required for patients with drug-resistant epilepsy. In such cases, the combinations of AEDs usually offer a significant enhancement of their protective effects against seizures. There has appeared a hypothesis that combining two AEDs, influencing the same neurotransmitter system, results in the potentialization of their anticonvulsant effects. For corroborating this hypothesis, a pharmacological character of interaction between tiagabine (TGB) and gabapentin F (GBP) two novel AEDs affecting the GABA-ergic system, in the maximal electroshock seizure threshold (MEST)-test in mice was evaluated. TGB at the dose of 4 mg/kg and GBP at 75 mg/kg significantly raised the electroconvulsive threshold. Further, using the isobolographic calculations, TGB was coadministered with GBP at three fixed-ratios (1 : 3, 1 : 1, and 3 : 1) of their respective protective drug doses. All examined combinations of TGB with GBP exerted supra-additive (synergistic) interactions against MEST-induced seizures in mice. The interaction index, describing the strength and magnitude of interaction, ranged between 0.25 and 0.50 indicating supra- additivity. -
HHS Template for Reports, with Instructions
Texas Vendor Drug Program 1.1 Drug Use Criteria: Substance P/Neurokinin1 Receptor Antagonists Publication History 1. Developed December 2003. 2. Revised September 2020; September 2018; September 2016; May 2015; August 2013; June 2013; September 2011; October 2009; February 2006; January 2006. Notes: Information on indications for use or diagnosis is assumed to be unavailable. All criteria may be applied retrospectively; prospective application is indicated with an asterisk [*]. The information contained is for the convenience of the public. The Texas Health and Human Services Commission is not responsible for any errors in transmission or any errors or omissions in the document. Medications listed in the tables and non-FDA approved indications included in these retrospective criteria are not indicative of Vendor Drug Program formulary coverage. Prepared by: • Drug Information Service, UT Health San Antonio. • The College of Pharmacy, The University of Texas at Austin. 1 1 Dosage [*] Current therapies for chemotherapy-induced nausea/vomiting (CINV) and post- operative nausea and vomiting (PONV) target corticosteroid, dopamine, and serotonin (5-HT3) receptors. In the central nervous system, tachykinins and neurokinins play a role in some autonomic reflexes and behaviors. Aprepitant is a selective human substance P/neurokinin 1 (NK1) antagonist with a high affinity for NK1 receptors and little, if any, attraction for corticosteroid, dopamine, or 5-HT3 receptors. Rolapitant (Varubi®), the newest substance P/NK1 antagonist, is FDA- approved to prevent delayed CINV with initial and repeat chemotherapy courses including, but not limited to, highly emetogenic chemotherapy in adults. Combination therapy including netupitant, a substance P/NK1 antagonist and palonosetron, a selective 5-HT3 receptor antagonist (Akynzeo®), is now available to prevent acute and delayed CINV with initial and repeat chemotherapy courses including, but not limited to, highly emetogenic chemotherapy in adults. -
Prefrontal Α7nachr Signaling Differentially Modulates Afferent
Research Articles: Systems/Circuits Prefrontal α7nAChR signaling differentially modulates afferent drive and trace fear conditioning behavior in adolescent and adult rats https://doi.org/10.1523/JNEUROSCI.1941-20.2020 Cite as: J. Neurosci 2021; 10.1523/JNEUROSCI.1941-20.2020 Received: 27 July 2020 Revised: 29 November 2020 Accepted: 23 December 2020 This Early Release article has been peer-reviewed and accepted, but has not been through the composition and copyediting processes. The final version may differ slightly in style or formatting and will contain links to any extended data. Alerts: Sign up at www.jneurosci.org/alerts to receive customized email alerts when the fully formatted version of this article is published. Copyright © 2021 the authors 1 Prefrontal α7nAChR signaling differentially modulates afferent drive 2 and trace fear conditioning behavior in adolescent and adult rats 3 4 5 6 7 Running title: Prefrontal α7nAChR control of afferent drive 8 9 10 11 Anabel M. M. Miguelez Fernandez, Hanna M. Molla, Daniel R. Thomases, and Kuei Y. Tseng* 12 13 Department of Anatomy and Cell Biology, University of Illinois at Chicago, IL 14 15 16 17 *Corresponding Author: Kuei Y. Tseng, MD, PhD 18 Department of Anatomy and Cell Biology 19 University of Illinois at Chicago – College of Medicine 20 Chicago, IL 60612, USA 21 Email: [email protected] 22 23 24 Number of figures: 8 25 Number of tables: 0 26 Abstract: 250 27 Main text: 4,030 words (Introduction: 451; Methods: 1,205; Results: 979; Discussion: 1,395) 28 29 30 31 32 Acknowledgements 33 Supported by NIH Grants R01-MH086507 and R01-MH105488 to KYT, and UIC College of Medicine 34 funds to KYT. -
WO 2015/072852 Al 21 May 2015 (21.05.2015) P O P C T
(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 2015/072852 Al 21 May 2015 (21.05.2015) P O P C T (51) International Patent Classification: (81) Designated States (unless otherwise indicated, for every A61K 36/84 (2006.01) A61K 31/5513 (2006.01) kind of national protection available): AE, AG, AL, AM, A61K 31/045 (2006.01) A61P 31/22 (2006.01) AO, AT, AU, AZ, BA, BB, BG, BH, BN, BR, BW, BY, A61K 31/522 (2006.01) A61K 45/06 (2006.01) BZ, CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, DO, DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, (21) International Application Number: HN, HR, HU, ID, IL, IN, IR, IS, JP, KE, KG, KN, KP, KR, PCT/NL20 14/050780 KZ, LA, LC, LK, LR, LS, LU, LY, MA, MD, ME, MG, (22) International Filing Date: MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, OM, 13 November 2014 (13.1 1.2014) PA, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SA, SC, SD, SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, TN, (25) Filing Language: English TR, TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW. (26) Publication Language: English (84) Designated States (unless otherwise indicated, for every (30) Priority Data: kind of regional protection available): ARIPO (BW, GH, 61/903,430 13 November 2013 (13. 11.2013) US GM, KE, LR, LS, MW, MZ, NA, RW, SD, SL, ST, SZ, TZ, UG, ZM, ZW), Eurasian (AM, AZ, BY, KG, KZ, RU, (71) Applicant: RJG DEVELOPMENTS B.V. -
Sedative Hypnotics
Louisiana Medicaid Sedative Hypnotics The Louisiana Uniform Prescription Drug Prior Authorization Form should be utilized to request: • Prior authorization for non-preferred sedative hypnotics; OR • Clinical authorization for tasimelteon (Hetlioz®, Hetlioz LQ™). Additional Point-of-Sale edits may apply. Some of tThese agents may have Black Box Warnings and/or may be subject to Risk Evaluation and Mitigation Strategy (REMS) under FDA safety regulations. Please refer to individual prescribing information for details. ___________________________________________________________________________________ Non-Preferred Agents Approval Criteria for Initial and Reauthorization Requests • There is no preferred alternative that is the exact same chemical entity, formulation, strength, etc.; AND • The requested medication has been prescribed for an approved diagnosis (if applicable); AND • Previous use of a preferred product - ONE of the following is required: o The recipient has had a treatment failure with at least one preferred product; OR o The recipient has had an intolerable side effect to at least one preferred product; OR o The recipient has documented contraindication(s) to all of the preferred products that are appropriate to use for the condition being treated; OR o There is no preferred product that is appropriate to use for the condition being treated; AND • By submitting the authorization request, the prescriber attests to the following: o The prescribing information for the requested medication has been thoroughly reviewed, including -
Gastroparesis: 2014
GASTROINTESTINAL MOTILITY AND FUNCTIONAL BOWEL DISORDERS, SERIES #1 Richard W. McCallum, MD, FACP, FRACP (Aust), FACG Status of Pharmacologic Management of Gastroparesis: 2014 Richard W. McCallum Joseph Sunny, Jr. Gastroparesis is characterized by delayed gastric emptying without mechanical obstruction of the gastric outlet or small intestine. The main etiologies are diabetes, idiopathic and post- gastric and esophageal surgical settings. The management of gastroparesis is challenging due to a limited number of medications and patients often have symptoms, which are refractory to available medications. This article reviews current treatment options for gastroparesis including adverse events and limitations as well as future directions in pharmacologic research. INTRODUCTION astroparesis is a syndrome characterized by documented gastroparesis are increasing.2 Physicians delayed emptying of gastric contents without have both medical and surgical approaches for these Gmechanical obstruction of the stomach, pylorus or patients (See Figure 1). Medical therapy includes both small bowel. Patients can present with nausea, vomiting, prokinetics and antiemetics (See Table 1 and Table 2). postprandial fullness, early satiety, pressure, fullness The gastroparesis population will grow as diabetes and abdominal distension. In addition, abdominal pain increases and new therapies will be required. What located in the epigastrium, and distinguished from the do we know about the size of the gastroparetic term discomfort, is increasingly being recognized population? According to a study from the Mayo Clinic as an important symptom. The main etiologies of group surveying Olmsted County in Minnesota, the gastroparesis are diabetes, idiopathic, and post gastric risk of gastroparesis in Type 1 diabetes mellitus was and esophageal surgeries.1 Hospitalizations from significantly greater than for Type 2.