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INVESTIGATION of NATURAL PRODUCT SCAFFOLDS for the DEVELOPMENT of OPIOID RECEPTOR LIGANDS by Katherine M
INVESTIGATION OF NATURAL PRODUCT SCAFFOLDS FOR THE DEVELOPMENT OF OPIOID RECEPTOR LIGANDS By Katherine M. Prevatt-Smith Submitted to the graduate degree program in Medicinal Chemistry and the Graduate Faculty of the University of Kansas in partial fulfillment of the requirements for the degree of Doctor of Philosophy. _________________________________ Chairperson: Dr. Thomas E. Prisinzano _________________________________ Dr. Brian S. J. Blagg _________________________________ Dr. Michael F. Rafferty _________________________________ Dr. Paul R. Hanson _________________________________ Dr. Susan M. Lunte Date Defended: July 18, 2012 The Dissertation Committee for Katherine M. Prevatt-Smith certifies that this is the approved version of the following dissertation: INVESTIGATION OF NATURAL PRODUCT SCAFFOLDS FOR THE DEVELOPMENT OF OPIOID RECEPTOR LIGANDS _________________________________ Chairperson: Dr. Thomas E. Prisinzano Date approved: July 18, 2012 ii ABSTRACT Kappa opioid (KOP) receptors have been suggested as an alternative target to the mu opioid (MOP) receptor for the treatment of pain because KOP activation is associated with fewer negative side-effects (respiratory depression, constipation, tolerance, and dependence). The KOP receptor has also been implicated in several abuse-related effects in the central nervous system (CNS). KOP ligands have been investigated as pharmacotherapies for drug abuse; KOP agonists have been shown to modulate dopamine concentrations in the CNS as well as attenuate the self-administration of cocaine in a variety of species, and KOP antagonists have potential in the treatment of relapse. One drawback of current opioid ligand investigation is that many compounds are based on the morphine scaffold and thus have similar properties, both positive and negative, to the parent molecule. Thus there is increasing need to discover new chemical scaffolds with opioid receptor activity. -
Opportunities and Pharmacotherapeutic Perspectives
biomolecules Review Anticoronavirus and Immunomodulatory Phenolic Compounds: Opportunities and Pharmacotherapeutic Perspectives Naiara Naiana Dejani 1 , Hatem A. Elshabrawy 2 , Carlos da Silva Maia Bezerra Filho 3,4 and Damião Pergentino de Sousa 3,4,* 1 Department of Physiology and Pathology, Federal University of Paraíba, João Pessoa 58051-900, Brazil; [email protected] 2 Department of Molecular and Cellular Biology, College of Osteopathic Medicine, Sam Houston State University, Conroe, TX 77304, USA; [email protected] 3 Department of Pharmaceutical Sciences, Federal University of Paraíba, João Pessoa 58051-900, Brazil; [email protected] 4 Postgraduate Program in Bioactive Natural and Synthetic Products, Federal University of Paraíba, João Pessoa 58051-900, Brazil * Correspondence: [email protected]; Tel.: +55-83-3216-7347 Abstract: In 2019, COVID-19 emerged as a severe respiratory disease that is caused by the novel coronavirus, Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2). The disease has been associated with high mortality rate, especially in patients with comorbidities such as diabetes, cardiovascular and kidney diseases. This could be attributed to dysregulated immune responses and severe systemic inflammation in COVID-19 patients. The use of effective antiviral drugs against SARS-CoV-2 and modulation of the immune responses could be a potential therapeutic strategy for Citation: Dejani, N.N.; Elshabrawy, COVID-19. Studies have shown that natural phenolic compounds have several pharmacological H.A.; Bezerra Filho, C.d.S.M.; properties, including anticoronavirus and immunomodulatory activities. Therefore, this review de Sousa, D.P. Anticoronavirus and discusses the dual action of these natural products from the perspective of applicability at COVID-19. -
Identifying New/Emerging Psychoactive Substances at the Time of COVID-19; a Web-Based Approach
ORIGINAL RESEARCH published: 09 February 2021 doi: 10.3389/fpsyt.2020.632405 Identifying New/Emerging Psychoactive Substances at the Time of COVID-19; A Web-Based Approach Valeria Catalani 1*, Davide Arillotta 1, John Martin Corkery 1, Amira Guirguis 1,2, Alessandro Vento 3,4,5 and Fabrizio Schifano 1 1 Psychopharmacology, Drug Misuse & Novel Psychoactive Substances Research Unit, School of Life & Medical Sciences, University of Hertfordshire, Hatfield, United Kingdom, 2 Swansea University Medical School, Institute of Life Sciences 2, Swansea University, Swansea, United Kingdom, 3 Department of Mental Health, ASL Roma 2, Rome, Italy, 4 Addictions’ Observatory (ODDPSS), Rome, Italy, 5 Department of Psychology, Guglielmo Marconi University, Rome, Italy COVID-19-related disruptions of people and goods’ circulation can affect drug markets, especially for new psychoactive substances (NPSs). Drug shortages could cause a change in available NPS, with the introduction of new, unknown, substances. The aims of the current research were to use a web crawler, NPSfinder®, to identify and categorize emerging NPS discussed on a range of drug enthusiasts/psychonauts’ websites/fora at the time of the pandemic; social media for these identified NPS were screened as Edited by: well. The NPSfinder® was used here to automatically scan 24/7 a list of psychonaut Ornella Corazza, University of Hertfordshire, websites and NPS online resources. The NPSs identified in the time frame between United Kingdom January and August 2020 were searched in both the European Monitoring Center Reviewed by: for Drugs and Drug Addictions (EMCDDA)/United Nations Office on Drugs and Crime Simona Zaami, Sapienza University of Rome, Italy (UNODC) databases and on social media (Facebook, Twitter, Instagram, Pinterest, Laura Hondebrink, and YouTube) as well, with a content qualitative analysis having been carried out on University Medical Center reddit.com. -
Β-Phenylethylamines and the Isoquinoline Alkaloids
-Phenylethylamines and the isoquinoline alkaloids Kenneth W. Bentley Marrview, Tillybirloch, Midmar, Aberdeenshire, UK AB51 7PS Received (in Cambridge, UK) 28th November 2000 First published as an Advance Article on the web 7th February 2001 Covering: July 1999 to June 2000. Previous review: Nat. Prod. Rep., 2000, 17, 247. 1 Introduction 2 -Phenylethylamines 3 Isoquinolines 4 Naphthylisoquinolines 5 Benzylisoquinolines 6 Bisbenzylisoquinolines 7 Pavines and isopavines 8 Berberines and tetrahydoberberines 9 Protopines 10 Phthalide-isoquinolines 11 Other modified berberines 12 Emetine and related alkaloids 13 Benzophenanthridines 14 Aporphinoid alkaloids 14.1 Proaporphines 14.2 Aporphines 14.3 Aporphine–benzylisoquinoline dimers 14.4 Phenanthrenes 14.5 Oxoaporphines 14.6 Dioxoaporphines 14.7 Aristolochic acids and aristolactams 14.8 Oxoisoaporphines 15 Alkaloids of the morphine group 16 Colchicine and related alkaloids 17 Erythrina alkaloids 17.1 Erythrinanes 17.2 Cephalotaxine and related alkaloids 18 Other isoquinolines 19 References 1 Introduction Reviews of the occurrence of isoquinoline alkaloids in some plant species 1,2 and of recent developments in the chemistry and synthesis of alkaloids of these groups 3–6 have been published. 2 -Phenylethylamines β-Phenylethylamine, tyramine, N-methyltyramine, hordenine, mescaline, N-methylmescaline and N,N-dimethylmescaline 1, which is reported as an alkaloid for the first time, have been isolated from an unspecified species of Turbinocarpus 7 and N-trans-feruloyltyramine has been isolated from Cananga odorata.8 The N-oxides of the known alkaloid culantraramine 2 and the unknown culantraraminol 3, together with the related avicennamine 4 have been isolated as new alkaloids from Zanthoxylum avicennae.9 Three novel amides of dehydrotyr- leucine and proline respectively. -
Serum Enterolactone
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Julkari Annamari Kilkkinen SERUM ENTEROLACTONE D E T E R M I N A N T S A N D A S S O C I A T I O N S W I T H B R E A S T A N D P R O S T A T E C A N C E R S A C A D E M I C D I S S E R T A T I O N To be presented with the permission of the Faculty of Medicine, University of Helsinki, for public examination in Auditorium XII, University Main Building, on June 11th, 2004, at 12 noon. National Public Health Institute, Helsinki, Finland and Department of Public Health, University of Helsinki, Finland Helsinki 2004 P u b l i c a t i o n s o f t h e N a t i o n a l P u b l i c H e a l t h I n s t i t u t e K T L A 1 0 / 2 0 0 4 Copyright National Public Health Institute Julkaisija-Utgivare-Publisher Kansanterveyslaitos (KTL) Mannerheimintie 166 00300 Helsinki Puh. vaihde (09) 474 41, telefax (09) 4744 8408 Folkhälsoinstitutet Mannerheimvägen 166 00300 Helsingfors Tel. växel (09) 474 41, telefax (09) 4744 8408 National Public Health Institute Mannerheimintie 166 FIN-00300 Helsinki, Finland Telephone +358 9 474 41, telefax +358 9 4744 8408 ISBN 951-740-448-4 ISSN 0359-3584 ISBN 951-740-449-2 (pdf) ISSN 1458-6290 (pdf) Hakapaino Oy Helsinki 2004 S u p e r v i s e d b y Professor Pirjo Pietinen Department of Epidemiology and Health Promotion National Public Health Institute, Helsinki, Finland Professor Jarmo Virtamo Department of Epidemiology and Health Promotion National Public Health Institute, Helsinki, Finland R e v i e w e d b y Associate Professor Sari -
Treatment Protocol Copyright © 2018 Kostoff Et Al
Prevention and reversal of Alzheimer's disease: treatment protocol Copyright © 2018 Kostoff et al PREVENTION AND REVERSAL OF ALZHEIMER'S DISEASE: TREATMENT PROTOCOL by Ronald N. Kostoffa, Alan L. Porterb, Henry. A. Buchtelc (a) Research Affiliate, School of Public Policy, Georgia Institute of Technology, USA (b) Professor Emeritus, School of Public Policy, Georgia Institute of Technology, USA (c) Associate Professor, Department of Psychiatry, University of Michigan, USA KEYWORDS Alzheimer's Disease; Dementia; Text Mining; Literature-Based Discovery; Information Technology; Treatments Prevention and reversal of Alzheimer's disease: treatment protocol Copyright © 2018 Kostoff et al CITATION TO MONOGRAPH Kostoff RN, Porter AL, Buchtel HA. Prevention and reversal of Alzheimer's disease: treatment protocol. Georgia Institute of Technology. 2018. PDF. https://smartech.gatech.edu/handle/1853/59311 COPYRIGHT AND CREATIVE COMMONS LICENSE COPYRIGHT Copyright © 2018 by Ronald N. Kostoff, Alan L. Porter, Henry A. Buchtel Printed in the United States of America; First Printing, 2018 CREATIVE COMMONS LICENSE This work can be copied and redistributed in any medium or format provided that credit is given to the original author. For more details on the CC BY license, see: http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License<http://creativecommons.org/licenses/by/4.0/>. DISCLAIMERS The views in this monograph are solely those of the authors, and do not represent the views of the Georgia Institute of Technology or the University of Michigan. This monograph is not intended as a substitute for the medical advice of physicians. The reader should regularly consult a physician in matters relating to his/her health and particularly with respect to any symptoms that may require diagnosis or medical attention. -
Mixed Antagonistic Effects of the Ginkgolides at Recombinant Human R1 GABAC Receptors
Neuropharmacology 63 (2012) 1127e1139 Contents lists available at SciVerse ScienceDirect Neuropharmacology journal homepage: www.elsevier.com/locate/neuropharm Mixed antagonistic effects of the ginkgolides at recombinant human r1 GABAC receptors Shelley H. Huang a, Trevor M. Lewis b, Sarah C.R. Lummis c, Andrew J. Thompson c, Mary Chebib d, Graham A.R. Johnston a, Rujee K. Duke a,* a Discipline of Pharmacology, School of Medical Sciences, Faculty of Medicine, University of Sydney, Australia b School of Medical Sciences, University of New South Wales, Australia c Department of Biochemistry, University of Cambridge, Cambridge, United Kingdom d Faculty of Pharmacy, University of Sydney, Australia article info abstract Article history: The diterpene lactones of Ginkgo biloba, ginkgolides A, B and C are antagonists at a range of Cys-loop Received 11 July 2011 receptors. This study examined the effects of the ginkgolides at recombinant human r1 GABAC recep- Received in revised form tors expressed in Xenopus oocytes using two-electrode voltage clamp. The ginkgolides were moderately 18 June 2012 potent antagonists with IC sinthemM range. At 10 mM, 30 mM and 100 mM, the ginkgolides caused Accepted 24 June 2012 50 rightward shifts of GABA doseeresponse curves and reduced maximal GABA responses, characteristic of noncompetitive antagonists, while the potencies showed a clear dependence on GABA concentration, Keywords: indicating apparent competitive antagonism. This suggests that the ginkgolides exert a mixed-type Ginkgolide Bilobalide antagonism at the r1 GABAC receptors. The ginkgolides did not exhibit any obvious use-dependent Mixed-antagonism inhibition. Fitting of the data to a number of kinetic schemes suggests an allosteric inhibition as Use-dependent a possible mechanism of action of the ginkgolides which accounts for their inhibition of the responses GABAr receptor without channel block or use-dependent inhibition. -
Anabolic-Androgenic Steroids in Horses: Natural Presence and Underlying Biomechanisms
ANABOLIC-ANDROGENIC STEROIDS IN HORSES: NATURAL PRESENCE AND UNDERLYING BIOMECHANISMS Anneleen Decloedt Dissertation submitted in the fulfilment of the requirements for the degree of Doctor of philosophy (PhD) in Veterinary Sciences, Faculty of Veterinary Medicine, Ghent University PROMOTER Prof. dr. ir. Lynn Vanhaecke Ghent University, Faculty of Veterinary Medicine Department of Veterinary Public Health and Food Safety Laboratory of Chemical Analysis MEMBERS OF THE READING COMMITTEE Prof. dr. James Scarth HFL Sport Science, Cambridgeshire, United-Kingdom Prof. dr. Peter Van Eenoo Ghent University, DoCoLab, Zwijnaarde, Belgium Prof. dr. Ann Van Soom Ghent University, Faculty of Veterinary Medicine, Merelbeke, Belgium MEMBERS OF THE EXAMINATION COMMITTEE Dr. Ludovic Bailly-Chouriberry Laboratoires des Courses Hippiques, Verrières-le-Buisson, France Dr. Leen Van Ginkel Wageningen University, RIKILT, Wageningen, The Netherlands Prof. dr. Myriam Hesta Ghent University, Faculty of Veterinary Medicine, Merelbeke, Belgium This work was funded by the Fédération Nationale des Courses Françaises (via the Laboratoire des Courses Hippiques) and executed at the Laboratory of Chemical Analysis (Faculty of Veterinary Medicine, Ghent University, Merelbeke). The author and the promoter give the authorisation to consult and to copy parts of this work for personal use only. Every other use is subject to the copyright laws. Permission to reproduce any material contained in this work should be obtained from the author. “The universe is full of magic, Just patiently waiting for our wits to grow sharper” TABLE OF CONTENTS TABLE OF CONTENTS Chapter I – General Introduction 1 1. Steroids 3 1.1 Chemical structure 1.2 (Steroid) hormones and their role in the endocrine system 1.3 Biosynthesis of steroid hormones 1.4 Anabolic-androgenic steroids (AAS) 1.5 Synthesis and absorption of the steroid precursor cholesterol 2. -
MICROCOMP Output File
108TH CONGRESS 2D SESSION S. 2195 AN ACT To amend the Controlled Substances Act to clarify the defini- tion of anabolic steroids and to provide for research and education activities relating to steroids and steroid precursors. 1 Be it enacted by the Senate and House of Representa- 2 tives of the United States of America in Congress assembled, 3 SECTION 1. SHORT TITLE. 4 This Act may be cited as the ‘‘Anabolic Steroid Con- 5 trol Act of 2004’’. 2 1 SEC. 2. AMENDMENTS TO THE CONTROLLED SUBSTANCES 2 ACT. 3 (a) DEFINITIONS.—Section 102 of the Controlled 4 Substances Act (21 U.S.C. 802) is amended— 5 (1) in paragraph (41)— 6 (A) by realigning the margin so as to align 7 with paragraph (40); and 8 (B) by striking subparagraph (A) and in- 9 serting the following: 10 ‘‘(A) The term ‘anabolic steroid’ means any drug or 11 hormonal substance, chemically and pharmacologically re- 12 lated to testosterone (other than estrogens, progestins, 13 corticosteroids, and dehydroepiandrosterone), and 14 includes— 15 ‘‘(i) androstanediol— 16 ‘‘(I) 3β,17β-dihydroxy-5α-androstane; and 17 ‘‘(II) 3α,17β-dihydroxy-5α-androstane; 18 ‘‘(ii) androstanedione (5α-androstan-3,17- 19 dione); 20 ‘‘(iii) androstenediol— 21 ‘‘(I) 1-androstenediol (3β,17β-dihydroxy- 22 5α-androst-1-ene); 23 ‘‘(II) 1-androstenediol (3α,17β-dihydroxy- 24 5α-androst-1-ene); 25 ‘‘(III) 4-androstenediol (3β,17β-dihydroxy- 26 androst-4-ene); and †S 2195 ES 3 1 ‘‘(IV) 5-androstenediol (3β,17β-dihydroxy- 2 androst-5-ene); 3 ‘‘(iv) androstenedione— 4 ‘‘(I) 1-androstenedione ([5α]-androst-1-en- 5 3,17-dione); -
California Essential Drug List
California Essential Drug List The Essential Drug List (formulary) includes a list of drugs covered by Health Net. The drug list is updated at least monthly and is subject to change. All previous versions are no longer in effect. You can view the most current drug list by going to our website at www.healthnet.com. Refer to Evidence of Coverage or Certificate of Insurance for specific cost share information. For California Individual & Family Plans: Drug Lists Select Health Net Large Group – Formulary (pdf). For Small Business Group: Drug Lists Select Health Net Small Business Group – Formulary (pdf). NOTE: To search the drug list online, open the (pdf) document. Hold down the “Control” (Ctrl) and “F” keys. When the search box appears, type the name of your drug and press the “Enter” key. If you have questions or need more information call us toll free. California Individual & Family Plans (off-Exchange) If you have questions about your pharmacy coverage call Customer Service at 1-800-839-2172 California Individual & Family Plans (on-Exchange) If you have questions about your pharmacy coverage call Customer Service at 1-888-926-4988 Hours of Operation 8:00am – 7:00pm Monday through Friday 8:00am – 5:00pm Saturday Small Business Group If you have questions about your pharmacy coverage call Customer Service at 1-800-361-3366 Hours of Operation 8:00am – 6:00pm Monday through Friday Updated September 1, 2021 Health Net of California, Inc. and Health Net Life Insurance Company are subsidiaries of Health Net, LLC and Centene Corporation. Health Net is a registered service mark of Health Net, LLC Table of Contents What If I Have Questions Regarding My Pharmacy Benefit? ................................... -
(12) United States Patent (10) Patent No.: US 9,713,596 B2 Hong Et Al
USOO9713596B2 (12) United States Patent (10) Patent No.: US 9,713,596 B2 Hong et al. (45) Date of Patent: Jul. 25, 2017 (54) BAKUCHOL COMPOSITIONS FOR FOREIGN PATENT DOCUMENTS TREATMENT OF POST INFLAMMATORY DE 1900 435 7, 1970 HYPERPGMENTATION DE 3417234 A1 * 11, 1985 JP H1171231 A * 3, 1999 ............... A61K 7.00 (75) Inventors: Mei Feng Hong, Lacey, WA (US); Qi JP 2000-327581 A 11 2000 Jia, Olympia, WA (US); Lidia Alfaro JP 2005325 120 A 11/2005 KR 2000-0007648 A 2, 2000 Brownell, Tacoma, WA (US) WO 2006/122160 A2 11/2006 WO 2008. 140673 A1 11, 2008 (73) Assignee: Unigen, Inc., Lacey, WA (US) (*) Notice: Subject to any disclaimer, the term of this OTHER PUBLICATIONS patent is extended or adjusted under 35 Ohno, O. Watabe, T., Kazuhiko, N., Kawagoshi, M., Uotsu, N., U.S.C. 154(b) by 0 days. Chiba, T., Yamada, M., Yamaguchi, K., Yamada, K., Miyamoto, K., Uemura, D. Inhibitory Effects of Bakuchiol, Bavachin, an (21) Appl. No.: 13/365,172 Isobavachalcone Isolated from Piper loungum on Melainin Produc (22) Filed: Feb. 2, 2012 tion in B 16 Mouse Melanoma Cells. Biosci. Biotechnol. Biochem. 74 (7), 1504-1506 (2010).* Prior Publication Data Hiroyuki Haraguchi, Junji Inoue, Yukiyoshi Tamura and Kenji (65) Mizutani.Antioxidative Components of Psoralea corylifolia US 2012/O2O1769 A1 Aug. 9, 2012 (Leguminosae). Phytother. Res. 16, 539-544 (2002).* Petra Clara Arck, et al. Towards a “free radical theory of graying: melanocyte apoptosis in the aging human hair follicle is an indicator Related U.S. Application Data of oxidative stress induced tissue damage. -
Effect of Atropine on Denervated Rabbit Ear Blood Vessels
http://www.paper.edu.cn Effect of Atropine on Denervated Rabbit Ear Blood Vessels *Shu-Qin Liu, *Wei-Jin Zang, *Zeng-Li Li, *Xiao-Jiang Yu, and †Bao-Ping Li similar to those of atropine and scopolamine. Henbane drugs Abstract: Surgical denervation of rabbit ear blood vessel beds was might exert multiple advantages in shock patients, but the va- combined with the isolated perfused rabbit ear technique to investi- sodilator effect is undoubtedly the main mechanism. Although gate the mechanism of atropine’s vasodilator action. Intramuscular many studies have been done throughout the world, the mecha- injection of atropine 0.2 mg/kg dilated the denervated blood vessels in the rabbit ear like innervated ones in vivo. Atropine at the maximal nisms of henbane drugs’ vasodilator action remain unclear. concentration (C )of3×10−6 to3×10−4 M did not increase ef- Atropine usually activates the central nervous system at max 8,9 fluent flow of the isolated perfused denervated rabbit ear under con- high doses. Scopolamine, in general, inhibits the central ner- −6 10–13 stant perfusion pressure, but chlorpromazine at a Cmax of 10 M and vous system at any dose. Anisodine slightly inhibits the acetylcholine (ACh) at 2.5 × 10−7 M significantly increased it and central nervous system compared with scopolamine.12,13 An- noradrenaline (NA) at 10−7 M significantly decreased it. Atropine at isodamine is so difficult to pass through the blood–brain bar- −7 −6 Cmax of3×10 M did not affect, but at3×10 M it abolished the rier that it might neither activate nor inhibit the central nervous −7 increase of the effluent flow induced by ACh 2.5 × 10 M.