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The 2021 List of Pharmacological Classes of Doping Agents and Doping Methods
BGBl. III - Ausgegeben am 8. Jänner 2021 - Nr. 1 1 von 23 The 2021 list of pharmacological classes of doping agents and doping methods www.ris.bka.gv.at BGBl. III - Ausgegeben am 8. Jänner 2021 - Nr. 1 2 von 23 www.ris.bka.gv.at BGBl. III - Ausgegeben am 8. Jänner 2021 - Nr. 1 3 von 23 THE 2021 PROHIBITED LIST WORLD ANTI-DOPING CODE DATE OF ENTRY INTO FORCE 1 January 2021 Introduction The Prohibited List is a mandatory International Standard as part of the World Anti-Doping Program. The List is updated annually following an extensive consultation process facilitated by WADA. The effective date of the List is 1 January 2021. The official text of the Prohibited List shall be maintained by WADA and shall be published in English and French. In the event of any conflict between the English and French versions, the English version shall prevail. Below are some terms used in this List of Prohibited Substances and Prohibited Methods. Prohibited In-Competition Subject to a different period having been approved by WADA for a given sport, the In- Competition period shall in principle be the period commencing just before midnight (at 11:59 p.m.) on the day before a Competition in which the Athlete is scheduled to participate until the end of the Competition and the Sample collection process. Prohibited at all times This means that the substance or method is prohibited In- and Out-of-Competition as defined in the Code. Specified and non-Specified As per Article 4.2.2 of the World Anti-Doping Code, “for purposes of the application of Article 10, all Prohibited Substances shall be Specified Substances except as identified on the Prohibited List. -
A Human Multi-Lineage Hepatic Organoid Model for Liver Fibrosis
bioRxiv preprint doi: https://doi.org/10.1101/2020.09.01.278473; this version posted September 2, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. A Human Multi-Lineage Hepatic Organoid Model for Liver Fibrosis Yuan Guan1, Annika Enejder2, Meiyue Wang1, Zhuoqing Fang1, Lu Cui3, Shih-Yu Chen4, Jingxiao Wang1, Yalun Tan1, Manhong Wu1, Xinyu Chen1, Patrik K. Johansson2, Issra Osman1, Koshi Kunimoto3, Pierre Russo5, Sarah C. Heilshorn2 and Gary Peltz1* 1Department of Anesthesia, Stanford University School of Medicine, Stanford CA, 94305; 2Department of Materials Science and Engineering, Stanford University, Stanford CA, 94305; 3Department of Pathology, Institute of Stem Cell Biology and Regenerative Medicine (ISCBRM), Stanford University School of Medicine, Stanford, 94305, CA, USA; 4Shih-Yu Chen, Institute of Biomedical Sciences, Academia Sinica, Taipei, 11529, Taiwan; 5Perelman School of Medicine at The University of Pennsylvania, Philadelphia, PA 19104 The authors have declared that no conflict of interest exists. *Address Correspondence to: [email protected] 300 Pasteur Dr. Room L232 Stanford, CA 94305. bioRxiv preprint doi: https://doi.org/10.1101/2020.09.01.278473; this version posted September 2, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Summary Despite its devastating consequences, liver fibrosis has no treatments. Genome engineering and a hepatic organoid system was used to produce the first in vitro model for human liver fibrosis. Hepatic organoids engineered to express the most common causative mutation for Autosomal Recessive Polycystic Kidney Disease (ARPKD) developed the key features of ARPKD liver pathology (abnormal bile ducts and hepatic fibrosis) in only 21 days. -
British Journal of Nutrition (2013), 110, 1524–1533 Doi:10.1017/S0007114513000743 Q the Authors 2013
Downloaded from British Journal of Nutrition (2013), 110, 1524–1533 doi:10.1017/S0007114513000743 q The Authors 2013 https://www.cambridge.org/core The dopamine b-hydroxylase inhibitor, nepicastat, suppresses chocolate self-administration and reinstatement of chocolate seeking in rats Alessandro Zaru1, Paola Maccioni1, Giancarlo Colombo1 and Gian Luigi Gessa1,2* . IP address: 1Neuroscience Institute, National Research Council of Italy, Section of Cagliari, S.S. 554 km. 4,500, I-09042 Monserrato (CA), Italy 170.106.40.40 2Department of Biomedical Sciences, University of Cagliari, Monserrato (CA), Italy (Submitted 26 July 2012 – Final revision received 5 February 2013 – Accepted 6 February 2013 – First published online 8 April 2013) , on 28 Sep 2021 at 03:11:02 Abstract Craving for chocolate is a common phenomenon, which may evolve to an addictive-like behaviour and contribute to obesity. Nepicastat is a selective dopamine b-hydroxylase (DBH) inhibitor that suppresses cocaine-primed reinstatement of cocaine seeking in rats. We verified whether nepicastat was able to modify the reinforcing and motivational properties of a chocolate solution and to prevent the reinstatement of chocolate seeking in rats. Nepicastat (25, 50 and 100 mg/kg, intraperitoneal) produced a dose-related inhibition of operant self-administration of the chocolate solution in rats under fixed-ratio 10 (FR10) and progressive-ratio schedules , subject to the Cambridge Core terms of use, available at of reinforcement, measures of the reinforcing and motivational properties of the chocolate solution, respectively. The effect of nepica- stat on the reinstatement of chocolate seeking was studied in rats in which lever-responding had been extinguished by removing the chocolate solution for approximately 8 d. -
JPET #212357 1 TITLE PAGE Effects of Pharmacologic Dopamine Β
JPET Fast Forward. Published on May 9, 2014 as DOI: 10.1124/jpet.113.212357 JPETThis Fast article Forward. has not been Published copyedited and on formatted. May 9, The 2014 final as version DOI:10.1124/jpet.113.212357 may differ from this version. JPET #212357 TITLE PAGE Effects of Pharmacologic Dopamine β-Hydroxylase Inhibition on Cocaine-Induced Reinstatement and Dopamine Neurochemistry in Squirrel Monkeys Debra A. Cooper, Heather L. Kimmel, Daniel F. Manvich, Karl T. Schmidt, David Weinshenker, Leonard L. Howell Yerkes National Primate Research Center Division of Neuropharmacology and Neurologic Diseases (D.A.C., H.L.K., L.L.H.), Department of Pharmacology (H.L.K., L.L.H.), Department of Human Genetics (D.A.C., D.F.M, K.T.S., D.W.), and Department of Psychiatry and Behavioral Sciences (L.L.H.) Emory University, Atlanta, Georgia Downloaded from jpet.aspetjournals.org at ASPET Journals on September 24, 2021 1 Copyright 2014 by the American Society for Pharmacology and Experimental Therapeutics. JPET Fast Forward. Published on May 9, 2014 as DOI: 10.1124/jpet.113.212357 This article has not been copyedited and formatted. The final version may differ from this version. JPET #212357 RUNNING TITLE PAGE Running Title: Effects of Dopamine β-Hydroxylase Inhibition in Monkeys Correspondence: Dr LL Howell, Yerkes National Primate Research Center, Emory University, 954 Gatewood Road, Atlanta, GA 30329, USA, Tel: +1 404 727 7786; Fax: +1 404 727 1266; E- mail: [email protected] Text Pages: 19 # Tables: 1 # Figures: 5 # References: 51 Abstract: 250 words Introduction: 420 words Discussion: 1438 words Downloaded from Abbreviations aCSF artificial cerebrospinal fluid DA dopamine jpet.aspetjournals.org DBH dopamine β-hydroxylase EDMax maximally-effective unit dose of cocaine (self-administration) EDPeak maximally-effective dose of pre-session drug prime (reinstatement) at ASPET Journals on September 24, 2021 FI fixed-interval FR fixed-ratio HPLC high-performance liquid chromatography i.m. -
Drug Testing Program
DRUG TESTING PROGRAM Copyright © 2021 CrossFit, LLC. All Rights Reserved. CrossFit is a registered trademark ® of CrossFit, LLC. 2021 DRUG TESTING PROGRAM 2021 DRUG TESTING CONTENTS 1. DRUG-FREE COMPETITION 2. ATHLETE CONSENT 3. DRUG TESTING 4. IN-COMPETITION/OUT-OF-COMPETITION DRUG TESTING 5. REGISTERED ATHLETE TESTING POOL (OUT-OF-COMPETITION DRUG TESTING) 6. REMOVAL FROM TESTING POOL/RETIREMENT 6A. REMOVAL FROM TESTING POOL/WATCH LIST 7. TESTING POOL REQUIREMENTS FOLLOWING A SANCTION 8. DRUG TEST NOTIFICATION AND ADMINISTRATION 9. SPECIMEN ANALYSIS 10. REPORTING RESULTS 11. DRUG TESTING POLICY VIOLATIONS 12. ENFORCEMENT/SANCTIONS 13. APPEALS PROCESS 14. LEADERBOARD DISPLAY 15. EDUCATION 16. DIETARY SUPPLEMENTS 17. TRANSGENDER POLICY 18. THERAPEUTIC USE EXEMPTION APPENDIX A: 2020-2021 CROSSFIT BANNED SUBSTANCE CLASSES APPENDIX B: CROSSFIT URINE TESTING PROCEDURES - (IN-COMPETITION) APPENDIX C: TUE APPLICATION REQUIREMENTS Drug Testing Policy V4 Copyright © 2021 CrossFit, LLC. All Rights Reserved. CrossFit is a registered trademark ® of CrossFit, LLC. [ 2 ] 2021 DRUG TESTING PROGRAM 2021 DRUG TESTING 1. DRUG-FREE COMPETITION As the world’s definitive test of fitness, CrossFit Games competitions stand not only as testaments to the athletes who compete but to the training methodologies they use. In this arena, a true and honest comparison of training practices and athletic capacity is impossible without a level playing field. Therefore, the use of banned performance-enhancing substances is prohibited. Even the legal use of banned substances, such as physician-prescribed hormone replacement therapy or some over-the-counter performance-enhancing supplements, has the potential to compromise the integrity of the competition and must be disallowed. With the health, safety, and welfare of the athletes, and the integrity of our sport as top priorities, CrossFit, LLC has adopted the following Drug Testing Policy to ensure the validity of the results achieved in competition. -
FLT3 Inhibitors in Acute Myeloid Leukemia Mei Wu1, Chuntuan Li2 and Xiongpeng Zhu2*
Wu et al. Journal of Hematology & Oncology (2018) 11:133 https://doi.org/10.1186/s13045-018-0675-4 REVIEW Open Access FLT3 inhibitors in acute myeloid leukemia Mei Wu1, Chuntuan Li2 and Xiongpeng Zhu2* Abstract FLT3 mutations are one of the most common findings in acute myeloid leukemia (AML). FLT3 inhibitors have been in active clinical development. Midostaurin as the first-in-class FLT3 inhibitor has been approved for treatment of patients with FLT3-mutated AML. In this review, we summarized the preclinical and clinical studies on new FLT3 inhibitors, including sorafenib, lestaurtinib, sunitinib, tandutinib, quizartinib, midostaurin, gilteritinib, crenolanib, cabozantinib, Sel24-B489, G-749, AMG 925, TTT-3002, and FF-10101. New generation FLT3 inhibitors and combination therapies may overcome resistance to first-generation agents. Keywords: FMS-like tyrosine kinase 3 inhibitors, Acute myeloid leukemia, Midostaurin, FLT3 Introduction RAS, MEK, and PI3K/AKT pathways [10], and ultim- Acute myeloid leukemia (AML) remains a highly resist- ately causes suppression of apoptosis and differentiation ant disease to conventional chemotherapy, with a me- of leukemic cells, including dysregulation of leukemic dian survival of only 4 months for relapsed and/or cell proliferation [11]. refractory disease [1]. Molecular profiling by PCR and Multiple FLT3 inhibitors are in clinical trials for treat- next-generation sequencing has revealed a variety of re- ing patients with FLT3/ITD-mutated AML. In this re- current gene mutations [2–4]. New agents are rapidly view, we summarized the preclinical and clinical studies emerging as targeted therapy for high-risk AML [5, 6]. on new FLT3 inhibitors, including sorafenib, lestaurtinib, In 1996, FMS-like tyrosine kinase 3/internal tandem du- sunitinib, tandutinib, quizartinib, midostaurin, gilteriti- plication (FLT3/ITD) was first recognized as a frequently nib, crenolanib, cabozantinib, Sel24-B489, G-749, AMG mutated gene in AML [7]. -
Disposition of T Oxic Drugs and Chemicals
Disposition of Toxic Drugs and Chemicals in Man, Eleventh Edition Eleventh Edition in Man and Chemicals Drugs Toxic Disposition of The purpose of this work is to present in a single convenient source the current essential information on the disposition of the chemi- cals and drugs most frequently encountered in episodes of human poisoning. The data included relate to the body fluid concentrations of substances in normal or therapeutic situations, concentrations in fluids and tissues in instances of toxicity and the known metabolic fate of these substances in man. Brief mention is made of specific analytical procedures that are applicable to the determination of each substance and its active metabolites in biological specimens. It is expected that such information will be of particular interest and use to toxicologists, pharmacologists, clinical chemists and clinicians who have need either to conduct an analytical search for these materials in specimens of human origin or to interpret 30 Amberwood Parkway analytical data resulting from such a search. Ashland, OH 44805 by Randall C. Baselt, Ph.D. Former Director, Chemical Toxicology Institute Bookmasters Foster City, California HARD BOUND, 7” x 10”, 2500 pp., 2017 ISBN 978-0-692-77499-1 USA Reviewer Comments on the Tenth Edition “...equally useful for clinical scientists and poison information centers and others engaged in practice and research involving drugs.” Y. Caplan, J. Anal. Tox. “...continues to be an invaluable and essential resource for the forensic toxicologist and pathologist.” D. Fuller, SOFT ToxTalk “...has become an essential reference book in many laboratories that deal with clinical or forensic cases of poisoning.” M. -
Disulfiram Attenuates Drug-Primed Reinstatement of Cocaine Seeking Via Inhibition of Dopamine B-Hydroxylase
Neuropsychopharmacology (2010) 35, 2440–2449 & 2010 Nature Publishing Group All rights reserved 0893-133X/10 $32.00 www.neuropsychopharmacology.org Disulfiram Attenuates Drug-Primed Reinstatement of Cocaine Seeking via Inhibition of Dopamine b-Hydroxylase 1,6 1,6 1 1 1 Jason P Schroeder , Debra A Cooper , Jesse R Schank , Megan A Lyle , Meriem Gaval-Cruz , 1 2 3 2,4 3 Yvonne E Ogbonmwan , Nikita Pozdeyev , Kimberly G Freeman , P Michael Iuvone , Gaylen L Edwards , Philip V Holmes5 and David Weinshenker*,1 1 2 Department of Human Genetics, Emory University School of Medicine, Atlanta, GA, USA; Department of Pharmacology, Emory University 3 4 School of Medicine, Atlanta, GA, USA; Department of Physiology and Pharmacology, University of Georgia, Athens, GA, USA; Department of 5 Ophthalmology, Emory University School of Medicine, Atlanta, GA, USA; Department of Psychology, University of Georgia, Athens, GA, USA The antialcoholism medication disulfiram (Antabuse) inhibits aldehyde dehydrogenase (ALDH), which results in the accumulation of acetaldehyde upon ethanol ingestion and produces the aversive ‘Antabuse reaction’ that deters alcohol consumption. Disulfiram has also been shown to deter cocaine use, even in the absence of an interaction with alcohol, indicating the existence of an ALDH-independent therapeutic mechanism. We hypothesized that disulfiram’s inhibition of dopamine b-hydroxylase (DBH), the catecholamine biosynthetic enzyme that converts dopamine (DA) to norepinephrine (NE) in noradrenergic neurons, underlies the drug’s ability to treat cocaine dependence. We tested the effects of disulfiram on cocaine and food self-administration behavior and drug-primed reinstatement of cocaine seeking in rats. We then compared the effects of disulfiram with those of the selective DBH inhibitor, nepicastat. -
Classification Decisions Taken by the Harmonized System Committee from the 47Th to 60Th Sessions (2011
CLASSIFICATION DECISIONS TAKEN BY THE HARMONIZED SYSTEM COMMITTEE FROM THE 47TH TO 60TH SESSIONS (2011 - 2018) WORLD CUSTOMS ORGANIZATION Rue du Marché 30 B-1210 Brussels Belgium November 2011 Copyright © 2011 World Customs Organization. All rights reserved. Requests and inquiries concerning translation, reproduction and adaptation rights should be addressed to [email protected]. D/2011/0448/25 The following list contains the classification decisions (other than those subject to a reservation) taken by the Harmonized System Committee ( 47th Session – March 2011) on specific products, together with their related Harmonized System code numbers and, in certain cases, the classification rationale. Advice Parties seeking to import or export merchandise covered by a decision are advised to verify the implementation of the decision by the importing or exporting country, as the case may be. HS codes Classification No Product description Classification considered rationale 1. Preparation, in the form of a powder, consisting of 92 % sugar, 6 % 2106.90 GRIs 1 and 6 black currant powder, anticaking agent, citric acid and black currant flavouring, put up for retail sale in 32-gram sachets, intended to be consumed as a beverage after mixing with hot water. 2. Vanutide cridificar (INN List 100). 3002.20 3. Certain INN products. Chapters 28, 29 (See “INN List 101” at the end of this publication.) and 30 4. Certain INN products. Chapters 13, 29 (See “INN List 102” at the end of this publication.) and 30 5. Certain INN products. Chapters 28, 29, (See “INN List 103” at the end of this publication.) 30, 35 and 39 6. Re-classification of INN products. -
Tanibirumab (CUI C3490677) Add to Cart
5/17/2018 NCI Metathesaurus Contains Exact Match Begins With Name Code Property Relationship Source ALL Advanced Search NCIm Version: 201706 Version 2.8 (using LexEVS 6.5) Home | NCIt Hierarchy | Sources | Help Suggest changes to this concept Tanibirumab (CUI C3490677) Add to Cart Table of Contents Terms & Properties Synonym Details Relationships By Source Terms & Properties Concept Unique Identifier (CUI): C3490677 NCI Thesaurus Code: C102877 (see NCI Thesaurus info) Semantic Type: Immunologic Factor Semantic Type: Amino Acid, Peptide, or Protein Semantic Type: Pharmacologic Substance NCIt Definition: A fully human monoclonal antibody targeting the vascular endothelial growth factor receptor 2 (VEGFR2), with potential antiangiogenic activity. Upon administration, tanibirumab specifically binds to VEGFR2, thereby preventing the binding of its ligand VEGF. This may result in the inhibition of tumor angiogenesis and a decrease in tumor nutrient supply. VEGFR2 is a pro-angiogenic growth factor receptor tyrosine kinase expressed by endothelial cells, while VEGF is overexpressed in many tumors and is correlated to tumor progression. PDQ Definition: A fully human monoclonal antibody targeting the vascular endothelial growth factor receptor 2 (VEGFR2), with potential antiangiogenic activity. Upon administration, tanibirumab specifically binds to VEGFR2, thereby preventing the binding of its ligand VEGF. This may result in the inhibition of tumor angiogenesis and a decrease in tumor nutrient supply. VEGFR2 is a pro-angiogenic growth factor receptor -
CAS Number Index
2334 CAS Number Index CAS # Page Name CAS # Page Name CAS # Page Name 50-00-0 905 Formaldehyde 56-81-5 967 Glycerol 61-90-5 1135 Leucine 50-02-2 596 Dexamethasone 56-85-9 963 Glutamine 62-44-2 1640 Phenacetin 50-06-6 1654 Phenobarbital 57-00-1 514 Creatine 62-46-4 1166 α-Lipoic acid 50-11-3 1288 Metharbital 57-22-7 2229 Vincristine 62-53-3 131 Aniline 50-12-4 1245 Mephenytoin 57-24-9 1950 Strychnine 62-73-7 626 Dichlorvos 50-23-7 1017 Hydrocortisone 57-27-2 1428 Morphine 63-05-8 127 Androstenedione 50-24-8 1739 Prednisolone 57-41-0 1672 Phenytoin 63-25-2 335 Carbaryl 50-29-3 569 DDT 57-42-1 1239 Meperidine 63-75-2 142 Arecoline 50-33-9 1666 Phenylbutazone 57-43-2 108 Amobarbital 64-04-0 1648 Phenethylamine 50-34-0 1770 Propantheline bromide 57-44-3 191 Barbital 64-13-1 1308 p-Methoxyamphetamine 50-35-1 2054 Thalidomide 57-47-6 1683 Physostigmine 64-17-5 784 Ethanol 50-36-2 497 Cocaine 57-53-4 1249 Meprobamate 64-18-6 909 Formic acid 50-37-3 1197 Lysergic acid diethylamide 57-55-6 1782 Propylene glycol 64-77-7 2104 Tolbutamide 50-44-2 1253 6-Mercaptopurine 57-66-9 1751 Probenecid 64-86-8 506 Colchicine 50-47-5 589 Desipramine 57-74-9 398 Chlordane 65-23-6 1802 Pyridoxine 50-48-6 103 Amitriptyline 57-92-1 1947 Streptomycin 65-29-2 931 Gallamine 50-49-7 1053 Imipramine 57-94-3 2179 Tubocurarine chloride 65-45-2 1888 Salicylamide 50-52-2 2071 Thioridazine 57-96-5 1966 Sulfinpyrazone 65-49-6 98 p-Aminosalicylic acid 50-53-3 426 Chlorpromazine 58-00-4 138 Apomorphine 66-76-2 632 Dicumarol 50-55-5 1841 Reserpine 58-05-9 1136 Leucovorin 66-79-5 -
LIGANDROL Comprometimento Ósseo
Apresenta ação anabólica com poucos efeitos androgênicos e virilizantes Auxilia no tratamento de condições onde há perda de massa muscular e LIGANDROL comprometimento ósseo Promove a hipertrofia e aumenta a força muscular O QUE É? RA especialmente pelos ligantes exógenos, como os esteróides anabolizantes androgênicos (EAA), pode estar envolvida com o O ligandrol, também conhecido como anabolicum ou LGD- desenvolvimento de patologias na próstata, coração e fígado. Isto 4033, é caracterizado como um modulador seletivo do receptor porque, o receptor RA está expresso em diferentes tecidos, o que de androgênio (SARM) de estrutura não esteroidal que atua de de certa forma limita o uso terapêutico dos EAA em condições forma seletiva sobre os tecidos que expressam os receptores mais específicas como sarcopenia, caquexia associada à doenças androgênicos (RA). Por sua especificidade e alta afinidade ao como câncer, osteoporose e hipogonadismo. RA, tem sido demonstrado que o ligandrol apresenta atividade anabólica no músculo e anti – reabsortiva e anabólica no tecido Com o intuito de contornar possíveis limitações que resultam da ósseo, ao passo que apresenta efeitos androgênicos mínimos ativação global dos RA, os moduladores seletivos de receptores sobre próstata, couro cabeludo e pele. 1 androgênicos, também conhecidos como SARMs, do inglês Selective Androgen Receptor Modulators, tem sido objeto de Os SARMs como o ligandrol e ostarine, têm sido avaliados como estudo uma vez que parecem ativar os RA de maneira específica uma alternativa eficaz e segura para o tratamento de perda e seletiva em determinados tecidos, reduzindo também a de massa muscular associada ao envelhecimento e a outras ocorrência de efeitos colaterais indesejados.