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  • Real World Efficacy and Tolerability of Acotiamide, in Relieving Meal
    testinal & in D o i tr g s e Journal of Gastrointestinal & a s t G i v f e o Narayanan et al., J Gastrointest Dig Syst 2018, 8:1 S l y a s n r ISSN: 2161-069Xt Digestive System DOI: 10.4172/2161-069X.1000553 e u m o J Research Article Open Access Real World Efficacy and Tolerability of Acotiamide, in Relieving Meal- related Symptoms of Functional Dyspepsia Varsha Narayanan*, Amit Bhargava and Shailesh Pallewar 1Department of Medical Services and Research, Lupin Ltd., India *Corresponding author: Narayanan V, Department of Medical Services and Research, Lupin Ltd., Mumbai, India, Tel: +912266402222; E-mail: [email protected] Received date: February 09, 2018; Accepted date: February 21, 2018; Published date: February 27, 2018 Copyright: © 2018 Narayanan V, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Background: Functional Dyspepsia (FD) is a highly prevalent clinical condition that imposes negative economic burden on health-care system as well as greatly impairs quality of life. Treatment of non-specific and bothersome meal-related FD symptoms like post-prandial fullness, upper abdominal bloating and early satiety, is a therapeutic challenge for the clinicians as poorly-defined and ill-understood pathogenesis has hampered efforts to develop effective treatments. Acotiamide is first-in-class drug that exerts its gastro-kinetic effect by enhancing acetylcholine release. Though evidence of its efficacy and tolerance are available through randomized clinical trials, real world data from its regular in-clinic use is lacking.
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  • Fig. L COMPOSITIONS and METHODS to INHIBIT STEM CELL and PROGENITOR CELL BINDING to LYMPHOID TISSUE and for REGENERATING GERMINAL CENTERS in LYMPHATIC TISSUES
    (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 Χ 23 February 2012 (23.02.2012) WO 2U12/U24519ft ft A2 (51) International Patent Classification: AO, AT, AU, AZ, BA, BB, BG, BH, BR, BW, BY, BZ, A61K 31/00 (2006.01) 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, IS, JP, KE, KG, KM, KN, KP, PCT/US201 1/048297 KR, KZ, LA, LC, LK, LR, LS, LT, LU, LY, MA, MD, (22) International Filing Date: ME, MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, 18 August 201 1 (18.08.201 1) NO, NZ, OM, PE, PG, PH, PL, PT, QA, RO, RS, RU, SC, SD, SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, (25) Filing Language: English TN, TR, TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, (26) Publication Language: English ZW. (30) Priority Data: (84) Designated States (unless otherwise indicated, for every 61/374,943 18 August 2010 (18.08.2010) US kind of regional protection available): ARIPO (BW, GH, 61/441,485 10 February 201 1 (10.02.201 1) US GM, KE, LR, LS, MW, MZ, NA, SD, SL, SZ, TZ, UG, 61/449,372 4 March 201 1 (04.03.201 1) US ZM, ZW), Eurasian (AM, AZ, BY, KG, KZ, MD, RU, TJ, TM), European (AL, AT, BE, BG, CH, CY, CZ, DE, DK, (72) Inventor; and EE, ES, FI, FR, GB, GR, HR, HU, IE, IS, ΓΓ, LT, LU, (71) Applicant : DEISHER, Theresa [US/US]; 1420 Fifth LV, MC, MK, MT, NL, NO, PL, PT, RO, RS, SE, SI, SK, Avenue, Seattle, WA 98101 (US).
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  • Minnesota Statutes 1979 Supplement
    MINNESOTA STATUTES 1979 SUPPLEMENT 152.01 PROHIBITED DRUGS CHAPTER 152. PROHIBITED DRUGS Sec. 152.01 Definitions. 152.02 Schedules of controlled substances; admin­ istration of chapter. 152.01 Definitions. [For text of subds 1 to 8, see M.S.1978] Subd. 9. Marijuana. "Marijuana" means all parts of the plant of any species of the genus Cannabis, including all agronomical varieties, whether growing or not; the seeds thereof; the resin extracted from any part of such plant; and every compound, manufacture, salt, derivative, mixture, or preparation of such plant, its seeds or resin, but shall not include the mature stalks of such plant, fiber from such stalks, oil or cake made from the seeds of such plant, any other compound, manufacture, salt, derivative, mix­ ture, or preparation of such mature stalks, except the resin extracted therefrom, fiber, oil, or cake, or the sterilized seed of such plant which is incapable of germination. [For text of subds 10 to 17, see M.S.1978] [ 1979 c 157 s 1 ] 152.02 Schedules of controlled substances; administration of chapter. [For text of subd 1, see M.S.1978) Subd. 2. The following items are listed in Schedule I: (1) Any of the following substances, including their isomers, esters, ethers, salts, and salts of isomers, esters, and ethers, unless specifically excepted, whenever the exis­ tence of such isomers, esters, ethers and salts is possible within the specific chemical des­ ignation: Acetylmethadol; Allylprodine; Alphacetylmethadol; Alphameprodine; Alpham- ethadol; Benzethidine; Betacetylmethadol; Betameprodine; Betamethadol; Betaprodine; Clonitazene; Dextromoramide; Dextrorphan; Diampromide; Diethyliambutene; Dime- noxadol; Dimepheptanol; Dimethyliambutene; Dioxaphetyl butyrate; Dipipanone; Ethylmethylthiambutene; Etonitazene; Etoxeridine; Furethidine; Hydroxypethidine; Ke- tobemidone; Levomoramide; Levophenacylmorphan; Morpheridine; Noracymethadol; Norlevorphanol; Normethadone; Norpipanone; Phenadoxone; Phenampromide; Pheno- morphan; Phenoperidine; Piritramide; Proheptazine; Properidine; Racemoramide; Tri­ meperidine.
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  • PN0496-Acotiamide.Pdf
    Acotiamide hydrochloride hydrate (Acofide®) 盐酸阿考替胺 Z-338 in Zeria; YM-443 in Astellas Tablet, oral, EQ 100 mg acotiamide Acotiamide is a peripheral acetylcholinesterase inhibitor, indicated for the treatment of functional dyspepsia (FD), which was first-in-class drug to treat FD in the world and approved in 2013 by Japan PMDA. It was originally discovered by Zeria, and co-developed with Astellas. The drug is co-marketing in Japan with a single brand name. The human recommended starting dose is 100 mg at a time, and 3 times a day before meals. Worldwide Key Approvals Global Sales ($Million) Key Substance Patent Expiration 2016-May (US5981557A) 2016-May (EP0870765B1) 2013-Mar (JP) Not available 2021-May (JP3181919B2) 2016-May (CN1063442C) Mechanism of Action Acotiamide hydrochloride hydrate is an acetylcholinesterase (AChE) inhibitor and enhanced the acetylcholine (ACh)-induced contraction and motility of the gastric antrum and the gastric body. Target Binding Selectivity In vitro Efficacy In vivo Efficacy Mixed pattern: Ki1= 0.61 µM Effect dose of contraction in gastric sample: Significantly improved the gastrointestinal motility: Ki2= 2.7 µM ACh-induced: at 1 µM In normal and gastric hypomotility dogs: at 10 mg/kg. Inhibition: IC50= 3 µM Electrical-induced: at 0.3 µM In gastric hypomotility rats: at 100 mg/kg. Pharmacokinetics Parameters Rats Dogs Healthy Humans 3 10 3 10 50 mg 100 mg 200 mg 400 mg 800 mg Dose (mg/kg) (i.v.) (p.o.) (i.v.) (p.o.) (p.o.) (p.o.) (p.o.) (p.o.) (p.o.) Tmax (hr) - 0.08 - 0.5 2.75 2.42 2.08 2.25 2.13 Cmax
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  • Combined Treatment with Epigenetic, Differentiating, and Chemotherapeutic
    Author Manuscript Published OnlineFirst on January 19, 2016; DOI: 10.1158/0008-5472.CAN-15-1619 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Combined treatment with epigenetic, differentiating, and chemotherapeutic agents cooperatively targets tumor-initiating cells in triple negative breast cancer. Vanessa F. Merino1,7, Nguyen Nguyen1,7, Kideok Jin1, Helen Sadik1, Soonweng Cho1, Preethi Korangath1, Liangfeng Han1, Yolanda M. N. Foster1, Xian C. Zhou1, Zhe Zhang1, Roisin M. Connolly1, Vered Stearns1, Syed Z. Ali2, Christina Adams2, Qian Chen3, Duojia Pan3, David L. Huso4, Peter Ordentlich5, Angela Brodie6, Saraswati Sukumar1*. 1Department of Oncology, 2Department of Pathology, Sol Goldman Pancreatic Cancer Research Center, 3Department of Molecular Biology and Genetics, 4Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA, 5Syndax Pharmaceuticals, Department of Translational Medicine, Waltham, MA, USA, 6Department of Pharmacology and Experimental Therapeutics, University of Maryland School of Medicine, Baltimore, MD, USA. 7These authors contributed equally. *Correspondence: Saraswati Sukumar, PhD, 1650 Orleans Street, Baltimore, MD, 21231, Ph. 410-614-2479, [email protected] and Vanessa F. Merino, PhD, 1650 Orleans Street, Baltimore, MD, 21231, Ph. 410-614-4075, [email protected]. Key words: Breast, cancer, entinostat, RAR-beta, epigenetic Grant Support: This work was funded by the DOD BCRP Center of Excellence Grant W81XWH-04-1-0595 to S.S, and DOD BCRP, W81XWH-09-1-0499 to V.M. Downloaded from cancerres.aacrjournals.org on September 27, 2021. © 2016 American Association for Cancer Research. Author Manuscript Published OnlineFirst on January 19, 2016; DOI: 10.1158/0008-5472.CAN-15-1619 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited.
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  • An Overview of the Role of Hdacs in Cancer Immunotherapy
    International Journal of Molecular Sciences Review Immunoepigenetics Combination Therapies: An Overview of the Role of HDACs in Cancer Immunotherapy Debarati Banik, Sara Moufarrij and Alejandro Villagra * Department of Biochemistry and Molecular Medicine, School of Medicine and Health Sciences, The George Washington University, 800 22nd St NW, Suite 8880, Washington, DC 20052, USA; [email protected] (D.B.); [email protected] (S.M.) * Correspondence: [email protected]; Tel.: +(202)-994-9547 Received: 22 March 2019; Accepted: 28 April 2019; Published: 7 May 2019 Abstract: Long-standing efforts to identify the multifaceted roles of histone deacetylase inhibitors (HDACis) have positioned these agents as promising drug candidates in combatting cancer, autoimmune, neurodegenerative, and infectious diseases. The same has also encouraged the evaluation of multiple HDACi candidates in preclinical studies in cancer and other diseases as well as the FDA-approval towards clinical use for specific agents. In this review, we have discussed how the efficacy of immunotherapy can be leveraged by combining it with HDACis. We have also included a brief overview of the classification of HDACis as well as their various roles in physiological and pathophysiological scenarios to target key cellular processes promoting the initiation, establishment, and progression of cancer. Given the critical role of the tumor microenvironment (TME) towards the outcome of anticancer therapies, we have also discussed the effect of HDACis on different components of the TME. We then have gradually progressed into examples of specific pan-HDACis, class I HDACi, and selective HDACis that either have been incorporated into clinical trials or show promising preclinical effects for future consideration.
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  • Predictive QSAR Tools to Aid in Early Process Development of Monoclonal Antibodies
    Predictive QSAR tools to aid in early process development of monoclonal antibodies John Micael Andreas Karlberg Published work submitted to Newcastle University for the degree of Doctor of Philosophy in the School of Engineering November 2019 Abstract Monoclonal antibodies (mAbs) have become one of the fastest growing markets for diagnostic and therapeutic treatments over the last 30 years with a global sales revenue around $89 billion reported in 2017. A popular framework widely used in pharmaceutical industries for designing manufacturing processes for mAbs is Quality by Design (QbD) due to providing a structured and systematic approach in investigation and screening process parameters that might influence the product quality. However, due to the large number of product quality attributes (CQAs) and process parameters that exist in an mAb process platform, extensive investigation is needed to characterise their impact on the product quality which makes the process development costly and time consuming. There is thus an urgent need for methods and tools that can be used for early risk-based selection of critical product properties and process factors to reduce the number of potential factors that have to be investigated, thereby aiding in speeding up the process development and reduce costs. In this study, a framework for predictive model development based on Quantitative Structure- Activity Relationship (QSAR) modelling was developed to link structural features and properties of mAbs to Hydrophobic Interaction Chromatography (HIC) retention times and expressed mAb yield from HEK cells. Model development was based on a structured approach for incremental model refinement and evaluation that aided in increasing model performance until becoming acceptable in accordance to the OECD guidelines for QSAR models.
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  • Immunotherapy in Various Cancers
    © 2021 JETIR June 2021, Volume 8, Issue 6 www.jetir.org (ISSN-2349-5162) Immunotherapy in various Cancers Nirav Parmar 1st Year MSc Student Department of Biosciences and Bioengineering, IIT- Roorkee India Abstract: Immunotherapy in the metastatic situation has changed the therapeutic landscape for a variety of cancers, including colorectal cancer. Immunotherapy has firmly established itself as a new pillar of cancer treatment in a variety of cancer types, from the metastatic stage to adjuvant and neoadjuvant settings. Immune checkpoint inhibitors have risen to prominence as a treatment option based on a better knowledge of the development of the tumour microenvironment immune cell-cancer cell regulation over time. Immunotherapy has lately appeared as the most potential field of cancer research by increasing effectiveness and reducing side effects, with FDA-approved therapies for more than 10 various tumours and thousands of new clinical studies. Key Words: Immunotherapy, metastasis, immune checkpoint. Introduction: In the late 1800s, William B. Coley, now generally regarded as the founder of immunotherapy, tried to harness the ability of immune system to cure cancer for the first time. Coley began injecting live and attenuated bacteria like Streptococcus pyogenes and Serratia marcescens into over a thousand patients in 1891 in the hopes of causing sepsis and significant immunological and antitumor responses. His bacterium mixture became known as "Coley's toxin" and is the first recorded active cancer immunotherapy treatment [1]. To better understand the processes of new and traditional immunological targets, the relationship between the immune system and tumour cells should be examined. Tumours have developed ways to evade immunological responses.
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  • (12) Patent Application Publication (10) Pub. No.: US 2017/0209462 A1 Bilotti Et Al
    US 20170209462A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2017/0209462 A1 Bilotti et al. (43) Pub. Date: Jul. 27, 2017 (54) BTK INHIBITOR COMBINATIONS FOR Publication Classification TREATING MULTIPLE MYELOMA (51) Int. Cl. (71) Applicant: Pharmacyclics LLC, Sunnyvale, CA A 6LX 3/573 (2006.01) A69/20 (2006.01) (US) A6IR 9/00 (2006.01) (72) Inventors: Elizabeth Bilotti, Sunnyvale, CA (US); A69/48 (2006.01) Thorsten Graef, Los Altos Hills, CA A 6LX 3/59 (2006.01) (US) A63L/454 (2006.01) (52) U.S. Cl. CPC .......... A61 K3I/573 (2013.01); A61K 3 1/519 (21) Appl. No.: 15/252,385 (2013.01); A61 K3I/454 (2013.01); A61 K 9/0053 (2013.01); A61K 9/48 (2013.01); A61 K (22) Filed: Aug. 31, 2016 9/20 (2013.01) (57) ABSTRACT Disclosed herein are pharmaceutical combinations, dosing Related U.S. Application Data regimen, and methods of administering a combination of a (60) Provisional application No. 62/212.518, filed on Aug. BTK inhibitor (e.g., ibrutinib), an immunomodulatory agent, 31, 2015. and a steroid for the treatment of a hematologic malignancy. US 2017/0209462 A1 Jul. 27, 2017 BTK INHIBITOR COMBINATIONS FOR Subject in need thereof comprising administering pomalido TREATING MULTIPLE MYELOMA mide, ibrutinib, and dexamethasone, wherein pomalido mide, ibrutinib, and dexamethasone are administered con CROSS-REFERENCE TO RELATED currently, simulataneously, and/or co-administered. APPLICATION 0008. In some aspects, provided herein is a method of treating a hematologic malignancy in a subject in need 0001. This application claims the benefit of U.S.
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  • Modifications to the Harmonized Tariff Schedule of the United States to Implement Changes to the Pharmaceutical Appendix
    United States International Trade Commission Modifications to the Harmonized Tariff Schedule of the United States to Implement Changes to the Pharmaceutical Appendix USITC Publication 4208 December 2010 U.S. International Trade Commission COMMISSIONERS Deanna Tanner Okun, Chairman Irving A. Williamson, Vice Chairman Charlotte R. Lane Daniel R. Pearson Shara L. Aranoff Dean A. Pinkert Address all communications to Secretary to the Commission United States International Trade Commission Washington, DC 20436 U.S. International Trade Commission Washington, DC 20436 www.usitc.gov Modifications to the Harmonized Tariff Schedule of the United States to Implement Changes to the Pharmaceutical Appendix Publication 4208 December 2010 (This page is intentionally blank) Pursuant to the letter of request from the United States Trade Representative of December 15, 2010, set forth at the end of this publication, and pursuant to section 1207(a) of the Omnibus Trade and Competitiveness Act, the United States International Trade Commission is publishing the following modifications to the Harmonized Tariff Schedule of the United States (HTS) to implement changes to the Pharmaceutical Appendix, effective on January 1, 2011. Table 1 International Nonproprietary Name (INN) products proposed for addition to the Pharmaceutical Appendix to the Harmonized Tariff Schedule INN CAS Number Abagovomab 792921-10-9 Aclidinium Bromide 320345-99-1 Aderbasib 791828-58-5 Adipiplon 840486-93-3 Adoprazine 222551-17-9 Afimoxifene 68392-35-8 Aflibercept 862111-32-8 Agatolimod
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  • )&F1y3x PHARMACEUTICAL APPENDIX to THE
    )&f1y3X PHARMACEUTICAL APPENDIX TO THE HARMONIZED TARIFF SCHEDULE )&f1y3X PHARMACEUTICAL APPENDIX TO THE TARIFF SCHEDULE 3 Table 1. This table enumerates products described by International Non-proprietary Names (INN) which shall be entered free of duty under general note 13 to the tariff schedule. The Chemical Abstracts Service (CAS) registry numbers also set forth in this table are included to assist in the identification of the products concerned. For purposes of the tariff schedule, any references to a product enumerated in this table includes such product by whatever name known. Product CAS No. Product CAS No. ABAMECTIN 65195-55-3 ACTODIGIN 36983-69-4 ABANOQUIL 90402-40-7 ADAFENOXATE 82168-26-1 ABCIXIMAB 143653-53-6 ADAMEXINE 54785-02-3 ABECARNIL 111841-85-1 ADAPALENE 106685-40-9 ABITESARTAN 137882-98-5 ADAPROLOL 101479-70-3 ABLUKAST 96566-25-5 ADATANSERIN 127266-56-2 ABUNIDAZOLE 91017-58-2 ADEFOVIR 106941-25-7 ACADESINE 2627-69-2 ADELMIDROL 1675-66-7 ACAMPROSATE 77337-76-9 ADEMETIONINE 17176-17-9 ACAPRAZINE 55485-20-6 ADENOSINE PHOSPHATE 61-19-8 ACARBOSE 56180-94-0 ADIBENDAN 100510-33-6 ACEBROCHOL 514-50-1 ADICILLIN 525-94-0 ACEBURIC ACID 26976-72-7 ADIMOLOL 78459-19-5 ACEBUTOLOL 37517-30-9 ADINAZOLAM 37115-32-5 ACECAINIDE 32795-44-1 ADIPHENINE 64-95-9 ACECARBROMAL 77-66-7 ADIPIODONE 606-17-7 ACECLIDINE 827-61-2 ADITEREN 56066-19-4 ACECLOFENAC 89796-99-6 ADITOPRIM 56066-63-8 ACEDAPSONE 77-46-3 ADOSOPINE 88124-26-9 ACEDIASULFONE SODIUM 127-60-6 ADOZELESIN 110314-48-2 ACEDOBEN 556-08-1 ADRAFINIL 63547-13-7 ACEFLURANOL 80595-73-9 ADRENALONE
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  • NINDS Custom Collection II
    ACACETIN ACEBUTOLOL HYDROCHLORIDE ACECLIDINE HYDROCHLORIDE ACEMETACIN ACETAMINOPHEN ACETAMINOSALOL ACETANILIDE ACETARSOL ACETAZOLAMIDE ACETOHYDROXAMIC ACID ACETRIAZOIC ACID ACETYL TYROSINE ETHYL ESTER ACETYLCARNITINE ACETYLCHOLINE ACETYLCYSTEINE ACETYLGLUCOSAMINE ACETYLGLUTAMIC ACID ACETYL-L-LEUCINE ACETYLPHENYLALANINE ACETYLSEROTONIN ACETYLTRYPTOPHAN ACEXAMIC ACID ACIVICIN ACLACINOMYCIN A1 ACONITINE ACRIFLAVINIUM HYDROCHLORIDE ACRISORCIN ACTINONIN ACYCLOVIR ADENOSINE PHOSPHATE ADENOSINE ADRENALINE BITARTRATE AESCULIN AJMALINE AKLAVINE HYDROCHLORIDE ALANYL-dl-LEUCINE ALANYL-dl-PHENYLALANINE ALAPROCLATE ALBENDAZOLE ALBUTEROL ALEXIDINE HYDROCHLORIDE ALLANTOIN ALLOPURINOL ALMOTRIPTAN ALOIN ALPRENOLOL ALTRETAMINE ALVERINE CITRATE AMANTADINE HYDROCHLORIDE AMBROXOL HYDROCHLORIDE AMCINONIDE AMIKACIN SULFATE AMILORIDE HYDROCHLORIDE 3-AMINOBENZAMIDE gamma-AMINOBUTYRIC ACID AMINOCAPROIC ACID N- (2-AMINOETHYL)-4-CHLOROBENZAMIDE (RO-16-6491) AMINOGLUTETHIMIDE AMINOHIPPURIC ACID AMINOHYDROXYBUTYRIC ACID AMINOLEVULINIC ACID HYDROCHLORIDE AMINOPHENAZONE 3-AMINOPROPANESULPHONIC ACID AMINOPYRIDINE 9-AMINO-1,2,3,4-TETRAHYDROACRIDINE HYDROCHLORIDE AMINOTHIAZOLE AMIODARONE HYDROCHLORIDE AMIPRILOSE AMITRIPTYLINE HYDROCHLORIDE AMLODIPINE BESYLATE AMODIAQUINE DIHYDROCHLORIDE AMOXEPINE AMOXICILLIN AMPICILLIN SODIUM AMPROLIUM AMRINONE AMYGDALIN ANABASAMINE HYDROCHLORIDE ANABASINE HYDROCHLORIDE ANCITABINE HYDROCHLORIDE ANDROSTERONE SODIUM SULFATE ANIRACETAM ANISINDIONE ANISODAMINE ANISOMYCIN ANTAZOLINE PHOSPHATE ANTHRALIN ANTIMYCIN A (A1 shown) ANTIPYRINE APHYLLIC
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