2012 Harmonized Tariff Schedule Pharmaceuticals Appendix
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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). -
Benfluorex: What Use? a SECOND LOOK POOR ASSESSMENT FILE
New products necessitating blood transfusions 3- “Paclitaxel” Prescr Intern 1994; 3 (14): 164-165. Literature 4- Rowisky EK et al. “Phase I and pharmacolog- occurred in 37% of patients (9). ic study of topotecan: a novel topoisomerase I The most frequent non haematologi- Our literature search was based on systematic inhibitor” J Clin Oncol 1992; 10: 647-656. cal side effects were nausea (68.1% of scrutiny of contents listings of the main inter- 5- Verweij L et al. “Phase I and pharmacokinet- ics study of topotecan, a new topoisomerase I patients, severe in 6.1% of patients), national journals and Current Contents at inhibitor” Ann Oncol 1993; 4: 673-678. vomiting (44.3%, severe in 4.5%), hair the Prescrire library, and on reference texts 6- Saltz L et al. “Phase I clinical and pharmacol- in clinical pharmacology (Martindale The ogy study of topotecan given daily for 5 consecu- loss (56.9%), fatigue (44.5%, severe in Extra Pharmacopoeia 31st ed., etc.). We also tive days to patients with advanced solid tumors, 6%), diarrhoea (26.1%, severe in 3.4%), consulted CD-ROM versions of Medline (1981- with attempt at dose intensification using recom- and stomatitis (20.2%, severe in 2%) (9). March 1998), Embase Drugs and binant granulocyte colony-stimulating factor” J Pharmacology (1991-January 1998), Cochrane Natl Cancer Inst 1993; 85 (18): 1499-1507. Paclitaxel solution contains a solvent, 7- Kudelka AP et al. “Phase II study of intravenous Cremophor EL°, that is incompatible with (1998, issue 1), Medidoc (1991-1994) and topotecan as a 5-day infusion for refractory epithe- Reactions (1983-June 1997), and the Minitel lial ovarian carcinoma” J Clin Oncol 1996; 14: the use of PVC infusion devices and war- version of the Pascal database up to 1552-1557. -
Review Article Targeting Beta Amyloid: a Clinical Review of Immunotherapeutic Approaches in Alzheimer’S Disease
Hindawi Publishing Corporation International Journal of Alzheimer’s Disease Volume 2012, Article ID 628070, 14 pages doi:10.1155/2012/628070 Review Article Targeting Beta Amyloid: A Clinical Review of Immunotherapeutic Approaches in Alzheimer’s Disease Kasia Lobello,1 J. Michael Ryan,1 Enchi Liu,2 Gregory Rippon,1 and Ronald Black1 1 Department of Clinical Sciences, Pfizer Inc., Collegeville, PA 19426, USA 2 Janssen Alzheimer Immunotherapy Research & Development, LLC., South San Francisco, CA 94080, USA Correspondence should be addressed to Kasia Lobello, kasia.lobello@pfizer.com Received 1 August 2011; Accepted 21 September 2011 Academic Editor: Marwan Sabbagh Copyright © 2012 Kasia Lobello et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. As the societal and economic burdens of Alzheimer’s disease (AD) continue to mount, so does the need for therapies that slow the progression of the illness. Beta amyloid has long been recognized as the pathologic hallmark of AD, and the past decade has seen significant progress in the development of various immunotherapeutic approaches targeting beta amyloid. This paper reviews active and passive approaches aimed at beta amyloid, with a focus on clinical trial data. 1. Introduction however, that it is the production and/or deposition of toxic forms of beta amyloid, along with the slowing of beta- Alzheimer’s disease (AD) is by far the most common form amyloid clearance, that act as the central and primary events of dementia, and the social and economic burdens of AD in AD pathogenesis, while neurofibrillary tangle formation continue to mount. -
Crohn's & Colitis Program, Patient Information Guide
Inflammatory Bowel Disease Program Patient Information Guide Page # Contents ..........................................................................................................................................1 Welcome! Welcome Letter ....................................................................................................................3 Important Things to Know Up Front ....................................................................................4 Meet Your Crohn’s & Colitis Team .....................................................................................6 How to Contact Us Crohn’s & Colitis Clinic Schedule .....................................................................................11 Physician and Nurse Contact Information..........................................................................12 Appointment Scheduling and Other Contact Information..................................................13 The Basics of Inflammatory Bowel Disease (IBD) Basic Information about Inflammatory Bowel Disease (IBD) ...........................................14 Frequently Asked Questions about Inflammatory Bowel Disease (IBD) ..........................18 Testing in IBD Colonoscopy and Flexible Sigmoidoscopy ........................................................................20 Upper Endoscopy ...............................................................................................................21 Capsule Endoscopy and Deep Enteroscopy .......................................................................22 -
Malignant B Lymphocyte Survival in Vivo CD22 Ligand Binding Regulates Normal
The Journal of Immunology CD22 Ligand Binding Regulates Normal and Malignant B Lymphocyte Survival In Vivo1 Karen M. Haas, Suman Sen, Isaac G. Sanford, Ann S. Miller, Jonathan C. Poe, and Thomas F. Tedder2 The CD22 extracellular domain regulates B lymphocyte function by interacting with ␣2,6-linked sialic acid-bearing ligands. To understand how CD22 ligand interactions affect B cell function in vivo, mouse anti-mouse CD22 mAbs were generated that inhibit CD22 ligand binding to varying degrees. Remarkably, mAbs which blocked CD22 ligand binding accelerated mature B cell turnover by 2- to 4-fold in blood, spleen, and lymph nodes. CD22 ligand-blocking mAbs also inhibited the survival of adoptively transferred normal (73–88%) and malignant (90%) B cells in vivo. Moreover, mAbs that bound CD22 ligand binding domains induced significant CD22 internalization, depleted marginal zone B cells (82–99%), and reduced mature recirculating B cell numbers by 75–85%. The CD22 mAb effects were independent of complement and FcRs, and the CD22 mAbs had minimal effects in CD22AA mice that express mutated CD22 that is not capable of ligand binding. These data demonstrate that inhibition of CD22 ligand binding can disrupt normal and malignant B cell survival in vivo and suggest a novel mechanism of action for therapeutics targeting CD22 ligand binding domains. The Journal of Immunology, 2006, 177: 3063–3073. D22 is a B cell-specific glycoprotein of the Ig superfam- cell surface CD22, IgM, and MHC class II expression on mature B ily expressed on the surface of maturing B cells coinci- cells, whereas normal BCR signaling and Ca2ϩ mobilization are dent with IgD expression (1, 2). -
Muscarinic Acetylcholine Receptor
mAChR Muscarinic acetylcholine receptor mAChRs (muscarinic acetylcholine receptors) are acetylcholine receptors that form G protein-receptor complexes in the cell membranes of certainneurons and other cells. They play several roles, including acting as the main end-receptor stimulated by acetylcholine released from postganglionic fibersin the parasympathetic nervous system. mAChRs are named as such because they are more sensitive to muscarine than to nicotine. Their counterparts are nicotinic acetylcholine receptors (nAChRs), receptor ion channels that are also important in the autonomic nervous system. Many drugs and other substances (for example pilocarpineand scopolamine) manipulate these two distinct receptors by acting as selective agonists or antagonists. Acetylcholine (ACh) is a neurotransmitter found extensively in the brain and the autonomic ganglia. www.MedChemExpress.com 1 mAChR Inhibitors & Modulators (+)-Cevimeline hydrochloride hemihydrate (-)-Cevimeline hydrochloride hemihydrate Cat. No.: HY-76772A Cat. No.: HY-76772B Bioactivity: Cevimeline hydrochloride hemihydrate, a novel muscarinic Bioactivity: Cevimeline hydrochloride hemihydrate, a novel muscarinic receptor agonist, is a candidate therapeutic drug for receptor agonist, is a candidate therapeutic drug for xerostomia in Sjogren's syndrome. IC50 value: Target: mAChR xerostomia in Sjogren's syndrome. IC50 value: Target: mAChR The general pharmacol. properties of this drug on the The general pharmacol. properties of this drug on the gastrointestinal, urinary, and reproductive systems and other… gastrointestinal, urinary, and reproductive systems and other… Purity: >98% Purity: >98% Clinical Data: No Development Reported Clinical Data: No Development Reported Size: 10mM x 1mL in DMSO, Size: 10mM x 1mL in DMSO, 1 mg, 5 mg 1 mg, 5 mg AC260584 Aclidinium Bromide Cat. No.: HY-100336 (LAS 34273; LAS-W 330) Cat. -
Tonsillopharyngitis - Acute (1 of 10)
Tonsillopharyngitis - Acute (1 of 10) 1 Patient presents w/ sore throat 2 EVALUATION Yes EXPERT Are there signs of REFERRAL complication? No 3 4 EVALUATION Is Group A Beta-hemolytic Yes DIAGNOSIS Streptococcus (GABHS) • Rapid antigen detection test infection suspected? (RADT) • roat culture No TREATMENT EVALUATION No A Supportive management Is GABHS confi rmed? B Pharmacological therapy (Non-GABHS) Yes 5 TREATMENT A EVALUATE RESPONSEMIMS Supportive management TO THERAPY C Pharmacological therapy • Antibiotics Poor/No Good D Surgery, if recurrent or complicated response response REASSESS PATIENT COMPLETE THERAPY & REVIEW THE DIAGNOSIS© Not all products are available or approved for above use in all countries. Specifi c prescribing information may be found in the latest MIMS. B269 © MIMS Pediatrics 2020 Tonsillopharyngitis - Acute (2 of 10) 1 ACUTE TONSILLOPHARYNGITIS • Infl ammation of the tonsils & pharynx • Etiologies include bacterial (group A β-hemolytic streptococcus, Haemophilus infl uenzae, Fusobacterium sp, etc) & viral (infl uenza, adenovirus, coronavirus, rhinovirus, etc) pathogens • Sore throat is the most common presenting symptom in older children TONSILLOPHARYNGITIS 2 EVALUATION FOR COMPLICATIONS • Patients w/ sore throat may have deep neck infections including epiglottitis, peritonsillar or retropharyngeal abscess • Examine for signs of upper airway obstruction Signs & Symptoms of Sore roat w/ Complications • Trismus • Inability to swallow liquids • Increased salivation or drooling • Peritonsillar edema • Deviation of uvula -
Inflammatory Bowel Disease Agents
Therapeutic Class Overview Inflammatory Bowel Disease Agents INTRODUCTION • Inflammatory bowel disease (IBD) is a spectrum of chronic idiopathic inflammatory intestinal conditions that cause gastrointestinal symptoms including diarrhea, abdominal pain, bleeding, fatigue, and weight loss. The exact cause of IBD is unknown; however, proposed etiologies involve a combination of infectious, genetic, and lifestyle factors (Bernstein et al 2015, Peppercorn 2019[a], Peppercorn 2020[c]). • Complications of IBD include hemorrhage, rectal fissures, fistulas, peri-rectal and intra-abdominal abscesses, and colon cancer. Possible extra-intestinal complications include hepatobiliary complications, anemia, arthritis and arthralgias, uveitis, skin lesions, and mood and anxiety disorders (Bernstein et al 2015). • Ulcerative colitis (UC) and Crohn’s disease (CD) are 2 forms of IBD that differ in pathophysiology and presentation; as a result of these differences, the approach to the treatment of each condition often differs (Peppercorn 2019[a]). • UC is characterized by recurrent episodes of inflammation of the mucosal layer of the colon. The inflammation, limited to the mucosa, commonly involves the rectum and may extend in a proximal and continuous fashion to affect other parts of the colon. The hallmark clinical symptom is an inflamed rectum with symptoms of urgency, bleeding, and tenesmus (Peppercorn 2020[c], Rubin et al 2019). • CD can involve any part of the gastrointestinal tract and is characterized by transmural inflammation and “skip areas.” Transmural inflammation may lead to fibrosis, strictures, sinus tracts, and fistulae (Peppercorn 2019[b]). • The immune system is known to play a critical role in the underlying pathogenesis of IBD. It is suggested that abnormal responses of both innate and adaptive immunity mechanisms induce aberrant intestinal tract inflammation in IBD patients (Geremia et al 2014). -
Endocrine Disrupting Compounds and Prostate Cell Proliferation
Review Article Clinics in Oncology Published: 18 Oct, 2016 Endocrine Disrupting Compounds and Prostate Cell Proliferation Joubert Banjop Kharlyngdoh and Per-Erik Olsson* Department of Biology, Örebro University, Sweden Abstract Epidemiological, in vitro and animal studies have indicated that Endocrine Disrupting Compounds (EDCs) influence the normal growth and development of the prostate as well as development and progression of prostate cancer. This has been linked to an increased presence of environmental chemicals that interfere with hormonal signaling. Many of these effects appear to be associated with interferences with steroid hormone receptor signaling or by affecting steroidogenesis. Currently, there is abundant evidence from epidemiological studies linking pesticides and EDCs with elevated prostate cancer risk. Bisphenol-A, a known EDC, has been shown to promote induction of Prostate Specific Antigen (PSA), which is a biomarker for prostate cancer, in the LNCaP human prostate carcinoma cells, and to increase prostate carcinogenesis in animal models. Our research has focused on AR signaling and identification of novel androgenic and anti-androgenic EDCs. Using prostate cancer cell lines we have shown that the AR agonist, TBECH, and antagonist ATE, which is also a partial ART877A agonist, induce PSA expression. With the increasing presence of these EDCs in indoor and outdoor air, follows an increased risk of disturbed prostate development, regulation and function. Hence, identification of the contribution of EDCs to prostate cancer -
Compositions and Methods to Improve the Oral Absorption of Antimicrobial Agents
(19) & (11) EP 2 263 654 A1 (12) EUROPEAN PATENT APPLICATION (43) Date of publication: (51) Int Cl.: 22.12.2010 Bulletin 2010/51 A61K 9/16 (2006.01) A61K 47/36 (2006.01) (21) Application number: 10181335.0 (22) Date of filing: 18.06.2001 (84) Designated Contracting States: (72) Inventors: AT BE CH CY DE DK ES FI FR GB GR IE IT LI LU • Choi, Seung-Ho MC NL PT SE TR Salt Lake City, UT 84109 (US) • Lee, Jeoung-Soo (30) Priority: 21.06.2000 US 598089 Salt Lake City, UT 84117 (US) 09.04.2001 US 829405 • Keith, Dennis 16.04.2001 US 283976 P Arlington, MA 02474 (US) (62) Document number(s) of the earlier application(s) in (74) Representative: Williams, Gareth Owen accordance with Art. 76 EPC: Marks & Clerk LLP 01944619.4 / 1 294 361 62-68 Hills Road Cambridge (71) Applicants: CB2 1LA (GB) • Cubist Pharmaceuticals, Inc. Lexington, MA 02421 (US) Remarks: • International Health Management Associates, This application was filed on 28-09-2010 as a Inc. divisional application to the application mentioned Schaumburg, IL 60173 (US) under INID code 62. • The University of Utah Research Foundation Salt Lake City, UT 84108 (US) (54) Compositions and methods to improve the oral absorption of antimicrobial agents (57) The present invention provides compositions sive, an antimicrobial agent, and a cationic binding agent and methods for increasing absorption of antibacterial contained within the biopolymer such that the binding agents, particularly third generation cephalosporin anti- agent is ionically bound or complexed to at least one bacterial agents, in oral dosage solid and/or suspension member selected from the group consisting of the biopol- forms. -
Obesity Drugs: Too Much Harm, for Far Too Long
Obesity drugs: too much harm, for far too long In 2016, a British team studied the causes for the market withdrawals of weight-loss drugs. They identified 25 drugs that had been withdrawn from markets around the world between 1964 and 2009. The mechanism of 22 of these drugs involved monoamine neurotransmitters (dopamine, noradrenaline or serotonin); examples include benfluorex, fenfluramine, phentermine (combined with topiramate in the United States) and sibutramine. One drug, rimonabant, was a cannabinoid EDITORIAL derivative, and the two others acted on the thyroid (1). 80% of the market withdrawals were based on data from spontaneous reports, involving cardiac disorders for 8 drugs, psychiatric disorders for 7 drugs, and abuse or dependence for 13 drugs. Drug-attributed deaths had occurred with 7 of the drugs. The median time between market introduction and the first report of a serious adverse effect was 10 years; and the median time between the first report of a serious adverse effect and the first market withdrawal anywhere in the world was 11 years. Fenfluramine was marketed for 24 years before its worldwide withdrawal in 1997 for heart valve disease. Benfluorex was marketed in France for 33 years before its withdrawal in 2009 for cardiotoxicity; yet the heart valve disorders resembled those caused by fenfluramine and the chemical structures of these two drugs are very similar (2). In France, phentermine was marketed from 1962 to 1988. Sibutramine was withdrawn in Europe in 2010, about 9 years after authorisation; and rimonabant was withdrawn in Europe in 2009, about 2 years after authorisation (1,3,4). -
As a Registered E-Materials Service User of the EBMT Annual Meeting in Marseille March 26-29Th 2017, You Have Been Granted Permi
Copyright Statement As a registered E-materials Service user of the EBMT Annual Meeting in Marseille March 26-29th 2017, you have been granted permission to access a copy of the presentation in the following pages for the purpose of scientific education. This presentation is copyrighted material and must not be copied, reproduced, transferred, distributed, leased, licensed, placed in a storage retrieval system, publicly performed or used in any way, except as specifically permitted in writing by the presenter or, as allowed under the terms and conditions under which it was received or as permitted by applicable copyright law or rules of proper citation. Any unauthorised distribution or use of this presentation, a subset of it or graphics taken from the presentation may be a direct infringement of the presenter’s rights. RACE DM training session: Immunusuppressive treatment for aplastic anemia Antonio M. Risitano, M.D., Ph.D. Head of Bone Marrow Transplantation Unit Federico II University of Naples Aplastic anemia Neutrophils for Incidence, age for SCT . Opha disease. Iidee ates peset geogaphi aiatios. to ‐fold highe ates i Asia tha Euope ad the Uited States . Gloal iidee ates age .‐. ases pe illio ihaitats. Aplasti aeia: AA • AA: hat does it ea? • Ho e do the diagosis? • Whe should e teat? • Ho e teat? Aplasti aeia: AA • AA: hat does it ea? • Ho e do the diagosis? • Whe should e teat? • Ho e teat? Aplastic anemia Normal Aplastic anemia CML AA Normal Marrow aplasia Takaku et al, Blood 2010 Takaku et al, Blood 2010 Contraction of stem cell pool Cytopenia AA: hat does it ea? (Oligo) clonal CD8+ T cells Auto-immunity = immune disorder = idiopathic AA AA: hat does it ea? Constitutionnal = inherited disorder (FA, dyskeratosis congenita) Hematopoietic stem cells in AA Hematopoietic progenitor cultures T-cell clonality in aplastic anemia A surrogate marker for Ag-driven immune response Experimental Hematology 23 (1995): 433 Establishment of a CD4+ T cell clone recognizing autologous hematopoietic progenitor cells from a patient with immune-mediated aplastic anemia.