Marine Antithrombotics
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Surfen, a Small Molecule Antagonist of Heparan Sulfate
Surfen, a small molecule antagonist of heparan sulfate Manuela Schuksz*†, Mark M. Fuster‡, Jillian R. Brown§, Brett E. Crawford§, David P. Ditto¶, Roger Lawrence*, Charles A. Glass§, Lianchun Wang*, Yitzhak Torʈ, and Jeffrey D. Esko*,** *Department of Cellular and Molecular Medicine, Glycobiology Research and Training Center, †Biomedical Sciences Graduate Program, ‡Department of Medicine, Division of Pulmonary and Critical Care Medicine and Veteran’s Administration San Diego Medical Center, ¶Moores Cancer Center, and ʈDepartment of Chemistry and Biochemistry, University of California at San Diego, La Jolla, CA 92093; and §Zacharon Pharmaceuticals, Inc, 505 Coast Blvd, South, La Jolla, CA 92037 Communicated by Carolyn R. Bertozzi, University of California, Berkeley, CA, June 18, 2008 (received for review May 26, 2007) In a search for small molecule antagonists of heparan sulfate, Surfen (bis-2-methyl-4-amino-quinolyl-6-carbamide) was first we examined the activity of bis-2-methyl-4-amino-quinolyl-6- described in 1938 as an excipient for the production of depot carbamide, also known as surfen. Fluorescence-based titrations insulin (16). Subsequent studies have shown that surfen can indicated that surfen bound to glycosaminoglycans, and the extent block C5a receptor binding (17) and lethal factor (LF) produced of binding increased according to charge density in the order by anthrax (18). It was also reported to have modest heparin- heparin > dermatan sulfate > heparan sulfate > chondroitin neutralizing effects in an oral feeding experiments in rats (19), sulfate. All charged groups in heparin (N-sulfates, O-sulfates, and but to our knowledge, no further studies involving heparin have carboxyl groups) contributed to binding, consistent with the idea been conducted, and its effects on HS are completely unknown. -
Dermatan Sulfate Composition
Europäisches Patentamt *EP000671414B1* (19) European Patent Office Office européen des brevets (11) EP 0 671 414 B1 (12) EUROPEAN PATENT SPECIFICATION (45) Date of publication and mention (51) Int Cl.7: C08B 37/00, A61K 31/715 of the grant of the patent: 02.01.2002 Bulletin 2002/01 (86) International application number: PCT/JP94/01643 (21) Application number: 94927827.9 (87) International publication number: (22) Date of filing: 30.09.1994 WO 95/09188 (06.04.1995 Gazette 1995/15) (54) DERMATAN SULFATE COMPOSITION AS ANTITHROMBOTIC DERMATANSULFATEZUSAMMENSETZUNG ALS ANTITHROMOTISCHES MITTEL COMPOSITION DE DERMATANE SULFATE UTILISE COMME ANTITHROMBOTIQUE (84) Designated Contracting States: • YOSHIDA, Keiichi AT BE CH DE DK ES FR GB IT LI NL PT SE Tokyo 189 (JP) (30) Priority: 30.09.1993 JP 26975893 (74) Representative: Davies, Jonathan Mark Reddie & Grose 16 Theobalds Road (43) Date of publication of application: London WC1X 8PL (GB) 13.09.1995 Bulletin 1995/37 (56) References cited: (60) Divisional application: EP-A- 0 112 122 EP-A- 0 199 033 01201321.5 / 1 125 977 EP-A- 0 238 994 WO-A-93/05074 JP-A- 59 138 202 JP-B- 2 100 241 (73) Proprietor: SEIKAGAKU KOGYO KABUSHIKI JP-B- 6 009 042 KAISHA Tokyo 103 (JP) • CARBOHYDRATE RESEARCH , vol. 131, no. 2, 1984 NL, pages 301-314, K. NAGASAWA ET AL. (72) Inventors: ’The structure of rooster-comb dermatan • TAKADA, Akikazu sulfate. Characterization and quantitative Shizuoka 431-31 (JP) determination of copolymeric, isomeric tetra- • ONAYA, Junichi and hexa-saccharides’ Higashiyamato-shi Tokyo 207 (JP) • ARAI, Mikio Remarks: Higashiyamato-shi Tokyo 207 (JP) The file contains technical information submitted • MIYAUCHI, Satoshi after the application was filed and not included in this Tokyo 208 (JP) specification • KYOGASHIMA, Mamoru Tokyo 207 (JP) Note: Within nine months from the publication of the mention of the grant of the European patent, any person may give notice to the European Patent Office of opposition to the European patent granted. -
Anticoagulant Effects of Statins and Their Clinical Implications
Review Article 1 Anticoagulant effects of statins and their clinical implications Anetta Undas1; Kathleen E. Brummel-Ziedins2; Kenneth G. Mann2 1Institute of Cardiology, Jagiellonian University School of Medicine, and John Paul II Hospital, Krakow, Poland; 2Department of Biochemistry, University of Vermont, Colchester, Vermont, USA Summary cleavage, factor V and factor XIII activation, as well as enhanced en- There is evidence indicating that statins (3-hydroxy-methylglutaryl dothelial thrombomodulin expression, resulting in increased protein C coenzyme A reductase inhibitors) may produce several cholesterol-inde- activation and factor Va inactivation. Observational studies and one ran- pendent antithrombotic effects. In this review, we provide an update on domized trial have shown reduced VTE risk in subjects receiving statins, the current understanding of the interactions between statins and blood although their findings still generate much controversy and suggest that coagulation and their potential relevance to the prevention of venous the most potent statin rosuvastatin exerts the largest effect. thromboembolism (VTE). Anticoagulant properties of statins reported in experimental and clinical studies involve decreased tissue factor ex- Keywords pression resulting in reduced thrombin generation and attenuation of Blood coagulation, statins, tissue factor, thrombin, venous throm- pro-coagulant reactions catalysed by thrombin, such as fibrinogen boembolism Correspondence to: Received: August 30, 2013 Anetta Undas, MD, PhD Accepted after major revision: October 15, 2013 Institute of Cardiology, Jagiellonian University School of Medicine Prepublished online: November 28, 2013 80 Pradnicka St., 31–202 Krakow, Poland doi:10.1160/TH13-08-0720 Tel.: +48 12 6143004, Fax: +48 12 4233900 Thromb Haemost 2014; 111: ■■■ E-mail: [email protected] Introduction Most of these additional statin-mediated actions reported are independent of blood cholesterol reduction. -
Antiplatelets, Anticoagulants and Bleeding Risk and Ppis
GP INFOSHEET – ANTITHROMBOTICS AND BLEEDING RISK Author(s): Dr. Stuart Rison; Dr. John Robson; Version: 1.6; Last updated 28/11/2019 ANTIPLATELETS, ANTICOAGULANTS AND BLEEDING RISK – WHICH AGENTS AND FOR HOW LONG?; WHY USE PPIs? KEY RECOMMENDATION Patients taking anticoagulants or antiplatelet medicines at high bleed risk should be considered for a Proton Pump Inhibitor (PPI). PPIs reduce bleeding risk by 70% or more. Patients age 65 years or more on anticoagulants or antiplatelet agents are at increased risk because of their age and bleeding risk continues to rise exponentially at older ages. PPIs are recommended in patients on anticoagulants or antiplatelet agents: o At any age with previous GI bleeding o Age 75 years or older o 65 years or older with additional risk factors (see box below) o Interacting medication Dual antiplatelet therapy (DAPT) for cardiac conditions - typically aspirin + clopidogrel - is rarely justified for more than 1 year. Review use for more than one 1 year and in conjunction with the cardiologist consider whether this can revert to a single agent. Dual-pathway therapy for atrial fibrillation - both an anticoagulant and one or more antiplatelet agents- is also rarely justified for longer than 1 year. Consider anticoagulant alone with appropriate specialist advice. ADDITIONAL GI-BLEED RISK FACTORS Anaemia Hb <11g/L Impaired renal function (eGFR<30) Upper GI inflammation (and of course previous GI bleeding) Liver disease Interacting medicines (NSAIDs, SSRI/SNRIs, bisphosphonates, lithium, spironolactone, phenytoin, carbamazepine) WHAT DO WE MEAN BY ANTITHROMBOTICS? Antithrombotics reduce blood clot formation1. There are two main categories: 1. Antiplatelet agent – inhibit platelet aggregation e.g. -
Current Status of Antifibrinolytics in Cardiopulmonary Bypass and Elective Deep Hypothermic Circulatory Arrest Jeffrey A
Anesthesiology Clin N Am 21 (2003) 527–551 Current status of antifibrinolytics in cardiopulmonary bypass and elective deep hypothermic circulatory arrest Jeffrey A. Green, MD*, Bruce D. Spiess, MD Department of Anesthesiology, Virginia Commonwealth University, Medical College of Virginia Campus, 1200 East Broad Street, PO Box 980695, Richmond, VA 23209 USA Bleeding after cardiopulmonary bypass Cardiopulmonary bypass (CPB) alters the hemostatic balance and predisposes cardiac surgery patients to an increased risk of microvascular bleeding. Bleeding and the need for transfusion are among the most common complications of cardiac surgery. In fact, until recently, blood transfusions seemed to be required for about 50% of all cardiac surgery patients [1]. Currently, CPB accounts for 10% to 20% of the transfusions performed in the United States [2,3]. Transfusion, however, exposes patients to added risks such as infectious disease transmission [4], transfusion reactions [5], graft-versus-host disease [6], transfusion-induced lung injury [7], and decreased resistance to postoperative infection [8,9]. Transfusion increases the risk of infection by 35% to 300% and increases the risk of pneumonia in coronary artery bypass (CABG) patients by 5% per unit transfused [10]. The primary purported benefit of transfusion, increased oxygen carrying capacity, has not been definitively proven. Excessive postoperative bleeding may necessitate surgical reexploration, increasing morbidity, and mortality. Postoperatively, the risk of excessive bleeding is 11% [11], and 5% to 7% of patients lose more than 2 L of blood in the first 24 hours after CPB [12]. Reexploration for hemorrhage is required in 3.6% to 4.2% of patients [13], and mortality rates range from 10% to 22% [14]. -
Antithrombotic Therapy for VTE Disease, 10Th Ed, 2016
[ Evidence-Based Medicine ] Antithrombotic Therapy for VTE Disease CHEST Guideline and Expert Panel Report Clive Kearon, MD, PhD; Elie A. Akl, MD, MPH, PhD; Joseph Ornelas, PhD; Allen Blaivas, DO, FCCP; David Jimenez, MD, PhD, FCCP; Henri Bounameaux, MD; Menno Huisman, MD, PhD; Christopher S. King, MD, FCCP; Timothy A. Morris, MD, FCCP; Namita Sood, MD, FCCP; Scott M. Stevens, MD; Janine R. E. Vintch, MD, FCCP; Philip Wells, MD; Scott C. Woller, MD; and COL Lisa Moores, MD, FCCP BACKGROUND: We update recommendations on 12 topics that were in the 9th edition of these guidelines, and address 3 new topics. METHODS: We generate strong (Grade 1) and weak (Grade 2) recommendations based on high- (Grade A), moderate- (Grade B), and low- (Grade C) quality evidence. RESULTS: For VTE and no cancer, as long-term anticoagulant therapy, we suggest dabigatran (Grade 2B), rivaroxaban (Grade 2B), apixaban (Grade 2B), or edoxaban (Grade 2B) over vitamin K antagonist (VKA) therapy, and suggest VKA therapy over low-molecular-weight heparin (LMWH; Grade 2C). For VTE and cancer, we suggest LMWH over VKA (Grade 2B), dabigatran (Grade 2C), rivaroxaban (Grade 2C), apixaban (Grade 2C), or edoxaban (Grade 2C). We have not changed recommendations for who should stop anticoagulation at 3 months or receive extended therapy. For VTE treated with anticoagulants, we recommend against an inferior vena cava filter (Grade 1B). For DVT, we suggest not using compression stockings routinely to prevent PTS (Grade 2B). For subsegmental pulmonary embolism and no proximal DVT, we suggest clinical surveillance over anticoagulation with a low risk of recurrent VTE (Grade 2C), and anticoagulation over clinical surveillance with a high risk (Grade 2C). -
Search Strategy, Baseline Risk Coronavirus and Prophylaxis For
Supplement 7: Search Strategy, Baseline Risk Coronavirus and prophylaxis for thrombotic events Search narrative, 23 July 2020 Bibliographic databases: EMBASE (1974 to, 22 July 2020) Epistemonikos COVID-19 Evidence (21 July 2020) (includes records from Cochrane Database of Systematic Reviews, Pubmed, EMBASE, CINAHL, PsycINFO, LILACS, Database of reviews of Effects, The Campbell Collaboration online library, JBI Database of Systematic Reviews and Implementation Reports, EPPI-Centre Evidence Library) MEDLINE (1946 to, 23 July 2020) SCOPUS (19 July 2020) WHO Global Research Database (COVID-19) (20 July 2020) Trial/study Databases: Cochrane COVID-19 study register (23 July 2020) (includes records from ClinicalTrials.gov, WHO ICTRN, and PubMed) CYTEL map of ongoing [COVID-19] clinical trials (20 July 2020) (WHO International Clinical Trials Registry Platform, European Clinical Trials Registry, clinicaltrials.gov, Chinese Clinical Trial Registry, German Clinical Trials registry, Japan Primary Registries Network, Iranian Clinical Trial Registry, and Australian New Zealand Clinical Trials Registry) Results were downloaded from sources and deduplicated in EndNote. Results from BioRxiV, ChemRxiV, MedRxiV (preprints indexed in Medline and Epistemonikos), or protocols for clinical trials were removed as they were beyond the scope of the search. COCHRANE COVID-19 (https://covid-19.cochrane.org/) Search 1: anticoagula* or anti-coagula* or coagulation or thromb* or antithromb* or antiplatelet* or heparin or LMWH or aspirin or embol* or phlebothrombos* -
Products for Heparin Analysis
Products for Heparin Analysis 2014 - 2015 Adhoc International Our Company Located in Beijing, Adhoc International is an integrated vendor who produces reagents used in researches and quality control of heparins and chondroitin sulfates. Adhoc International also uses its engineering prowess to develop novel devices for microbial mutation, such as multifunctional plasma mutagenesis systems. Our Focuses Heparinases and chondroitinases Reagents for chromogenic assays Determination of heparin sources Multifunctional plasma mutagenesis systems Chemicals used in personal health products Table of Contents Heparinases 2 Chondroitinases 4 Chromogenic Assays 6 GAG Disaccharides 8 Heparin Analogs 10 Heparin Polysaccharides 11 Benzethonium Chloride 12 1 www.aglyco.com Heparinases from Flavobacterium heparinum Heparinases, or heparin lyases, are widely used in studies of heparin and heparan sulfate as well as in quality control of heparin products. With improved fermentation capabilities and advanced purification techniques, we promise a large supply of natural heparinases. Specificity Heparinase I & II Heparinase II & III D-Glucosamine D-Glucosamine L-Iduronic acid D-Glucuronic acid N-Acetyl-D-glucosamine Heparinases can clave glycosidic bonds of heparin and/or heparan sulfate by a β-elimination mechanism, generating unsaturated products (mostly disaccharides) with a double bond be- tween C4 and C5 of the uronate residue. The resulting unsaturated products can be measured at 232 nm wavelength. Enzyme Substrate Heparinase I Heparin and heparan -
AHFS Pharmacologic-Therapeutic Classification (2012).Pdf
AHFS Pharmacologic-Therapeutic Classification 4:00 Antihistamine Drugs 4:04 First Generation Antihistamines 4:04.04 Ethanolamine Derivatives 4:04.08 Ethylenediamine Derivatives 4:04.12 Phenothiazine Derivatives 4:04.16 Piperazine Derivatives 4:04.20 Propylamine Derivatives 4:04.92 Miscellaneous Derivatives 4:08 Second Generation Antihistamines 4:92 Other Antihistamines* 8:00 Anti-infective Agents 8:08 Anthelmintics 8:12 Antibacterials 8:12.02 Aminoglycosides 8:12.06 Cephalosporins 8:12.06.04 First Generation Cephalosporins 8:12.06.08 Second Generation Cephalosporins 8:12.06.12 Third Generation Cephalosporins 8:12.06.16 Fourth Generation Cephalosporins 8:12.07 Miscellaneous -Lactams 8:12.07.04 Carbacephems 8:12.07.08 Carbapenems 8:12.07.12 Cephamycins 8:12.07.16 Monobactams 8:12.08 Chloramphenicol 8:12.12 Macrolides 8:12.12.04 Erythromycins 8:12.12.12 Ketolides 8:12.12.92 Other Macrolides 8:12.16 Penicillins 8:12.16.04 Natural Penicillins 8:12.16.08 Aminopenicillins 8:12.16.12 Penicillinase-resistant Penicillins 8:12.16.16 Extended-spectrum Penicillins 8:12.18 Quinolones 8:12.20 Sulfonamides 8:12.24 Tetracyclines 8:12.24.12 Glycylcyclines 8:12.28 Antibacterials, Miscellaneous 8:12.28.04 Aminocyclitols 8:12.28.08 Bacitracins 8:12.28.12 Cyclic Lipopeptides 8:12.28.16 Glycopeptides 8:12.28.20 Lincomycins 8:12.28.24 Oxazolidinones 8:12.28.28 Polymyxins 8:12.28.30 Rifamycins 8:12.28.32 Streptogramins 8:12.28.92 Other Miscellaneous Antibacterials* 8:14 Antifungals 8:14.04 Allylamines 8:14.08 Azoles 8:14.16 Echinocandins 8:14.28 Polyenes 8:14.32 -
Dermatan Sulfate Is the Predominant Antithrombotic Glycosaminoglycan in Vessel Walls: Implications for a Possible Physiological Function of Heparin Cofactor II
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Biochimica et Biophysica Acta 1740 (2005) 45–53 http://www.elsevier.com/locate/bba Dermatan sulfate is the predominant antithrombotic glycosaminoglycan in vessel walls: Implications for a possible physiological function of heparin cofactor II Ana M.F. Tovar, Diogo A. de Mattos, Mariana P. Stelling, Branca S.L. Sarcinelli-Luz, Roˆmulo A. Nazareth, Paulo A.S. Moura˜o* Laborato´rio de Tecido Conjuntivo, Hospital Universita´rio Clementino Fraga Filho and Instituto de Bioquı´mica Me´dica, Centro de Cieˆncias da Sau´de, Universidade Federal do Rio de Janeiro, Caixa Postal 68041, Rio de Janeiro, RJ, 21941-590, Brazil Received 10 December 2004; received in revised form 17 February 2005; accepted 23 February 2005 Available online 11 March 2005 Abstract The role of different glycosaminoglycan species from the vessel walls as physiological antithrombotic agents remains controversial. To further investigate this aspect we extracted glycosaminoglycans from human thoracic aorta and saphenous vein. The different species were highly purified and their anticoagulant and antithrombotic activities tested by in vitro and in vivo assays. We observed that dermatan sulfate is the major anticoagulant and antithrombotic among the vessel wall glycosaminoglycans while the bulk of heparan sulfate is a poorly sulfated glycosaminoglycan, devoid of anticoagulant and antithrombotic activities. Minor amounts of particular a heparan sulfate (b5% of the total arterial glycosaminoglycans) with high anticoagulant activity were also observed, as assessed by its retention on an antithrombin-affinity column. Possibly, this anticoagulant heparan sulfate originates from the endothelial cells and may exert a significant physiological role due to its location in the interface between the vessel wall and the blood. -
Antithrombotic Therapy in Hypertension: a Cochrane Systematic Review
Journal of Human Hypertension (2005) 19, 185–196 & 2005 Nature Publishing Group All rights reserved 0950-9240/05 $30.00 www.nature.com/jhh ORIGINAL ARTICLE Antithrombotic therapy in hypertension: a Cochrane Systematic review DC Felmeden and GYH Lip Haemostasis, Thrombosis, and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, UK Although elevated systemic blood pressure (BP) results on one large trial, ASA taken for 5 years reduced in high intravascular pressure, the main complications myocardial infarction (ARR, 0.5%, NNT 200 for 5 years), of hypertension are related to thrombosis rather than increased major haemorrhage (ARI, 0.7%, NNT 154), and haemorrhage. It therefore seemed plausible that use of did not reduce all cause mortality or cardiovascular antithrombotic therapy may be useful in preventing mortality. In two small trials, warfarin alone or in thrombosis-related complications of elevated BP. The combination with ASA did not reduce stroke or coronary objectives were to conduct a systematic review of the events. Glycoprotein IIb/IIIa inhibitors as well as ticlopi- role of antiplatelet therapy and anticoagulation in dine and clopidogrel have not been sufficiently eval- patients with BP, to address the following hypotheses: uated in patients with elevated BP. To conclude for (i) antiplatelet agents reduce total deaths and/or major primary prevention in patients with elevated BP, anti- thrombotic events when compared to placebo or other platelet therapy with ASA cannot be recommended active treatment; and (ii) oral anticoagulants reduce total since the magnitude of benefit, a reduction in myocar- deaths and/or major thromboembolic events when dial infarction, is negated by a harm of similar magni- compared to placebo or other active treatment. -
Use of Antithrombotic Medications in the Presence of Neuraxial Anesthesia
Guideline: Use of Antithrombotic Medications In The Presence of Neuraxial Anesthesia Use of Antithrombotic Medications In The Presence of Neuraxial Anesthesia Purpose of Guidelines: To establish appropriate administration and timing of antithrombotic medications before, during, and after the use of neuraxial anesthesia to minimize the risk of bleeding. Definitions: Neuraxial Anesthesia = Delivery of anesthetic medication requiring placement of catheters or needles into the epidural or spinal space Antithrombotic Medications = Anticoagulant, antiplatelet, and thrombolytic medications Background1-3: Spinal (or epidural) hematomas are a rare but catastrophic complication of neuraxial anesthesia. The risk of hematoma development is increased in the presence of antithrombotic medication. Patients undergoing neuraxial anesthesia must have the risks of bleeding from neuraxial interventions balanced with the underlying and ongoing risk of thromboembolism necessitating anticoagulation. Recommendations for the management of specific antithrombotics in patients undergoing neuraxial anesthesia are provided in the following Tables: o Table 1. Management of Intravenous and Subcutaneous Anticoagulation Therapy in Patients Undergoing Neuraxial Anesthesia o Table 2. Management of ORAL Anticoagulation Therapy in Patients Undergoing Neuraxial Anesthesia o Table 3. Management of ORAL and Intravenous Antiplatelet and Thrombolytic Therapy in Patients Undergoing Neuraxial Anesthesia Workflow if a Contradicted Medication is Prescribed: Providers will have