Treatments for Atopic Eczema
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Thymic Peptides and Preparations: an Update
¡ Archivum Immunologiae et Therapiae Experimentalis, 1999, 47¢ , 77–82 £ PL ISSN 0004-069X Review Thymic Peptides and Preparations: an Update ¤ O. J. Cordero et al.: Thymic Peptides ¦ ¨ § OSCAR J. CORDERO, A¥ LICIA PIÑEIRO and MONTSERRAT NOGUEIRA Department of Biochemistry and Molecular Biology, University of Santiago de Compostela, 15706 Santiago de Compostela, Spain Abstract. The possibilities of thymic peptides in human therapy are still being described. Here, we focus on their © general characteristics and on recent advances in this area. Key words: thymus; thymic peptides; preclinical investigation; therapeutic use; clinical trials. Thymic peptides, as well as a variety of other purified from porcine and human serum and from calf modulators (IL-1, IL-3, IL-6, GM-CSF) and cell-cell thymus, and named “facteur thymique serique”11. interactions, regulate the process known as thymic se- According to the classical criteria, TH is the unique lection by which pro-thymocytes become mature and peptide that can be recognized as a hormone. Its secre- functional T cells. tion by a subpopulation of thymic epithelial cells (TEC) Several polypeptides have been extracted, mainly is controlled by a pleiotropic mechanism involving its from young calves, and some of them have been suc- own levels and those of prolactine (PRL), growth hor- cessfully isolated and prepared synthetically (Fig. 1). mone (GH) through insulin growth factor 1 (IGF-1) se- The precise role of much of these factors purported to cretion, adrenocorticotropin (ACTH), thyroxin (T4), β- have intrathymic effects is still unknown, although endorphin and β-leukencephalin and IL-1α and β8. many of these compounds exhibit immunobiological Furthermore, reciprocal regulatory actions on the activity. -
(12) Patent Application Publication (10) Pub. No.: US 2008/0317805 A1 Mckay Et Al
US 20080317805A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2008/0317805 A1 McKay et al. (43) Pub. Date: Dec. 25, 2008 (54) LOCALLY ADMINISTRATED LOW DOSES Publication Classification OF CORTICOSTEROIDS (51) Int. Cl. A6II 3/566 (2006.01) (76) Inventors: William F. McKay, Memphis, TN A6II 3/56 (2006.01) (US); John Myers Zanella, A6IR 9/00 (2006.01) Cordova, TN (US); Christopher M. A6IP 25/04 (2006.01) Hobot, Tonka Bay, MN (US) (52) U.S. Cl. .......... 424/422:514/169; 514/179; 514/180 (57) ABSTRACT Correspondence Address: This invention provides for using a locally delivered low dose Medtronic Spinal and Biologics of a corticosteroid to treat pain caused by any inflammatory Attn: Noreen Johnson - IP Legal Department disease including sciatica, herniated disc, Stenosis, mylopa 2600 Sofamor Danek Drive thy, low back pain, facet pain, osteoarthritis, rheumatoid Memphis, TN38132 (US) arthritis, osteolysis, tendonitis, carpal tunnel syndrome, or tarsal tunnel syndrome. More specifically, a locally delivered low dose of a corticosteroid can be released into the epidural (21) Appl. No.: 11/765,040 space, perineural space, or the foramenal space at or near the site of a patient's pain by a drug pump or a biodegradable drug (22) Filed: Jun. 19, 2007 depot. E Day 7 8 Day 14 El Day 21 3OO 2OO OO OO Control Dexamethasone DexamethasOne Dexamethasone Fuocinolone Fluocinolone Fuocinolone 2.0 ng/hr 1Ong/hr 50 ng/hr 0.0032ng/hr 0.016 ng/hr 0.08 ng/hr Patent Application Publication Dec. 25, 2008 Sheet 1 of 2 US 2008/0317805 A1 900 ----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------- 80.0 - 7OO – 6OO - 5OO - E Day 7 EDay 14 40.0 - : El Day 21 2OO - OO = OO – Dexamethasone Dexamethasone Dexamethasone Fuocinolone Fluocinolone Fuocinolone 2.0 ng/hr 1Ong/hr 50 ng/hr O.OO32ng/hr O.016 ng/hr 0.08 nghr Patent Application Publication Dec. -
Nitrate Prodrugs Able to Release Nitric Oxide in a Controlled and Selective
Europäisches Patentamt *EP001336602A1* (19) European Patent Office Office européen des brevets (11) EP 1 336 602 A1 (12) EUROPEAN PATENT APPLICATION (43) Date of publication: (51) Int Cl.7: C07C 205/00, A61K 31/00 20.08.2003 Bulletin 2003/34 (21) Application number: 02425075.5 (22) Date of filing: 13.02.2002 (84) Designated Contracting States: (71) Applicant: Scaramuzzino, Giovanni AT BE CH CY DE DK ES FI FR GB GR IE IT LI LU 20052 Monza (Milano) (IT) MC NL PT SE TR Designated Extension States: (72) Inventor: Scaramuzzino, Giovanni AL LT LV MK RO SI 20052 Monza (Milano) (IT) (54) Nitrate prodrugs able to release nitric oxide in a controlled and selective way and their use for prevention and treatment of inflammatory, ischemic and proliferative diseases (57) New pharmaceutical compounds of general effects and for this reason they are useful for the prep- formula (I): F-(X)q where q is an integer from 1 to 5, pref- aration of medicines for prevention and treatment of in- erably 1; -F is chosen among drugs described in the text, flammatory, ischemic, degenerative and proliferative -X is chosen among 4 groups -M, -T, -V and -Y as de- diseases of musculoskeletal, tegumental, respiratory, scribed in the text. gastrointestinal, genito-urinary and central nervous sys- The compounds of general formula (I) are nitrate tems. prodrugs which can release nitric oxide in vivo in a con- trolled and selective way and without hypotensive side EP 1 336 602 A1 Printed by Jouve, 75001 PARIS (FR) EP 1 336 602 A1 Description [0001] The present invention relates to new nitrate prodrugs which can release nitric oxide in vivo in a controlled and selective way and without the side effects typical of nitrate vasodilators drugs. -
(CD-P-PH/PHO) Report Classification/Justifica
COMMITTEE OF EXPERTS ON THE CLASSIFICATION OF MEDICINES AS REGARDS THEIR SUPPLY (CD-P-PH/PHO) Report classification/justification of medicines belonging to the ATC group D07A (Corticosteroids, Plain) Table of Contents Page INTRODUCTION 4 DISCLAIMER 6 GLOSSARY OF TERMS USED IN THIS DOCUMENT 7 ACTIVE SUBSTANCES Methylprednisolone (ATC: D07AA01) 8 Hydrocortisone (ATC: D07AA02) 9 Prednisolone (ATC: D07AA03) 11 Clobetasone (ATC: D07AB01) 13 Hydrocortisone butyrate (ATC: D07AB02) 16 Flumetasone (ATC: D07AB03) 18 Fluocortin (ATC: D07AB04) 21 Fluperolone (ATC: D07AB05) 22 Fluorometholone (ATC: D07AB06) 23 Fluprednidene (ATC: D07AB07) 24 Desonide (ATC: D07AB08) 25 Triamcinolone (ATC: D07AB09) 27 Alclometasone (ATC: D07AB10) 29 Hydrocortisone buteprate (ATC: D07AB11) 31 Dexamethasone (ATC: D07AB19) 32 Clocortolone (ATC: D07AB21) 34 Combinations of Corticosteroids (ATC: D07AB30) 35 Betamethasone (ATC: D07AC01) 36 Fluclorolone (ATC: D07AC02) 39 Desoximetasone (ATC: D07AC03) 40 Fluocinolone Acetonide (ATC: D07AC04) 43 Fluocortolone (ATC: D07AC05) 46 2 Diflucortolone (ATC: D07AC06) 47 Fludroxycortide (ATC: D07AC07) 50 Fluocinonide (ATC: D07AC08) 51 Budesonide (ATC: D07AC09) 54 Diflorasone (ATC: D07AC10) 55 Amcinonide (ATC: D07AC11) 56 Halometasone (ATC: D07AC12) 57 Mometasone (ATC: D07AC13) 58 Methylprednisolone Aceponate (ATC: D07AC14) 62 Beclometasone (ATC: D07AC15) 65 Hydrocortisone Aceponate (ATC: D07AC16) 68 Fluticasone (ATC: D07AC17) 69 Prednicarbate (ATC: D07AC18) 73 Difluprednate (ATC: D07AC19) 76 Ulobetasol (ATC: D07AC21) 77 Clobetasol (ATC: D07AD01) 78 Halcinonide (ATC: D07AD02) 81 LIST OF AUTHORS 82 3 INTRODUCTION The availability of medicines with or without a medical prescription has implications on patient safety, accessibility of medicines to patients and responsible management of healthcare expenditure. The decision on prescription status and related supply conditions is a core competency of national health authorities. -
Classification of Medicinal Drugs and Driving: Co-Ordination and Synthesis Report
Project No. TREN-05-FP6TR-S07.61320-518404-DRUID DRUID Driving under the Influence of Drugs, Alcohol and Medicines Integrated Project 1.6. Sustainable Development, Global Change and Ecosystem 1.6.2: Sustainable Surface Transport 6th Framework Programme Deliverable 4.4.1 Classification of medicinal drugs and driving: Co-ordination and synthesis report. Due date of deliverable: 21.07.2011 Actual submission date: 21.07.2011 Revision date: 21.07.2011 Start date of project: 15.10.2006 Duration: 48 months Organisation name of lead contractor for this deliverable: UVA Revision 0.0 Project co-funded by the European Commission within the Sixth Framework Programme (2002-2006) Dissemination Level PU Public PP Restricted to other programme participants (including the Commission x Services) RE Restricted to a group specified by the consortium (including the Commission Services) CO Confidential, only for members of the consortium (including the Commission Services) DRUID 6th Framework Programme Deliverable D.4.4.1 Classification of medicinal drugs and driving: Co-ordination and synthesis report. Page 1 of 243 Classification of medicinal drugs and driving: Co-ordination and synthesis report. Authors Trinidad Gómez-Talegón, Inmaculada Fierro, M. Carmen Del Río, F. Javier Álvarez (UVa, University of Valladolid, Spain) Partners - Silvia Ravera, Susana Monteiro, Han de Gier (RUGPha, University of Groningen, the Netherlands) - Gertrude Van der Linden, Sara-Ann Legrand, Kristof Pil, Alain Verstraete (UGent, Ghent University, Belgium) - Michel Mallaret, Charles Mercier-Guyon, Isabelle Mercier-Guyon (UGren, University of Grenoble, Centre Regional de Pharmacovigilance, France) - Katerina Touliou (CERT-HIT, Centre for Research and Technology Hellas, Greece) - Michael Hei βing (BASt, Bundesanstalt für Straßenwesen, Germany). -
PRODUCT MONOGRAPH MYLAN-CLOBETASOL SCALP APPLICATION (Clobetasol 17-Propionate 0.05% W/W in Aqueous-Alcohol Base) (60 Ml Bottles
PRODUCT MONOGRAPH MYLAN-CLOBETASOL SCALP APPLICATION (Clobetasol 17-propionate 0.05% w/w in aqueous-alcohol base) (60 ml bottles) Topical Corticosteroid Mylan Pharmaceuticals ULC DATE OF PREPARATION: 85 Advance Road Etobicoke, June 5, 2009 Ontario M8Z 2S6 DATE OF REVISION: Control#: 129665 NAME OF DRUG MYLAN-CLOBETASOL SCALP APPLICATION (Clobetasol 17-propionate 0.05 %w/w) (60 mL bottles) THERAPEUTIC CLASSIFICATION Topical Corticosteroid ACTIONS AND CLINICAL PHARMACOLOGY MYLAN-CLOBETASOL SCALP APPLICATION (Clobetasol 17-propionate) is a very potent topical corticosteroid with anti-inflammatory, antipruritic, and vasoconstrictive actions. Pharmacokinetics In man, the extent of percutaneous absorption of topical corticosteroids, including clobetasol 17-propionate, is determined by many factors, including the vehicle, the integrity of the epidermal barrier, and the use of occlusive dressing. As with all topical corticosteroids, clobetasol 17-propionate can be absorbed from normal intact skin. Inflammation and/or other disease processes in the skin may increase percutaneous absorption. Occlusive dressings substantially increase the percutaneous absorption of topical corticosteroids. 2 Once absorbed through the skin, topical corticosteroids enter pharmacokinetic pathways similar to systemically administered corticosteroids. Corticosteroids are bound to plasma proteins in varying degrees. Corticosteroids are metabolized primarily in the liver and are then excreted by the kidneys. Some of the topical corticosteroids, including clobetasol 17-propionate and its metabolites, are also excreted in the bile. Bioavailability The relative potency of corticosteroids is usually assayed by the vasoconstriction test which reflects the potency of the steroid molecule, its topical activity as well as its bioavailaility from the particular formulation. The vascoconstrictor response of MYLAN-CLOBETASOL SCALP APPLICATION was compared with Dermovate Scalp Application as well as a placebo in a randomised and double blind study involving twelve healthy subjects. -
United States Patent (10) Patent No.: US 7,524,836 B2 Del Soldato (45) Date of Patent: Apr
USOO7524836B2 (12) United States Patent (10) Patent No.: US 7,524,836 B2 Del Soldato (45) Date of Patent: Apr. 28, 2009 (54) NITROOXYDERIVATIVESTEROIDAL JP 58-045724 3, 1983 COMPOUNDS JP 5-39.261 2, 1992 JP 4-273892 9, 1992 (75) Inventor: Piero Del Soldato, Milan (IT) WO 98.15568 4f1998 OTHER PUBLICATIONS (73) Assignee: Nicox S.A., Paris (FR) English language abstract of JP 58-045724. (*) Notice: Subject to any disclaimer, the term of this English language abstract of JP4-273892. patent is extended or adjusted under 35 English language abstract of DE 19634793. U.S.C. 154(b) by 173 days. K. B. Schwarz, “Oxidative Sress During Viral Infection: A Review”. Free Radical Biology & Medicine, vol. 21, No. 5, 1996, pp. 641-649. Goodman & Gillman, “The Pharmacological Basis of Therapeutics'. (21) Appl. No.: 11/643,887 9" Edition, 1996, McGraw-Hill Health preffsions Division, pp. 1-1. 1459–1465 and 1474. (22) Filed: Dec. 22, 2006 Martindale, The Extraphamacopeia,30" Edition, 1993, pp. 712-723. O O Nenseter et al., “Paracetamol inhibits Copper Ion-Induced, AZO Com (65) Prior Publication Data pound-Initialed, and Mononuclear Cell-Mediated Oxidative Modifi US 2007/O142342 A1 June 21, 2007 cation of LDL', Arterioscierosis, Thombosis, and Vascular Biology, s vol. 15, No. 9, Sep. 1995, pp. 1338-1344. O O Baylis et al. “Chronic Blockade of Nitric Oxide Synthesis in the Rat Related U.S. Application Data Produces Syntemic Hypertension and Glomemerular Damage'. J. (62) Division of application No. 1 1/028, 198, filed on Jan. 4, Clin. Investigation, vol.90, 1992, pp. -
Thymopentin and Splenopentin As Immunomodulators Current Stutus
Immunologic Research 1998;17/3:345-368 Thymopentin and Splenopentin as Immunomodulators Current Stutus 1Department of Immunology, Sanjay Gandhi Post-Graduate Institute of Medical Sciences, Lucknow, India. 2Division of Biopolymers, Central Drug Research Institute, Lucknow, India. 3Department of Microbiology, RML Awadh University, Faizabad, India. Abstract Key Words Splenopentin (SP-5, Arg-Lys-Glu-Val-Tyr) and thymopentin (TP-5, Immunomodulation Arg-Lys-Asp-Val-Tyr) are synthetic immunomodulating peptides Splenin corresponding to the region 32-34 of a splenic product called splenin Splenopentin (SP) and the thymic hormone thymopoietin (TP), respectively. TP Thymopoietin was originally isolated as a 5-kDa (49-amino acids) protein from Thymopentin bovine thymus while studying effects of the thymic extracts on neuro- muscular transmission and was subsequently observed to affect T cell differentiation and function. TP I and II are two closely related polypeptides isolated from bovine thymus. A radioimmunoassay for TP revealed a crossreaction with a product found in spleen and lymph node. This product, named splenin, differs from TP only in position 34, aspartic acid for bovine TP and glutamic acid for bovine splenin and it was called TP III as well. Synthetic pentapeptides (TP-5) and (SP-5), reproduce the biological activities of TP and SP, respectively. It is now evident that various forms of TPs were created by proteolytic cleavage of larger proteins during isolation, cDNA clones have been isolated for three alternatively spliced mRNAs that encodes three distinct human T cell TPs. The immunomodulatory properties of TP, SP, TP-5, SP-5 and some of their synthetic analogs reported in the literature have been briefly reviewed. -
)&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 -
A New Robust Technique for Testing of Glucocorticosteroids in Dogs and Horses Terry E
Iowa State University Capstones, Theses and Retrospective Theses and Dissertations Dissertations 2007 A new robust technique for testing of glucocorticosteroids in dogs and horses Terry E. Webster Iowa State University Follow this and additional works at: https://lib.dr.iastate.edu/rtd Part of the Veterinary Toxicology and Pharmacology Commons Recommended Citation Webster, Terry E., "A new robust technique for testing of glucocorticosteroids in dogs and horses" (2007). Retrospective Theses and Dissertations. 15029. https://lib.dr.iastate.edu/rtd/15029 This Thesis is brought to you for free and open access by the Iowa State University Capstones, Theses and Dissertations at Iowa State University Digital Repository. It has been accepted for inclusion in Retrospective Theses and Dissertations by an authorized administrator of Iowa State University Digital Repository. For more information, please contact [email protected]. A new robust technique for testing of glucocorticosteroids in dogs and horses by Terry E. Webster A thesis submitted to the graduate faculty in partial fulfillment of the requirements for the degree of MASTER OF SCIENCE Major: Toxicology Program o f Study Committee: Walter G. Hyde, Major Professor Steve Ensley Thomas Isenhart Iowa State University Ames, Iowa 2007 Copyright © Terry Edward Webster, 2007. All rights reserved UMI Number: 1446027 Copyright 2007 by Webster, Terry E. All rights reserved. UMI Microform 1446027 Copyright 2007 by ProQuest Information and Learning Company. All rights reserved. This microform edition is protected against unauthorized copying under Title 17, United States Code. ProQuest Information and Learning Company 300 North Zeeb Road P.O. Box 1346 Ann Arbor, MI 48106-1346 ii DEDICATION I want to dedicate this project to my wife, Jackie, and my children, Shauna, Luke and Jake for their patience and understanding without which this project would not have been possible. -
Canine Vascular Tissues Are Targets for Androgens, Estrogens, Progestins, and Glucocorticoids
Canine vascular tissues are targets for androgens, estrogens, progestins, and glucocorticoids. K B Horwitz, L D Horwitz J Clin Invest. 1982;69(4):750-758. https://doi.org/10.1172/JCI110513. Research Article Sex differences and steroid hormones are known to influence the vascular system as shown by the different incidence of atherosclerosis in men and premenopausal women, or by the increased risk of cardiovascular diseases in women taking birth control pills or men taking estrogens. However, the mechanisms for these effects in vascular tissues are not known. Since steroid actions in target tissues are mediated by receptors, we have looked for cytoplasmic steroid receptor proteins in vascular tissues of dogs. We find specific saturable receptors, sedimenting at 8S on sucrose density gradients for estrogens (measured with [3H]estradiol +/- unlabeled diethylstilbestrol), androgens (measured with [3H]R1881 +/- unlabeled R1881 and triamcinolone acetonide), and glucocorticoids (measured with [3H]dexamethasone +/- unlabeled dexamethasone); they are absent for progesterone (measured with [3H]R5020 +/- unlabeled R5020 and dihydrotestosterone). Progesterone receptors can, however, be induced by 1-wk treatment of dogs with physiological estradiol concentrations (100 pg/ml serum estrogen), indicating a functional estrogen receptor. Receptor levels range from 20 to 2,000 fmol/mg DNA. They are specific for each hormone; unrelated steroids fail to complete for binding. Low dissociation constants, measured by Scatchard analyses, show that binding is of high affinity. Steroid binding sites are in the media and/or adventitia since they persist when the intima is removed. Compared with the arteries, receptor levels are reduced 80% in inferior venae cavae of […] Find the latest version: https://jci.me/110513/pdf Canine Vascular Tissues Are Targets for Androgens, Estrogens, Progestins, and Glucocorticoids KATHRYN B. -
Dexamethasone Inhibits the Induction of NAD+-Dependent 15
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Biochimica et Biophysica Acta 1497 (2000) 61^68 www.elsevier.com/locate/bba Dexamethasone inhibits the induction of NAD-dependent 15-hydroxyprostaglandin dehydrogenase by phorbol ester in human promonocytic U937 cells Min Tong 1, Hsin-Hsiung Tai * Division of Pharmaceutical Sciences, College of Pharmacy, University of Kentucky, Lexington, KY 40536-0082, USA Received 29 December 1999; received in revised form 2 March 2000; accepted 9 March 2000 Abstract Pro-inflammatory prostaglandins are known to be first catabolized by NAD-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH) to inactive metabolites. This enzyme is under regulatory control by various inflammation-related agents. Regulation of this enzyme was investigated in human promonocytic U937 cells. 15-PGDH activity was found to be optimally induced by phorbol 12-myristate 13-acetate (PMA) at 10 nM after 24 h of treatment. The induction was blocked by staurosporine or GF 109203X indicating that the induction was mediated by protein kinase C. The induction by PMA was inhibited by the concurrent addition of dexamethasone. Nearly complete inhibition was observed at 50 nM. Other glucocorticoids, such as hydrocortisone and corticosterone, but not sex hormones, were also inhibitory. Inhibition by dexamethasone could be reversed by the concurrent addition of antagonist mifepristone (RU-486) indicating that the inhibition was a receptor-mediated event. Either induction by PMA or inhibition by dexamethasone the 15-PGDH activity correlated well with the enzyme protein expression as shown by the Western blot analysis. These results provide the first evidence that prostaglandin catabolism is regulated by glucocorticoids at the therapeutic level.