Hydroxychloroquine and Sulphasalazine Alone and in Combination in Rheumatoid Arthritis: a Randomised Double Blind Trial
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Wo 2009/082437 A9
(12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) CORRECTED VERSION (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date 2 July 2009 (02.07.2009) WO 2009/082437 A9 (51) International Patent Classification: KZ, LA, LC, LK, LR, LS, LT, LU, LY, MA, MD, ME, C07D 207/08 (2006.01) A61K 31/402 (2006.01) MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, C07D 207/09 (2006.01) A61P 5/26 (2006.01) NZ, OM, PG, PH, PL, PT, RO, RS, RU, SC, SD, SE, SG, C07D 498/04 (2006.01) SK, SL, SM, ST, SV, SY, TJ, TM, TN, TR, TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW. (21) International Application Number: PCT/US2008/013657 (84) Designated States (unless otherwise indicated, for every kind of regional protection available): ARIPO (BW, GH, (22) International Filing Date: G M M N S D S L s z τ z U G Z M 12 December 2008 (12.12.2008) z w Eurasian (A M B γ KG> M D RU> τ (25) Filing Language: English TM), European (AT, BE, BG, CH, CY, CZ, DE, DK, EE, ES, FI, FR, GB, GR, HR, HU, IE, IS, IT, LT, LU, LV, (26) Publication Language: English M C M T N L N O P L P T R O S E S I s T R OAPI (30) Priority Data: B F ' B J ' C F ' C G ' C I' C M ' G A ' G N ' 0 G W ' M L ' M R ' 61/008,731 2 1 December 2007 (21 .12.2007) US N E ' S N ' T D ' T G ) - (71) Applicant (for all designated States except US): LIG- Declarations under Rule 4.17: AND PHARMACEUTICALS INCORPORATED [US/ — as to applicant's entitlement to apply for and be granted US]; 11085 N. -
Dietary L-Citrulline Supplementation Modulates Nitric Oxide Synthesis and Anti-Oxidant Status of Laying Hens During Summer Seaso
Uyanga et al. Journal of Animal Science and Biotechnology (2020) 11:103 https://doi.org/10.1186/s40104-020-00507-5 RESEARCH Open Access Dietary L-citrulline supplementation modulates nitric oxide synthesis and anti- oxidant status of laying hens during summer season Victoria A. Uyanga, Hongchao Jiao, Jingpeng Zhao, Xiaojuan Wang and Hai Lin* Abstract Background: L-citrulline (L-Cit), a non-protein amino acid, has been implicated in several physiological functions including anti-inflammatory, anti-oxidative, and hypothermic roles, however, there is a paucity of information with regards to its potential in poultry production. Methods: This study was designed to investigate the effects of dietary L-Cit supplementation on the production performance, nitric oxide production, and antioxidant status of laying hens during summer period. Hy-Line Brown laying hens (n = 288, 34 weeks old) were allotted to four treatment, 6 replicates of 12 chickens each. Dietary treatments of control (basal diets), 0.25%, 0.50% and 1.00% L-Cit supplementation were fed to chickens for eight (8) weeks. Production performance, free amino acid profiles, nitric oxide production, and antioxidant properties were measured. Blood samples were collected at the 4th and 8th weeks of the experiment. Results: Air temperature monitoring indicated an average daily minimum and maximum temperatures of 25.02 °C and 31.01 °C respectively. Dietary supplementation with L-Cit did not influence (P > 0.05) the production performance, and rectal temperature of laying hens. Egg shape index was increased (P < 0.05) with increasing levels of L-Cit. Serum-free content of arginine, citrulline, ornithine, tryptophan, histidine, GABA, and cystathionine were elevated, but taurine declined with L-Cit diets. -
D-Penicillamine-Induced Status Dystonicus in a Patient with Wilson’S Disease: a Diagnostic & Therapeutic Challenge
A. Satyasrinivas, et al. D-penicillamine-induced Status Dystonicus | Case Report D-penicillamine-induced Status Dystonicus in A Patient with Wilson’s Disease: A Diagnostic & Therapeutic Challenge A. Satyasrinivas*, Y.S. Kanni, N.Rajesh, M.SaiSravanthi, Vijay kumar Department of General Medicine, Kamineni Institute Of Medical Sciences, Narketpally 508254 Andhra Pradesh, India. DOI Name http://dx.doi.org/10.3126/jaim.v3i2.14066 Keywords Dystonia,Gabapentin Kayser-Fleischer ring, ABSTRACT Trientein hydrochloride, Wilson’s disease. Wilson's disease is an autosomal-recessive disorder of copper metabolism Citation resulting from the absence or dysfunction of a copper-transporting protein. A. Satyasrinivas, Y.S. Kanni, N.Rajesh, The disease is mainly seen in children, adolescents and young adults, and is M.SaiSravanthi, Vijay kumar. D-penicillamine- induced Status Dystonicus in A Patient with characterized by hepatobiliary, neurologic, psychiatric and ophthalmologic Wilson’s Disease: A Diagnostic & Therapeutic (Kayser-Fleischer rings) manifestations. Mechanism of status dystonicus in WD Challenge. Journal of Advances in Internal Medicine is not clear We present here a case study of Wil. son’s disease in 14 year old 2014;03(01):62-64. child with dystonia not responed with routine therapy. INTRODUCTION but patient had developed loose stools, difficulty in speaking and pronouncing linguals. With these compliants he was Wilson’s disease (WD), also known as hepatolenticular admitted in the hospital. On Radio imaging and ophthalmic degeneration was first described in 1912 by Kinnear Wilson as examination he was diagnosed as a case of Wilson’s disease progressive lenticular degeneration. WD is an inherited, fatal and was started with tablet calcium Pantothenate and neurological disorder accompanied by chronic liver disease tablets D-Penicillamine and was discharged. -
(Sodium Aurothiomalate Injection, Mfr. Std.) 10, 25 and 50 Mg/Ml Anti
PRESCRIBING INFORMATION PrMYOCHRYSINE® (sodium aurothiomalate injection, Mfr. Std.) 10, 25 and 50 mg/mL Anti-Rheumatic Agent (disease modifying) sanofi-aventis Canada Inc. Date of Revision: 2150 St. Elzear Blvd. West November 29, 2007 Laval, Quebec H7L 4A8 Submission Control No.: 114637 s-a Version 2.0 dated NAME OF DRUG PrMYOCHRYSINE® Sodium aurothiomalate injection, Mfr. Std. 10, 25 and 50 mg/mL THERAPEUTIC CLASSIFICATION Anti-rheumatic agent (disease modifying) ACTIONS AND CLINICAL PHARMACOLOGY Sodium aurothiomalate exhibits anti-inflammatory, antiarthritic and immunomodulating effects. The predominant clinical effect of MYOCHRYSINE (sodium aurothiomalate) appears to be suppression of the synovitis in the active stage of the rheumatoid disease. The precise mechanism of action is unknown but it has been suggested that the drug may act by inhibiting cell-mediated and humoral immune mechanisms. Additional modes of action include alteration or inhibition of various enzyme systems, suppression of phagocytic activity of macrophage and polymorphonuclear leukocytes, and alteration of collagen biosynthesis. The metabolic fate of sodium aurothiomalate in humans is unknown but it is believed not to be broken down to elemental gold. It is very highly bound to plasma proteins. Sixty to 90% is excreted very slowly by the renal route while 10 to 40% is eliminated in the feces mostly via biliary secretion. The biologic half-life of gold following a single 50 mg dose of parenteral gold has been reported to range from 6 to 25 days. It increases following successive weekly doses. The appearance of clinical effect is slow. It may take at least 8 weeks to become significant and the maximum benefits may not be achieved for at least 6 months. -
Should I Take Methotrexate
I have never taken medication for rheumatoid arthritis before. Should I take methotrexate (Rheumatrex®) alone or with other disease- modifying anti-rheumatic drugs for rheumatoid arthritis? A Cochrane decision aid to discuss options with your doctor This decision aid is for you if: □ You are16 or older. □ Your doctor has told you that you have active rheumatoid arthritis (RA). □ You have never taken methotrexate or any disease-modifying anti-rheumatic drug before such as azathioprine (Imuran®), cyclosporine (Neoral®), gold therapy or sodium aurothiomalate (Myochrysine®), hydroxychloroquine (Plaquenil®), leflunomide (Arava®), penicillamine (Cuprimine®) sulfasalazine (Salazopyrin®, generics), tacrolimus (Prograf®) or others. What is Rheumatoid Arthritis (RA)? When you have rheumatoid arthritis, your immune system, which normally fights infection, attacks the lining of your joints making them inflamed. This inflammation causes your joints to be hot, swollen, stiff, and painful. The small joints of your hands and feet are usually affected first. If the inflammation goes on without treatment, it can lead to damaged joints. Once the joint is damaged it cannot be repaired, so treating rheumatoid arthritis early is important. What is Methotrexate? Methotrexate is a disease-modifying antirheumatic drug (DMARD). It is the most commonly used DMARD in rheumatoid arthritis. It works to control inflammation in your joints. Methotrexate is taken once per week and it comes in pill form or as an injection. Methotrexate only works while you are taking it. It will take 6 to 8 weeks for the methotrexate to work. It is important for you to keep taking the medicine. Your doctor may start you on a low dose and gradually increase your dose. -
D-Penicillamine)
IMPORTANT PRESCRIBING INFORMATION: D-PENAMINE (D-penicillamine) Subject: Temporary importation of D-PENAMINE (D-penicillamine) 125 mg tablets to address shortage November 15, 2018 Dear Health Care Provider: Due to the shortage of penicillamine titratable tablets in the United States (U.S.) market, Mylan is coordinating with the U.S. Food and Drug Administration (FDA) to temporarily import penicillamine 125 mg tablets to address a critical drug shortage of penicillamine 250 mg titratable tablets. Mylan has initiated temporary importation of D-Penamine (D-penicillamine) tablets, 125 mg (not scored) distributed in Australia by Alphapharm Pty Limited, an FDA- inspected Mylan facility in Carole Park, Australia. At this time no other entity except Mylan is authorized by the FDA to import or distribute D- Penamine (D-penicillamine) tablets, 125 mg in the U.S. FDA has not approved Mylan’s D- Penamine (D-penicillamine) tablets, 125 mg in the United States. Please note that during this temporary period and only for this product lot, FDA does not intend to initiate regulatory action for violations of applicable section 582(b) requirements of the Federal Food, Drug, and Cosmetic Act. Effective immediately, and during this temporary period, Mylan will offer the following: Product name and Size Product code NDC code description (Bottle Count) D-PENAMINE (D- penicillamine) – 125mg tablets 100 tablets AUST R 14625 N/A for oral administration The U.S. product labeling should be followed as prescribed by the treating physician except patients should be instructed to take the correct multiple of D-Penamine 125 mg tablets to equal their currently prescribed Depen® dose. -
Designing Peptidomimetics
CORE Metadata, citation and similar papers at core.ac.uk Provided by UPCommons. Portal del coneixement obert de la UPC DESIGNING PEPTIDOMIMETICS Juan J. Perez Dept. of Chemical Engineering ETS d’Enginyeria Industrial Av. Diagonal, 647 08028 Barcelona, Spain 1 Abstract The concept of a peptidomimetic was coined about forty years ago. Since then, an enormous effort and interest has been devoted to mimic the properties of peptides with small molecules or pseudopeptides. The present report aims to review different approaches described in the past to succeed in this goal. Basically, there are two different approaches to design peptidomimetics: a medicinal chemistry approach, where parts of the peptide are successively replaced by non-peptide moieties until getting a non-peptide molecule and a biophysical approach, where a hypothesis of the bioactive form of the peptide is sketched and peptidomimetics are designed based on hanging the appropriate chemical moieties on diverse scaffolds. Although both approaches have been used in the past, the former has been more widely used to design peptidomimetics of secretory peptides, whereas the latter is nowadays getting momentum with the recent interest in designing protein-protein interaction inhibitors. The present report summarizes the relevance of the information gathered from structure-activity studies, together with a short review on the strategies used to design new peptide analogs and surrogates. In a following section there is a short discussion on the characterization of the bioactive conformation of a peptide, to continue describing the process of designing conformationally constrained analogs producing first and second generation peptidomimetics. Finally, there is a section devoted to review the use of organic scaffolds to design peptidomimetics based on the information available on the bioactive conformation of the peptide. -
Report of the Expert Committee for the Selection and Inclusion Of
Report of the Expert Committee / A Report of the Expert Committee for the Selection and Inclusion of Medicines in the Pan American Health Organization Strategic Fund – July 2013 Report of the Expert Committee for the Selection and Inclusion of Medicines in the Pan American Health Organization Strategic Fund – July 2013 PAHO HQ Library Cataloguing-in-Publication Data ***************************************************************************************** Pan American Health Organization. Report of the Expert Committee for the Selection and Inclusion of Medicines in the Pan American Health Organization Strategic Fund – July 2013. Washington, DC : PAHO, 2013. 1. Pharmaceutical Preparations. 2. Chronic Disease. 3. Cardiovascular Diseases. 4. Neoplasms. 5. Immunosuppressive Agents. 6. Complementary Therapies. 7. Americas. I. Title. II. PAHO Strategic Fund. ISBN 978-92-75-11814-6 (NLM Classification: QV55) The Pan American Health Organization welcomes requests for permission to reproduce or translate its publications, in part or in full. Applications and inquiries should be addressed to the Department of Knowledge Management and Communications (KMC), Pan American Health plansOrganization, for new Washington,editions, and D.C.,reprints U.S.A. and ([email protected]). translations already available. The Department of Health Systems and Services (HSS) will be glad to provide the latest information on any changes made to the text, © Pan American Health Organization, 2013. All rights reserved. Publications of the Pan American Health Organization enjoy copyright protection in accordance with the provisions of Protocol 2 of the Universal Copyright Convention. All rights are reserved. The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the Secretariat of the Pan American Health Organization concerning the status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. -
Effects of Penicillamine on Distribution of B6 Vitamers in Rat Urine
J. Nutr. Sci. Vitaminol., 24, 1-7, 1978 EFFECTS OF PENICILLAMINE ON DISTRIBUTION OF B6 VITAMERS IN RAT URINE Toshihide KAJIWARA1 and Makoto MATSUDA2 1 Department of Orthopedic Surgery and 2Department of Biochemistry, Jikei University School of Medicine, Minato-ku, Tokyo 105, Janan (Received June 8, 1977) Summary The antivitamin B6 effect of DL and D-penicillamine has been studied in rats. A considerable elevation in the urinary excretion of vitamin B6 activity (pyridoxal and its thiazolidine derivative) has been shown as a parameter of B6 antagonism. Both DL and D-penicillamine have been shown to have an antivitamin B6 effect in rats, although that induced by the DL-form is considerably greater, as would be expected from previous studies. We suggest that B6 supplementation should be included in any long term penicillamine therapy, regardless of the isomer that is employed. Penicillamine (PeA) is now accepted as the treatment of choice of patients with WILSON'Sdisease because of its copper-chelating properties (1), and for cystinuric patients, in whom urinary cystine stone formation is prevented by the formation of a soluble PeA-cysteinemixed disulfide (2). It is currently under investigation in the treatment of rheumatoid arthritis, where it has been shown to produce various clinical improvements (3, 4). With the first description of its use as a drug with WILSON'sdisease (1), it was pointed out that certain toxic reactions might be expected in view of the works of Du VIGNEAUDet al. (5-7) who had shown that the inclusion of L-isomer of PeA (L-PeA) in the diet of rats caused vitamin B6 deficiency, resulting in inhibition of growth, reduced transaminase activity and abnormal excretion of xanthurenic acid following the administration of tryptophan: the D-isomer (D-PeA) appeared to have no toxic action under the conditions described (5, 8). -
Topical Photodynamic Therapy for Localized Scleroderma
Acta Derm Venereol 2000; 80: 26±27 Topical Photodynamic Therapy for Localized Scleroderma SIGRID KARRER, CHRISTOPH ABELS, MICHAEL LANDTHALER and ROLF-MARKUS SZEIMIES Department of Dermatology, University of Regensburg, Regensburg, Germany Therapy of localized scleroderma is unsatisfactory, with MATERIAL AND METHODS numerous treatments being used that have only limited success Patients or considerable side-effects. The aim of this trial was to determine whether topical photodynamic therapy would be Five patients aged between 21 and 63 years with biopsy-proven effective in patients with localized scleroderma. Five patients localized scleroderma (morphoea) were studied. All patients had evidence of progressive disease, i.e. lesions showed an in¯ammatory with progressive disease, in whom conventional therapies had reaction and increase in size. In each patient the condition had failed, were treated by application of a gel containing 3% previously failed to respond to potent topical corticosteroids, systemic 5-aminolevulinic acid followed by irradiation with an incoherent therapy with penicillin and/or PUVA bath photochemotherapy. lamp (40 mW/cm2, 10 J/cm2). The treatment was performed Patients were required to discontinue all therapy at least 4 weeks once or twice weekly for 3 ± 6 months. In all patients the before study initiation. The most affected sclerotic plaque of each therapy was highly effective for sclerotic plaques, as measured patient was judged at baseline and then every 2 weeks during by a quantitative durometer score and a clinical skin score. The treatment. Sclerotic plaques were assessed by a clinical skin score (10) only side-effect was a transient hyperpigmentation of the and the durometer score (11). -
Gold Levels Produced by Treatment with Auranofin and Sodium Aurothiomalate
Ann Rheum Dis: first published as 10.1136/ard.42.5.566 on 1 October 1983. Downloaded from Annals ofthe Rheumatic Diseases, 1983, 42, 566-570 Gold levels produced by treatment with auranofin and sodium aurothiomalate D. LEWIS,' H. A. CAPELL,1 C. J. McNEIL,2 M. S. IQBAL,2 D. H. BROWN, 2 AND W. E. SMITH2 From the 1CentreforRheumatic Diseases, University DepartmentofMedicine, Baird Street, Glasgow G4 OEH, and the 2Department ofPure and Applied Chemistry, University ofStrathclyde, Glasgow GJ IXL SUMMARY Sixty-three patients with rheumatoid arthritis were randomly divided into 3 groups, and treated with either sodium aurothiomalate (Myocrisin), auranofin, or placebo. Gold levels in whole blood, plasma, and haemolysate were measured serially along with clinical and laboratory para- meters of efficacy. Auranofin produced a higher ratio of haemolysate to plasma gold than Myocrisin, and it appears that the affinity of the red cell for gold is reduced during therapy with auranofin. Gold levels did not correlate with changes in the pain score, erythrocyte sedimentation rate, and C-reactive protein, nor with the development of toxicity. In the Myocrisin group the haemolysate gold level achieved was dependent on the number of cigarettes smoked. In the auranofin group there was no such correlation, but the haemolysate gold level was higher for smokers than non-smokers. The likely action of gold is discussed. copyright. Gold compounds have been used in the treatment of The purpose of the present study was to measure rheumatoid arthritis for over 50 years, and theirplace the distribution ofgold in the blood of patients receiv- in clinical practice is firmly established.' 2 However, ing Myocrisin or auranofin, both in order to deter- there remains a need to monitor the use of these mine whether or not parameters such as haemolysate compounds very carefully to establish efficacy and to gold or the ratio of haemolysate to plasma gold are anticipate the onset of any toxic reaction which may correlated with efficacy or toxicity and to improve http://ard.bmj.com/ occur. -
The Antiproliferative Effect of Sodium Aurothiomalate
Annals of the Rheumatic Diseases, 1986; 45, 389-395 Cultured human cells can acquire resistance to the antiproliferative effect of sodium aurothiomalate A GLENNAS' 2 AND H E RUGSTAD' From the 'Division of Clinical Pharmacology, Institute for Surgical Research, Rikshospitalet, the National Hospital, and the 2Oslo Sanitetsforening Rheumatism Hospital, Oslo, Norway SUMMARY Cultured human epithelial cells (HE), grown as monolayers, acquired resistance to otherwise lethal concentrations (300 [tmol/l, culture medium) of sodium aurothiomalate during five months' exposure to stepwise increased concentrations of the drug. The resistance acquired was shown by exposure to drug concentrations ranging from 25 to 300 [mol/, resulting in 100% of the resistant cells (HeMy(,) surviving compared with controls. Only 13% of the sensitive parent cells survived when exposed to 300 [tmol/l for four days. The IHEMV, cells were also resistant to the antiproliferative effects of equimolar concentrations of thiomalic acid without gold. The cytosolic gold concentration and the association of '99Au with cytosolic proteins after gel filtration were similar in both cell lines after sodium aurothiomalate exposure to the exponentially growing cells. No synthesis of gold binding proteins of metallothionein character was observed in the HEMyo cells. The concentration of free thiomalate in the sonicates and cytosols of the HeMV, cells was decreased to 25-30% of the concentration found in the HE cells. Comparison with previous data for the cytosolic concentration of total thiomalate in the HE cells suggests that most of the cytosolic thiomalate present was free thiomalate. We conclude that the cells can develop resistance to the antiproliferative effect of sodium aurothiomalate, and that the resistance may be due to their capacity to maintain low concentrations of free thiomalate in the sonicates and cytosols.