DOCSLIB.ORG

Induced by Non-Steroidal Anti-Inflammatory Drugs (NSAID)

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Induced by Non-Steroidal Anti-Inflammatory Drugs (NSAID) 936 Letters to the editor 3 Tominaga A, Takaki S, Koyama N, Katoh S, Changes in incidences ofhepatitis (cases per months of treatment) due to NSAID in France Matsumoto R, Migita M, et al. Transgenic mice expressing a B cell growth and differen- Ann Rheum Dis: first published as 10.1136/ard.55.12.936 on 1 December 1996. Downloaded from tiation factor gene (interleukin 5) develop Incidence of NSAID eosinophilia and autoantibody production. J Exp Med 1991;173:429-37. Grouphepatitis 1985 1989 4 Sanderson CJ, Campbell HD, Young IG. 1 > 1/50 000 Oxyphenbutazone Molecular and cellular biology of eosinophil fenbufen, phenylbutazone differentiation factor (interleukin-5) and its 2 1/50 000 to Isoxicam, pirprofen, sulindac Pirprofen, effects on human and mouse B cells. Immunol 1/100 000 Rev 1988;102:29-50. 3 1/100 000 to Fenbufen, ibuprofen, indomethacin, Ketoprofen, sulindac, diclofenac, 5 Barnes L, Rodnan GP, Medsger TA, Short D. 1/300 000 ketoprofen mefenamic acid Eosinophilic fasciitis. A pathologic study of 4 1/300 000 to Diclofenac, piroxicam Ibuprofen, etodolac, piroxicam, tenoxicam twenty cases. AmJ Pathol 1979;96:493-518. 1/500 000 6 Rosenthal J, Benson MD. Diffuse fasciitis and 5 < 1/500 000 Flurbiprofen, sodium naproxen, Indomethacin, sodium naproxen, niflumic eosinophilia with symmetric polyarthritis. Ann niflumic acid, tiaprofenic acid acid, tiaprofenic acid, fenoprofen Intern Med 1980;92:507-9. 7 Matsumoto R, Ando M, Kohrogi H, Araki S, Takatsu K. Interleukin-5 levels of pleural fluid and serum samples in a patient with PIE syn- tigate for a number of reasons: blood test drome. Chest 1992;102:1296-7. [24], acute cholestatic hepatitis (17) [9], or findings are extremely variable and may show 8 Hirashima M, Ueno M, Higuchi S, Matsumoto mixed hepatitis (7) [15]. The remainder were cytolytic, cholestatic, or mixed pattern T, Sakata KM, Matsumoto R, et al. Establish- may or may not ment of a human T-cell line constitutively pro- subclinical biochemical abnormalities (20) effects; the clinical picture ducing several eosinophil chemotactic lym- [8]. suggest an immunoallergic response; the his- phokines and their functional heterogeneity on In 1989 all patients recovered after the tology is rarely pathognomonic; and, finally, eosinophils. Lymphokine Cytokine Res 1992; drug was stopped [in 1985 three patients died]. little is known about the mechanisms that 11:331-8. On the basis of the later study, NSAID initiate it, and little basic research has been 9 Kopf M, Brombacher F, Hodgkin PD, Ramsay AJ, Milbourne EA, Dai WJ, et al. IL-5- were reclassified according to the incidence done on the subject. deficient mice have a developmental defect in of hepatitis expressed as the number of cases PHILIPPE TRECHOT CD5+ B-1 cells and lack eosinophilia but have per months of treatment, and the 1985 and PIERRE GILLET normal antibody and cytotoxic T cell re- 1989 classifications are compared (table). sponses. Immunity 1996;4: 15-24. It is noteworthy that: (a) two drugs in GERARD GAY 10 Meeker TC, Hardy D, Willman C, Hogan T, BERNADETTE HANESSE groups 1 and 2 in 1985 were withdrawn from Abrams J. Activation of the interleulin-3 gene PATRICK NETTER by chromosome translocation in acute lym- the market that year: oxyphenbutazone phocytic leukemia with eosinophilia. Blood because of haematological toxicity and isoxi- Centre de Pharmacovigilance de Nancy 1990;76:285-9. cam because of skin toxicity; (b) pirprofen, ANNE CASTOT which was eventually withdrawn (in 1990) Centre de Pharmacovigilance de Paris because of hepatic toxicity with, according to Fernand-Widal Incidence ofhepatitis the manufacturer,6 a frequency of one case induced by non-steroidal per 69 000 months of treatment, was in DOMNIQUE LARREY group 2 in both of our studies; (c) piroxicam H6pital Saint Eloi Montpellier anti-inflammatory drugs and tenoxicam, which were put on the market 1 Netter P, Castot A, Larrey D, Carlier P, (NSAID) at different times (1981 and 1988 Bannwarth B, Trechot P. Hepatitis induced by respectively), were both in group 4 in 1989. non-steroidal anti-inflammatory drugs. Ann Netter et al 'reported the incidence of hepati- The hepatotoxicity ofNSAID has been the Rheum Dis 1989;48:439. some years.4 From these 2 Castot A, Netter P, Larrey D, Carlier P, Gaire tis due to NSAID after a French drug subject of reports for M, Bannwarth B. Hepatites aux anti- surveillance study in 1985.2 This work, which reports and our pair of studies emerge a inflammatoires non steroidiens. Bilan is regularly cited in reference books and other number of broad ideas about NSAID cooperatif des Centres Regionaux de pharma- induced hepatotoxicity: covigilance pour l'annee 1985. Therapie 1988; publications,34 has been updated with the 43:229-3. http://ard.bmj.com/ results of a second cooperative study carried * side effects are non-negligible, with regard 3 O'Brien WN. Hepatitis due to non-steroidal out in the same way, by the same team, to to either morbidity or mortality anti-inflammatory drugs (NSAIDs). In: Rains- compare and measure any changes in risk * different chemical structures can produce ford KD, Velo GP, eds. Side-effects of anti- inflammatory drugs. Lancaster: Kluwer Aca- after a three year interval. As we have pointed similar hepatotoxic responses demic Publishers, 1992:211-22. out,5 this approach should minimise the bias * older women greatly predominate among 4 Stricker BHCH. Drug-induced hepatic injury. inherent in such studies of drug surveillance. affected patients In: Dukes MNG ed. Drug-induced disorders. * a hepatotoxic response is unpredictable and Amsterdam: Elsevier Science Publishers, In 1989 the drug surveillance centres 1992:93-149. collected 51 cases (30 women and 21 men) sometimes is unaccompanied by symptoms 5 Bresler Castot A, Gay Trechot P, Moore N, N, on September 26, 2021 by guest. Protected copyright. [the comparable figures for 1985 were 56 * when a drug is reintroduced, side effect is G, Netter P, Royer R. Potassium chloride tab- cases-37 women and 19 men] of hepatitis frequently more sudden and severe, thus the lets and small bowel stenoses and perforations: of the same must be two studies in the French pharmacovigilance associated with NSAID in patients without readministration drug system. AmJ Gastroenterol 1994;89:1268. any previous history of hepatic disorder. strictly avoided 6 Anonymous. Arret de la commercialisation de They comprised acute cytolytic hepatitis (7) * these hepatotoxicities are difficult to inves- Rangasil. Rev Prescr 1990;10:243..
Load more

Recommended publications
  • United States Patent (19) 11 Patent Number: 5,955,504 Wechter Et Al
    USOO5955504A United States Patent (19) 11 Patent Number: 5,955,504 Wechter et al. (45) Date of Patent: Sep. 21, 1999 54 COLORECTAL CHEMOPROTECTIVE Marnett, “Aspirin and the Potential Role of Prostaglandins COMPOSITION AND METHOD OF in Colon Cancer, Cancer Research, 1992; 52:5575–89. PREVENTING COLORECTAL CANCER Welberg et al., “Proliferation Rate of Colonic Mucosa in Normal Subjects and Patients with Colonic Neoplasms: A 75 Inventors: William J. Wechter; John D. Refined Immunohistochemical Method.” J. Clin Pathol, McCracken, both of Redlands, Calif. 1990; 43:453-456. Thun et al., “Aspirin Use and Reduced Risk of Fatal Colon 73 Assignee: Loma Linda University Medical Cancer." N Engl J Med 1991; 325:1593-6. Center, Loma Linda, Calif. Peleg, et al., “Aspirin and Nonsteroidal Anti-inflammatory Drug Use and the Risk of Subsequent Colorectal Cancer.” 21 Appl. No.: 08/402,797 Arch Intern Med. 1994, 154:394–399. 22 Filed: Mar 13, 1995 Gridley, et al., “Incidence of Cancer among Patients With Rheumatoid Arthritis J. Natl Cancer Inst 1993 85:307-311. 51) Int. Cl. .......................... A61K 31/19; A61K 31/40; Labayle, et al., “Sulindac Causes Regression Of Rectal A61K 31/42 Polyps. In Familial Adenomatous Polyposis” Gastroenterol 52 U.S. Cl. .......................... 514/568; 514/569; 514/428; ogy 1991 101:635-639. 514/416; 514/375 Rigau, et al., “Effects Of Long-Term Sulindac Therapy On 58 Field of Search ..................................... 514/568, 570, Colonic Polyposis” Annals of Internal Medicine 1991 514/569, 428, 416, 375 11.5:952-954. Giardiello.et al., “Treatment Of Colonic and Rectal 56) References Cited Adenomas With Sulindac In Familial Adenomatous Poly U.S.
    [Show full text]
  • What Are the Acute Treatments for Migraine and How Are They Used?
    2. Acute Treatment CQ II-2-1 What are the acute treatments for migraine and how are they used? Recommendation The mainstay of acute treatment for migraine is pharmacotherapy. The drugs used include (1) acetaminophen, (2) non-steroidal anti-inflammatory drugs (NSAIDs), (3) ergotamines, (4) triptans and (5) antiemetics. Stratified treatment according to the severity of migraine is recommended: use NSAIDs such as aspirin and naproxen for mild to moderate headache, and use triptans for moderate to severe headache, or even mild to moderate headache when NSAIDs were ineffective in the past. It is necessary to give guidance and cautions to patients having acute attacks, and explain the methods of using medications (timing, dose, frequency of use) and medication use during pregnancy and breast-feeding. Grade A Background and Objective The objective of acute treatment is to resolve the migraine attack completely and rapidly and restore the patient’s normal functions. An ideal treatment should have the following characteristics: (1) resolves pain and associated symptoms rapidly; (2) is consistently effective; (3) no recurrence; (4) no need for additional use of medication; (5) no adverse effects; (6) can be administered by the patients themselves; and (7) low cost. Literature was searched to identify acute treatments that satisfy the above conditions. Comments and Evidence The acute treatment drugs for migraine generally include (1) acetaminophens, (2) non-steroidal anti-inflammatory drugs (NSAIDs), (3) ergotamines, (4) triptans, and (5) antiemetics. For severe migraines including status migrainosus and migraine attacks refractory to treatment, (6) anesthetics, and (7) corticosteroids (dexamethasone) are used (Tables 1 and 2).1)-9) There are two approaches to the selection and sequencing of these medications: “step care” and “stratified care”.
    [Show full text]
  • (12) Patent Application Publication (10) Pub. No.: US 2010/0221245 A1 Kunin (43) Pub
    US 2010O221245A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2010/0221245 A1 Kunin (43) Pub. Date: Sep. 2, 2010 (54) TOPICAL SKIN CARE COMPOSITION Publication Classification (51) Int. Cl. (76) Inventor: Audrey Kunin, Mission Hills, KS A 6LX 39/395 (2006.01) (US) A6II 3L/235 (2006.01) A638/16 (2006.01) Correspondence Address: (52) U.S. Cl. ......................... 424/133.1: 514/533: 514/12 HUSCH BLACKWELL SANDERS LLP (57) ABSTRACT 4801 Main Street, Suite 1000 - KANSAS CITY, MO 64112 (US) The present invention is directed to a topical skin care com position. The composition has the unique ability to treat acne without drying out the user's skin. In particular, the compo (21) Appl. No.: 12/395,251 sition includes a base, an antibacterial agent, at least one anti-inflammatory agent, and at least one antioxidant. The (22) Filed: Feb. 27, 2009 antibacterial agent may be benzoyl peroxide. US 2010/0221 245 A1 Sep. 2, 2010 TOPCAL SKIN CARE COMPOSITION stay of acne treatment since the 1950s. Skin irritation is the most common side effect of benzoyl peroxide and other anti BACKGROUND OF THE INVENTION biotic usage. Some treatments can be severe and can leave the 0001. The present invention generally relates to composi user's skin excessively dry. Excessive use of some acne prod tions and methods for producing topical skin care. Acne Vul ucts may cause redness, dryness of the face, and can actually garis, or acne, is a common skin disease that is prevalent in lead to more acne. Therefore, it would be beneficial to provide teenagers and young adults.
    [Show full text]
  • Comparative Study of the Efficacy of Flunixin, Ketoprofen and Phenylbutazone in Delman Horses with Mild Colic
    Sys Rev Pharm 2020; 11(5): 464 468 A multifaceted review journal in the field of pharmacy E-ISSN 0976-2779 P-ISSN 0975-8453 Comparative Study of the Efficacy of Flunixin, Ketoprofen and Phenylbutazone in Delman Horses with Mild Colic Agus Purnomo1, Arya Pradana Wicaksono2, Dodit Hendrawan2, Muhammad Thohawi Elziyad Purnama3* 1Department of Veterinary Surgery and Radiology, Faculty of Veterinary Medicine, Universitas Gadjah Mada, DI Yogyakarta, 55281, Indonesia 2Postgraduate Studies, Faculty of Veterinary Medicine, Universitas Airlangga, Surabaya, 60115, Indonesia 3Department of Veterinary Anatomy, Faculty of Veterinary Medicine, Universitas Airlangga, Surabaya, 60115, Indonesia *Corresponding author E-mail: [email protected] Article History: Submitted: 26.02.2020 Revised: 16.04.2020 Accepted: 21.05.2020 ABSTRACT This study aimed to evaluate the efficacy of flunixin, ketoprofen and multiple range test. The results showed a significant alleviation in all phenylbutazone on serum biochemistry, plasma catecholamines and observed variables on Day 13, although the use of various NSAIDs serum cortisol in Delman horses with mild colic. During the study showed no significant difference. period, 32 horses were evaluated due to mild colic. Flunixin, Keywords: serum biochemical, catecholamine, cortisol, colic, NSAIDs ketoprofen, and phenylbutazone were administered intravenously at Correspondence: the recommended dose rates of 1.0; 2.2 and 4.4 mg/kg, respectively. Muhammad Thohawi Elziyad Purnama Administration of the NSAIDs commenced on Day 1 and continued Department of Veterinary Anatomy, Faculty of Veterinary Medicine, every 12 h for 12 days. Blood samples collected between days 2, 5, 9 Universitas Airlangga, Surabaya, 60115, Indonesia and 13 to evaluate AST, ALP, GGT, creatinine, urea, epinephrine, E-mail: [email protected] norepinephrine, and cortisol level.
    [Show full text]
  • Acute Renal Failure Associated with Diflunisal J. G. WHARTON D. 0
    Postgrad Med J: first published as 10.1136/pgmj.58.676.104 on 1 February 1982. Downloaded from Postgraduate Medical Journal (February 1982) 58, 104-105 Acute renal failure associated with diflunisal J. G. WHARTON D. 0. OLIVER B.Sc., M.R.C.P. F.R.C.P., F.R.A.C.P. M. S. DUNNILL F.R.C.P., F.R.C.Path. Renal Unit, Churchill Hospital, and Department of Pathology, John Radcliffe Hospital, Oxford Summary eosinophils 224 x 106/1; ESR 30 mm/hr; urea 305 The case of a 44-year-old man with acute oliguric mmol/l; creatinine 1651 ,Lmol/l; potassium 6-43 renal failure due to tubulo-interstitial nephritis after mmol/l; serum amylase 88 Somogyi units; urine 3 months' diflunisal is reported. The possible mecha- contained no casts; no red cells but 10 neutrophils, nisms are discussed. no eosinophils and no growth. Antistreptolysin 0 titre 50 i.u./ml; IgG 16-5 g/l; IgA 3-8 g/l; IgM 1.1 g/l antinuclear factor negative; C3 122 mg/dl, C4 54Protected by copyright. Introduction mg/dl; hepatitis B surface antigen negative; chest Diflunisal has been reported as causing acute radiograph, cardiomegaly plus congestion; intra- allergic interstitial nephritis (Chan et al., 1980) venous urogram with tomograms, no obstruction, resulting in acute oliguric renal failure. A case of poor nephrogram. A renal biopsy showed tubulo- acute renal failure due to tubulo-interstitial nephritis interstitial nephritis with no eosinophil infiltrate. after 3 months of diflunisal is reported here. Recently, Diflunisal had been stopped 2 days before admission phenylakalonic acids with analgesic and anti- to this renal unit.
    [Show full text]
  • Non-Steroidal Anti-Inflammatory Drugs (Nsaids)
    NON-STEROIDAL ANTI-INFLAMMATORY DRUGS ANALYSIS IN MILK BY QUECHERS AND LC-MS: LOW AND HIGH RESOLUTION DETECTION AND CONFIRMATION APPROACHES A. Rúbies1, L. Guo2, I. Beguiristain1, F. Centrich1, M. Granados2 1. Laboratori Agència de Salut Pública de Barcelona, 2. Departament de Química Analítica - Universitat de Barcelona. * INTRODUCTION NON-STEROIDAL ANTI-INFLAMATORY DRUGS (NSAIDs) Non-steroidal anti-inflammatory drugs (NSAIDs) are used as anti-inflammatory, analgesic and OXICAMS ANTHRANILIC ACID DERIVATIVES ACETIC ACID antipyretic drugs in medicine and veterinary. Their action mechanism is based on the blocking of PROPIONIC ACID DERIVATIVES DERIVATIVES the biosynthesis of prostaglandins. NSAIDs are highly effective and extensively used, but they have some adverse side effects, such as hepatotoxicity, renal disorders or allergic reactions. In the European Union, to assure food safety and protect consumers, maximum residue limits have been established for some authorised NSAIDs in food products. Therefore, high throughput and reliable analytical methodology is required for the effective control of NSAIDs in food from animal Flufenamic acid origin. Liquid chromatography (LC) coupled to mass spectrometry (MS) is currently the technique of choice in confirmatory analysis of NSAIDs residues. We present a new method for the determination of representative NSAIDs in milk based on QuEChERS methodology, LC-MS/MS and UHPLC-HRMS. Meloxicam Ketoprofen Diclofenac EU Maximum Residue Limits (MRLs) Recommended NSAIDs concentrations for NSAIDs in milk.
    [Show full text]
  • Contrasting Effects of Diclofenac and Ibuprofen on Active Imatinib Uptake Into Leukaemic Cells British Journal of Cancer, 2012; 106(11):1772-1778
    PUBLISHED VERSION Wang, Jueqiong; Hughes, Timothy Peter; Kok, Chung Hoow; Saunders, Verity Ann; Frede, Amity; Groot- Obbink, Kelvin Stuart; Osborn, M.; Somogyi, Andrew Alexander; D'Andrea, Richard James; White, Deborah Lee Contrasting effects of diclofenac and ibuprofen on active imatinib uptake into leukaemic cells British Journal of Cancer, 2012; 106(11):1772-1778 © 2012 Cancer Research UK From twelve months after its original publication, this work is licensed under the Creative Commons Attribution-NonCommercial-Share Alike 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/ The electronic version of this article is the complete one and can be found online at: http://www.nature.com/bjc/journal/v106/n11/full/bjc2012173a.html PERMISSIONS http://www.nature.com/bjc/authors/submit.html#open BJC publishes BJC OPEN articles under a Creative Commons Attribution-Non commercial-Share Alike 3.0 Unported licence. This licence allows users to: share - to copy, distribute and transmit the work remix - to adapt the work Under the following conditions: attribution - users must attribute the work in the manner specified by the author or licensor (but not in any way that suggests an endorsement ) non commercial - users may not use this work for commercial purposes share alike - If users alter, transform, or build upon this work, they may distribute the resulting work only under the same or similar license to this one 20th May 2013 http://hdl.handle.net/2440/72375 British Journal of Cancer
    [Show full text]
  • Non-Steroidal Anti-Inflammatory Drugs (Nsaids)* *See List of Prescription NSAID Nsaids Are Used to Treat Pain, Redness, Swelling, and Heat (Inflammation)
    Medication Guide Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)* *see list of prescription NSAID NSAIDs are used to treat pain, redness, swelling, and heat (inflammation). medicines at the end of this guide WHAT IS THE MOST IMPORTANT INFORMATION YOU SHOULD KNOW ABOUT NSAIDS? NSAIDs can increase the risk of kidney failure, gastrointestinal damage, heart attack or stroke. Heart Kidney Gastrointestinal Attack Damage Damage (GI) Never use right before or You should not take NSAIDs Beware of life-threatening after coronary bypass graft if you have one of these ulcers and bleeding that may ! (CABG) surgery. ! high-risk conditions: ! happen without warning. Your risk† of heart attack or • Kidney disease Your GI risk increases with: stroke increases if: • Diabetes • Taking medicines called corticosteroids • You have heart disease • High blood pressure and anticoagulants • Even with short-term use • You take water pills or pills with • Old age or having poor health † • Smoking and drinking alcohol low dose aspirin does not pose this risk names that end in ‘pril’ or ‘sartan’ Your health risks increase the longer you take NSAIDs WHO SHOULD NOT TAKE NSAIDS? Do talk to your doctor if you: Do not take NSAIDs if you: • have medical conditions • have had an allergic reaction to aspirin or other NSAID • are breastfeeding • are a pregnant woman late in your pregnancy • take more than one medication: show your health provider a list of all of your medicines — some may cause serious side effects when combined with NSAIDs. WHAT ARE SERIOUS SIDE EFFECTS YOU
    [Show full text]
  • Arthritis Treatment Comparison Arthritis Treatment Comparison
    ARTHRITIS TREATMENT COMPARISON ARTHRITIS TREATMENT COMPARISON GENERIC OA of (BRAND) HOW SUPPLIED AS GA JIA JRA OA Knee PsA RA CHELATING AGENTS Penicillamine Cap: 250mg ✓ (Cuprimine) Penicillamine Tab: 250mg ✓ (Depen) CYCLIC POLYPEPTIDE IMMUNOSUPPRESSANTS Cyclosporine Cap: 25mg, 100mg; ✓ (Gengraf, Neoral) Sol: 100mg/mL CYCLOOXYGENASE-2 INHIBITORS Celecoxib Cap: 50mg, 100mg, ✓ ✓ ✓ ✓ (Celebrex) 200mg, 400mg DIHYDROFOLIC ACID REDUCTASE INHIBITORS Methotrexate Inj: 25mg/mL; ✓ ✓ Tab: 2.5mg Methotrexate Tab: 5mg, 7.5mg, ✓ ✓ (Trexall) 10mg, 15mg INTERLEUKIN RECEPTOR ANTAGONISTS Anakinra Inj: 100mg/0.67mL ✓ (Kineret) Tocilizumab Inj: 20mg/mL, ✓ ✓ (Actemra) 162mg/0.9mL GOLD COMPOUNDS Auranofin Cap: 3mg ✓ (Ridaura) Gold sodium thiomalate Inj: 50mg/mL ✓ ✓ (Myochrysine) HYALURONAN AND DERIVATIVES Hyaluronan Inj: 30mg/2mL ✓ (Orthovisc) Sodium hyaluronate Inj: 1% ✓ (Euflexxa) Sodium hyaluronate Inj: 10mg/mL ✓ (Hyalgan) Sodium hyaluronate Inj: 2.5mL ✓ (Supartz) HYLAN POLYMERS Hylan G-F 20 Inj: 8mg/mL ✓ (Synvisc, Synvisc One) KINASE INHIBITORS Tofacitinib Tab: 5mg ✓ (Xeljanz) MONOCLONAL ANTIBODIES Ustekinumab Inj: 45mg/0.5mL, ✓ (Stelara) 90mg/mL MONOCLONAL ANTIBODIES/CD20-BLOCKERS Rituximab Inj: 100mg/10mL, ✓ (Rituxan) 500mg/50mL (Continued) ARTHRITIS TREATMENT COMPARISON GENERIC OA of (BRAND) HOW SUPPLIED AS GA JIA JRA OA Knee PsA RA MONOCLONAL ANTIBODIES/TNF-BLOCKERS Adalimumab Inj: 20mg/0.4mL, ✓ ✓ ✓ ✓ (Humira) 40mg/0.8mL Golimumab Inj: 50mg/0.5mL, ✓ ✓ ✓ (Simponi) 100mg/mL Infliximab Inj: 100mg ✓ ✓ ✓ (Remicade) NON-STEROIDAL ANTI-INFLAMMATORY DRUGS
    [Show full text]
  • Fenbufen | Medchemexpress
    Inhibitors Product Data Sheet Fenbufen • Agonists Cat. No.: HY-B1138 CAS No.: 36330-85-5 Molecular Formula: C₁₆H₁₄O₃ • Molecular Weight: 254.28 Screening Libraries Target: COX; Caspase Pathway: Immunology/Inflammation; Apoptosis Storage: Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month SOLVENT & SOLUBILITY In Vitro DMSO : 50 mg/mL (196.63 mM; Need ultrasonic) H2O : 0.67 mg/mL (2.63 mM; Need ultrasonic) Mass Solvent 1 mg 5 mg 10 mg Concentration Preparing 1 mM 3.9327 mL 19.6634 mL 39.3267 mL Stock Solutions 5 mM 0.7865 mL 3.9327 mL 7.8653 mL 10 mM 0.3933 mL 1.9663 mL 3.9327 mL Please refer to the solubility information to select the appropriate solvent. In Vivo 1. Add each solvent one by one: 10% DMSO >> 90% (20% SBE-β-CD in saline) Solubility: 2.5 mg/mL (9.83 mM); Suspended solution; Need ultrasonic 2. Add each solvent one by one: 10% DMSO >> 90% corn oil Solubility: ≥ 2.5 mg/mL (9.83 mM); Clear solution BIOLOGICAL ACTIVITY Description Fenbufen (CL-82204) is an orally active non-steroidal anti-inflammatory drug (NSAID), with analgetic and antipyretic effects. Fenbufen has potent activity in a variety of animal model, including carageenin edema, UV erythema and adjuvant arthritis. Fenbufen has inhibitory activities against COX-1 and COX-2 with IC50s of 3.9 μM and 8.1 μM, respectively. Fenbufen is a caspases (caspase-1, 3, 4, 5, 9) inhibitor[1][2][3][4][5].
    [Show full text]
  • In 1977 a Conclusion of the National Association of State Racing Commissioners Veterinary-Chemist Advisory Board Concluded That
    Lawrence R. Soma, VMD, University of Pennsylvania, School of Veterinary Medicine. This review was undertaken at the request of the Racing Medication and Testing Consortium, Medication Advisory Committee. Review: The use of phenylbutazone in the horse This review presents a brief historical prospective of the genesis of regulated medication in the US racing industry of which the non-steroidal anti-inflammatory drug phenylbutazone (PBZ) is the focus. It presents some historical guide posts in the development of the current rules on the use on PBZ by racing jurisdictions in the US. Based on its prevalent use, PBZ still remains a focus of attention. The review examines the information presented in a number of different models used to determine the effects and duration of PBZ in the horse. They include naturally occurring lameness and reversible induced lameness models that directly examine the effects and duration of the administration of various doses of PBZ. The review also examines indirect plasma and tissue models studying the suppression of the release of arachidonic acid- derived mediators of inflammation. The majority of studies suggest an effect of PBZ at 24 hours at 4.4 mg/kg. This reflects and substantiates the opinion of many clinical veterinarians, many of whom will not perform a pre-purchase lameness examination unless the horse is shown to be free of NSAID. This remains the opinion of many Commission Veterinarians in that they wish to examine a horse pre-race without the possibility of a NSAID interfering with the examination and masking possible musculoskeletal conditions. Based on scientific studies, residual effects of PBZ remain at 24 hours following administration.
    [Show full text]
  • (12) United States Patent (10) Patent No.: US 6,221,377 B1 Meyer (45) Date of Patent: Apr
    USOO6221377B1 (12) United States Patent (10) Patent No.: US 6,221,377 B1 Meyer (45) Date of Patent: Apr. 24, 2001 (54) ADMINISTRATION MEDIA FOR (56) References Cited ANALGESIC, ANTI-INFLAMMATORY AND ANT-PYRETC DRUGS CONTAINING FOREIGN PATENT DOCUMENTS NITROUS OXDE AND PHARMACEUTICAL 2 277 264 10/1994 (GB). COMPOSITIONS CONTAINING SUCH MEDIA AND DRUGS OTHER PUBLICATIONS (75) Inventor: Petrus Johannes Meyer, Randburg Chemical ABstracts AN 1985:464783, Hertz et al., Jan. (ZA) 1985.* Chemical Abstracts AN 1978:44978, Berkowitz et al., Jan. (73) Assignee: Pitmy International N.V., Bonaire 1977.* (NL) International Publication No. WO93/25213, published Dec. 23, 1993. (*) Notice: Subject to any disclaimer, the term of this Mikrochim. Acta, vol. 2, No. 5-6, 1980 pp. 464–474, Stahl patent is extended or adjusted under 35 et al., Extraction of natural Substances using Supercritical U.S.C. 154(b) by 0 days. and liquified gases. (21) Appl. No.: 09/068,543 Reynolds J.E.F. et al., “Martindale', 1989, The Pharmaceu tical Press. (22) PCT Filed: Nov. 13, 1996 Science, vol. 194, No. 4268, 1976, pp. 967–968, Berkowitz (86) PCT No.: PCT/IB96/01366 et al., "Nitrous oxide “analgesia': resemblance to opiate action'. S371 Date: May 13, 1998 Steinegger et al., “Lehrbuch der Pharmakognosie und Phy S 102(e) Date: May 13, 1998 topharmazie', Edition 4, 1988. (87) PCT Pub. No.: WO97/17978 * cited by examiner PCT Pub. Date: May 22, 1997 Primary Examiner Jyothsna Venkat (30) Foreign Application Priority Data ASSistant Examiner-Grace Hsu (74) Attorney, Agent, or Firm-Arent Fox Kintner Plotkin Nov. 13, 1995 (ZA) ...................................................
    [Show full text]