Evaluation of Antiulcer Properties of Ethanolic and Hot Aqueous Stem Extracts of Synclisia Scabrida on Experimentally Induced Ulcer Models in Albino Mice
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A Comparative Study of DA-9601 and Misoprostol for Prevention of NSAID-Associated Gastroduodenal Injury in Patients Undergoing Chronic NSAID Treatment
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Springer - Publisher Connector Arch. Pharm. Res. (2014) 37:1308–1316 DOI 10.1007/s12272-014-0408-3 RESEARCH ARTICLE A comparative study of DA-9601 and misoprostol for prevention of NSAID-associated gastroduodenal injury in patients undergoing chronic NSAID treatment Oh Young Lee • Dae-Hwan Kang • Dong Ho Lee • Il-Kwun Chung • Jae-Young Jang • Jin-Il Kim • Jin-Woong Cho • Jong-Sun Rew • Kang-Moon Lee • Kyoung Oh Kim • Myung-Gyu Choi • Sang-Woo Lee • Soo-Teik Lee • Tae-Oh Kim • Yong-Woon Shin • Sang-Yong Seol Received: 25 April 2014 / Accepted: 2 May 2014 / Published online: 30 May 2014 Ó The Author(s) 2014. This article is published with open access at Springerlink.com Abstract Misoprostol is reported to prevent non-steroidal The primary endpoint was the gastric protection rate, and anti-inflammatory drug (NSAID)-associated gastroduode- secondary endpoints were the duodenal protection rate and nal complications. There is, however, limited information ulcer incidence rate. Endpoints were assessed by endos- regarding the efficacy of DA-9601 in this context. We copy after the 4-week treatment period. Drug-related performed a comparative study on the relative efficacy of adverse effects, including gastrointestinal (GI) symptoms, DA-9601 and misoprostol for prevention of NSAID-asso- were also compared. At week 4, the gastric protection rates ciated complications. In this multicenter, double-blinded, with DA-9601 and misoprostol were 81.4 % (192/236) and active-controlled, stratified randomized, parallel group, 89.3 % (216/242), respectively. -
Patent Application Publication ( 10 ) Pub . No . : US 2019 / 0192440 A1
US 20190192440A1 (19 ) United States (12 ) Patent Application Publication ( 10) Pub . No. : US 2019 /0192440 A1 LI (43 ) Pub . Date : Jun . 27 , 2019 ( 54 ) ORAL DRUG DOSAGE FORM COMPRISING Publication Classification DRUG IN THE FORM OF NANOPARTICLES (51 ) Int . CI. A61K 9 / 20 (2006 .01 ) ( 71 ) Applicant: Triastek , Inc. , Nanjing ( CN ) A61K 9 /00 ( 2006 . 01) A61K 31/ 192 ( 2006 .01 ) (72 ) Inventor : Xiaoling LI , Dublin , CA (US ) A61K 9 / 24 ( 2006 .01 ) ( 52 ) U . S . CI. ( 21 ) Appl. No. : 16 /289 ,499 CPC . .. .. A61K 9 /2031 (2013 . 01 ) ; A61K 9 /0065 ( 22 ) Filed : Feb . 28 , 2019 (2013 .01 ) ; A61K 9 / 209 ( 2013 .01 ) ; A61K 9 /2027 ( 2013 .01 ) ; A61K 31/ 192 ( 2013. 01 ) ; Related U . S . Application Data A61K 9 /2072 ( 2013 .01 ) (63 ) Continuation of application No. 16 /028 ,305 , filed on Jul. 5 , 2018 , now Pat . No . 10 , 258 ,575 , which is a (57 ) ABSTRACT continuation of application No . 15 / 173 ,596 , filed on The present disclosure provides a stable solid pharmaceuti Jun . 3 , 2016 . cal dosage form for oral administration . The dosage form (60 ) Provisional application No . 62 /313 ,092 , filed on Mar. includes a substrate that forms at least one compartment and 24 , 2016 , provisional application No . 62 / 296 , 087 , a drug content loaded into the compartment. The dosage filed on Feb . 17 , 2016 , provisional application No . form is so designed that the active pharmaceutical ingredient 62 / 170, 645 , filed on Jun . 3 , 2015 . of the drug content is released in a controlled manner. Patent Application Publication Jun . 27 , 2019 Sheet 1 of 20 US 2019 /0192440 A1 FIG . -
PHARMACEUTICAL APPENDIX to the TARIFF SCHEDULE 2 Table 1
Harmonized Tariff Schedule of the United States (2011) Annotated for Statistical Reporting Purposes PHARMACEUTICAL APPENDIX TO THE HARMONIZED TARIFF SCHEDULE Harmonized Tariff Schedule of the United States (2011) Annotated for Statistical Reporting Purposes PHARMACEUTICAL APPENDIX TO THE TARIFF SCHEDULE 2 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. -
Prevalence of Anti-Ulcer Drug Use in a Chinese Cohort
P.O.Box 2345, Beijing 100023,China World J Gastroenterol 2003;9(6):1365-1369 Fax: +86-10-85381893 World Journal of Gastroenterology E-mail: [email protected] www.wjgnet.com Copyright © 2003 by The WJG Press ISSN 1007-9327 • CLINICAL RESEARCH • Prevalence of anti-ulcer drug use in a Chinese cohort Tzeng-Ji Chen, Li-Fang Chou, Shinn-Jang Hwang Tzeng-Ji Chen, Shinn-Jang Hwang, Department of Family anti-ulcer drugs, e.g. H2-receptor antagonists, synthetic Medicine, Taipei Veterans General Hospital and National Yang-Ming prostaglandins, proton pump inhibitors, and cytoprotective University School of Medicine, Taipei, Taiwan, China agents, has changed the physicians’ treatment patterns in Li-Fang Chou, Department of Public Finance, National Chengchi gastroenterology and greatly improved the ulcer-healing rate University, Taipei, Taiwan, China of patients with peptic ulcer disease[1-6]. In spite of effectiveness Correspondence to: Professor Shinn-Jang Hwang, Department of and popularity, the cost of these drugs has also aroused concern Family Medicine, Taipei Veterans General Hospital, 201, Sec. 2, Shih- [7-11] Pai Road, Taipei 11217, Taiwan, China. [email protected] in the health care systems of developed countries . The concern Telephone: +86-2-28757458 Fax: +86-2-28737901 has been aggravating in recent years because of expanding use of Received: 2003-02-25 Accepted: 2003-03-16 proton pump inhibitors in treating gastroesophageal reflux disease. Although prescribing of these potent acid-suppressing drugs is popular, their patterns of utilization have been infrequently [12-21] Abstract documented in national surveys . In Taiwan area, a single and universal health insurance AIM: To estimate the age-specific prevalence of anti-ulcer program started in 1995 and covered nearly all inhabitants drug use and to calculate the usage of different anti-ulcer (21 653 555 beneficiaries at the end of 2001)[22]. -
Functional Dyspepsia
Erwin Budi Cahyono DEFINITION : Symptoms like pain or nausea in epigastrium accompanied by disgust, vomit, bloat, easy to full, fullness or nitre, which is suspected come from the abnormality of upper gastro- intestinal tractus. Dyspepsia: pathogenic mechanisms Dysmotility H. pylori infection/ Altered gastric inflammation acid secretion Mechanisms of dyspepsia Psychosocial Gut hypersensitivity factors Witteman & Tytgat, Netherlands J Med 1995; 46: 205–11. Talley et al., BMJ 2001; 323:1294–7. Tack et al., Curr Gastroenterol Rep 2001; 3: 503–8. Dyspepsia: symptom assessment Nature of symptoms Severity of Character symptoms Radiation Timing, duration and frequency Modifying factors Assessment of symptoms Patient’s degree Alarm features of distress Paré, Can J Gastroenterol 1999; 13: 647–54. acute dyspepsia (new onset dyspepsia) Suddenly Sigh with the quality of sigh which is usually more tremendous with a longer response to the medication. chronic dyspepsia Sigh which is sometimes disappear, sometimes appear, more than two weeks. The sigh is not as tremendous as acute dyspepsia with a quick response to the medication. Organic Dyspepsia : There is an organ abnormality as ulcer gastro- duodenal, gastro esofageal reflux and gastric carcinoma (Talley, 1998) A common term which is given to the patient as : abdominal pain or nausea on the upper of stomach which is repeatedly happen more than three months, and at least a long of that time 25% symptoms of dyspepsia appear and no evidence organic disease which is responsible to that symptoms -
Supplement Ii to the Japanese Pharmacopoeia Seventeenth Edition
SUPPLEMENT II TO THE JAPANESE PHARMACOPOEIA SEVENTEENTH EDITION O‹cial from June 28, 2019 English Version THE MINISTRY OF HEALTH, LABOUR AND WELFARE Notice: This English Version of the Japanese Pharmacopoeia is published for the convenience of users unfamiliar with the Japanese language. When and if any discrepancy arises between the Japanese original and its English translation, the former is authentic. Printed in Japan The Ministry of Health, Labour and Welfare Ministerial Notification No. 49 Pursuant to Paragraph 1, Article 41 of Act on Securing Quality, Efficacy and Safety of Products Including Pharmaceuticals and Medical Devices (Act No. 145, 1960), this notification stated that a part of the Japanese Pharmacopoeia was revised as follows*. NEMOTO Takumi The Minister of Health, Labour and Welfare June 28, 2019 A part of the Japanese Pharmacopoeia (Ministerial Notification No. 64, 2016) was revised as follows*. (The text referred to by the term ``as follows'' are omitted here. All of the revised Japanese Pharmacopoeia in accordance with this notification (hereinafter referred to as ``new Pharmacopoeia'' in Supplement 2) are made available for public exhibition at the Pharmaceutical Evaluation Division, Pharmaceutical Safety and Environmen- tal Health Bureau, Ministry of Health, Labour and Welfare, at each Regional Bureau of Health and Welfare, and at each Prefectural Office in Japan). Supplementary Provisions (Effective Date) Article 1 This Notification is applied from June 28, 2019. (Transitional measures) Article 2 In the case of drugs which are listed in the Japanese Pharmacopoeia (hereinafter referred to as ``previous Pharmacopoeia'') [limited to those listed in new Pharmacopoeia] and drugs which have been approved as of June 28, 2019 as prescribed under Paragraph 1, Article 14 of Act on Securing Quality, Efficacy and Safety of Products Including Pharmaceuticals and Medical Devices [including drugs the Minister of Health, Labour and Welfare specifies (the Ministry of Health and Welfare Ministerial Notification No. -
United States Patent (19) 11) Patent Number: 5,457,128 Yanagawa 45 Date of Patent: Oct
USOO5457128A United States Patent (19) 11) Patent Number: 5,457,128 Yanagawa 45 Date of Patent: Oct. 10, 1995 54 TOPICAL PREPARATION FOR HEALING Derwent & C.A. 112:84201 Sucralfate-topical. WOUNDS OF THE SKN Baldoni et al. WO/PCT90/02133 (Mar. 8, 1990) Derwent 75 Inventor: Akira Yanagawa, Yokohama, Japan Sucralfate sounds topical/dermal. Caramella et al. EP402933 (Dec. 19, 1990) Derwinet Sucral 73) Assignee: Dott Limited Company, Japan fate Topical. Peterson et al. WO/PCT9104034 (Apr. 4, 1991) Derwent & (21) Appl. No.: 142,468 C.A. 115:42011 Sucralfate Topical Ulcers/Lesions. 22) PCT Filed: Mar. 26, 1993 Fabre FR 2646604 (Nov. 9, 1990) CA.114:129165. 86 PCT No.: PCT/P93/00379 Burch et al. Agents Actions 34(1/2)229-231 (1991) CA. S 371 Date: Nov. 29, 1993 115:174597. Hayashi et al. J. Pediatr. Sug. 26(11):1279–81 Nov. 1991 S 102(e) Date: Nov. 29, 1993 Medline Abstrot. 87). PCT Pub. No.: WO93/19744 Michaeli EP230023 (Jul. 29, 1987) Derwent & C.A. 08:11249. PCT Pub. Date: Oct. 14, 1993 30 Foreign Application Priority Data Primary Examiner–Shep K. Rose Mar. 28, 1992 JP Japan .................................... 4-10862 Attorney, Agent, or Firm-Lorusso & Loud (51 Int. Cl. .................... A61K 31/045; A61 K9/06 57 ABSTRACT 52 U.S. Cl. ............................................. 514/532, 514/546 58 Field of Search ...................................... 514/532, 546 Disclosed is a topical preparation for healing wounds of the skin, which can demonstrate remarkable effects of the treat (56) References Cited ment of wounds of the skin, such as an ulcer of the skin, traumatogenic wounds caused by the abrasion of the skin, U.S. -
A Comparison of Efficacy Between Rebamipide and Omeprazole in the Treatment of Nsaids Gastropathy
ORIGINAL ARTICLE A Comparison of Efficacy between Rebamipide and Omeprazole in the Treatment of NSAIDs Gastropathy Suyata, Erita Bustami, Syadra Bardiman, Fuad Bakry Division of Gastroentero-Hepatology, Department of Internal Medicine, Faculty of Medicine, University Sriwijaya/M Hoesin Hospital, Palembang ABSTRACT Background: Gastropathy represent a disparity of gastric mucosal characterized by sub-epithelial bleeding and erosion. Gastropathy can be induced by non steroidal anti-inflammatory drugs (NSAIDs), alcohol, stressor, and chemical agents with various sign and symptoms. NSAIDs-induced gastropathy is the second most common etiology of gastric ulcer and variceal haemorrhages. Aims: To investigate the effectivity of rebamipide compare with omeprazole in treatment of NSAIDs- induced gastropathy. Method: This triple blind randomized study was enrolled from January to June 2004 with 38 subjects who were recruited from outpatient and inpatient clinic in M Hoesin Hospital in Palembang. Subject was divided into two groups. Endoscopic examination was performed in every patients. Results: There was an improvement of symptom in rebamipide group (78.9%) and omeprazole group (79.0%) after treatment but it didn’t have significant difference statistically. Improvement of NSAIDs induced gastropathy after treatment between two groups have significant difference (P = 0.02), and improvement of gradation of gastropathy after treatment has significant difference (P = 0.007).There was no side effect of administration of rebamipide and omeprazole in each group. Conclusion: Rebamipide as effective as omeprazole in improvement of symptom. Omeprazole is more effective than rebamipide in improvement of NSAIDs induced gastropathy and is as safe as rebamipide in the treatment of NSAIDs induced gastropathy. Keywords: Gastropathy, NSAIDs, rebamipide, omeprazole. -
Ranitidine and Sucralfate As Maintenance Therapy for Gastric Ulcer Disease: Endoscopic Control and Assessment of Scarring
Gut: first published as 10.1136/gut.30.12.1692 on 1 December 1989. Downloaded from Gut, 1989, 30, 1692-1697 Ranitidine and sucralfate as maintenance therapy for gastric ulcer disease: endoscopic control and assessment of scarring T TAKEMOTO, M NAMIKI, M ISHIKAWA, K TSUNEOKA, S OSHIBA, K KAWAI, AND N OGAWA From the Yamaguchi University School ofMedicine, Asahikawa Medical College, Yamagata University School of Medicine, Nippon Medical School, Osaka Medical College, Kyoto Prefectural University of Medicine, Ehime University School of Medicine, Japan SUMMARY The efficacy of ranitidine (150 mg nocte), and sulcralfate (1 g tds) as maintenance therapy to prevent gastric ulcer relapse was evaluated in a 12 month trial in 363 patients. The relapse rates were 8.8% at three months, 14.7% at six months, 18/1% at nine months, and 21V0% at 12 months for the ranitidine group and 1477%, 21/3%, 29.9%, and 30.2% respectively for the sucralfate group. At nine and 12 months the cumulative relapse rates for the ranitidine group were significantly lower than those for the sucralfate group (p<005). In both groups ulcers recurred mainly from red scars observed at the endoscopic scarring stage. This indicated the necessity of drug treatment up to the white scar stage. The results suggest that ranitidine is effective in preventing gastric ulcer relapse. Gastric acid is generally considered to be a key factor Methods http://gut.bmj.com/ in peptic ulcer development and the histamine H receptor blockers which inhibit its formation have PATIENTS become standard therapy for treatment of both Patients whose gastric ulcers had healed after any duodenal and gastric ulcer. -
PHARMACEUTICAL APPENDIX to the HARMONIZED TARIFF SCHEDULE Harmonized Tariff Schedule of the United States (2011) (Rev
Harmonized Tariff Schedule of the United States (2011) (Rev. 1) Annotated for Statistical Reporting Purposes PHARMACEUTICAL APPENDIX TO THE HARMONIZED TARIFF SCHEDULE Harmonized Tariff Schedule of the United States (2011) (Rev. 1) Annotated for Statistical Reporting Purposes PHARMACEUTICAL APPENDIX TO THE TARIFF SCHEDULE 2 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. ABACAVIR 136470-78-5 ACEVALTRATE 25161-41-5 ABAFUNGIN 129639-79-8 ACEXAMIC ACID 57-08-9 ABAGOVOMAB 792921-10-9 ACICLOVIR 59277-89-3 ABAMECTIN 65195-55-3 ACIFRAN 72420-38-3 ABANOQUIL 90402-40-7 ACIPIMOX 51037-30-0 ABAPERIDONE 183849-43-6 ACITAZANOLAST 114607-46-4 ABARELIX 183552-38-7 ACITEMATE 101197-99-3 ABATACEPT 332348-12-6 ACITRETIN 55079-83-9 ABCIXIMAB 143653-53-6 ACIVICIN 42228-92-2 ABECARNIL 111841-85-1 ACLANTATE 39633-62-0 ABETIMUS 167362-48-3 ACLARUBICIN 57576-44-0 ABIRATERONE 154229-19-3 ACLATONIUM NAPADISILATE 55077-30-0 ABITESARTAN 137882-98-5 ACLIDINIUM BROMIDE 320345-99-1 ABLUKAST 96566-25-5 ACODAZOLE 79152-85-5 ABRINEURIN 178535-93-8 ACOLBIFENE 182167-02-8 ABUNIDAZOLE 91017-58-2 ACONIAZIDE 13410-86-1 ACADESINE 2627-69-2 ACOTIAMIDE 185106-16-5 -
Chemical Structure-Related Drug-Like Criteria of Global Approved Drugs
Molecules 2016, 21, 75; doi:10.3390/molecules21010075 S1 of S110 Supplementary Materials: Chemical Structure-Related Drug-Like Criteria of Global Approved Drugs Fei Mao 1, Wei Ni 1, Xiang Xu 1, Hui Wang 1, Jing Wang 1, Min Ji 1 and Jian Li * Table S1. Common names, indications, CAS Registry Numbers and molecular formulas of 6891 approved drugs. Common Name Indication CAS Number Oral Molecular Formula Abacavir Antiviral 136470-78-5 Y C14H18N6O Abafungin Antifungal 129639-79-8 C21H22N4OS Abamectin Component B1a Anthelminithic 65195-55-3 C48H72O14 Abamectin Component B1b Anthelminithic 65195-56-4 C47H70O14 Abanoquil Adrenergic 90402-40-7 C22H25N3O4 Abaperidone Antipsychotic 183849-43-6 C25H25FN2O5 Abecarnil Anxiolytic 111841-85-1 Y C24H24N2O4 Abiraterone Antineoplastic 154229-19-3 Y C24H31NO Abitesartan Antihypertensive 137882-98-5 C26H31N5O3 Ablukast Bronchodilator 96566-25-5 C28H34O8 Abunidazole Antifungal 91017-58-2 C15H19N3O4 Acadesine Cardiotonic 2627-69-2 Y C9H14N4O5 Acamprosate Alcohol Deterrant 77337-76-9 Y C5H11NO4S Acaprazine Nootropic 55485-20-6 Y C15H21Cl2N3O Acarbose Antidiabetic 56180-94-0 Y C25H43NO18 Acebrochol Steroid 514-50-1 C29H48Br2O2 Acebutolol Antihypertensive 37517-30-9 Y C18H28N2O4 Acecainide Antiarrhythmic 32795-44-1 Y C15H23N3O2 Acecarbromal Sedative 77-66-7 Y C9H15BrN2O3 Aceclidine Cholinergic 827-61-2 C9H15NO2 Aceclofenac Antiinflammatory 89796-99-6 Y C16H13Cl2NO4 Acedapsone Antibiotic 77-46-3 C16H16N2O4S Acediasulfone Sodium Antibiotic 80-03-5 C14H14N2O4S Acedoben Nootropic 556-08-1 C9H9NO3 Acefluranol Steroid -
Studies on the Mechanism for the Gastric Mucosal Protection by Famotidine in Rats
Japan. J. Pharmacol. 55, 211-222 (1991) 211 Studies on the Mechanism for the Gastric Mucosal Protection by Famotidine in Rats KeijiMiyata, Takeshi Kamato, Akito Nishida and Kazuo Honda DepartmentofPharmacology, Medicinal Research Laboratories 1, YamanouchiPharmaceutical Co.,Ltd., 21 Miyukigaoka, Tsukuba, Ibaraki 305, Japan ReceivedAugust 10, 1990 AcceptedNovember 15,1990 ABSTRACT-Theeffect of famotidineon gastriclesions induced by the decreasein mucosaldefensive resistance was investigatedin rats and comparedwith those of cimetidine,pirenzepine and cetraxate.Famotidine (0.03, 0.1 and 0.3 mg/kg,p.o.) in- hibiteddose-dependently the developmentof gastriclesions produced by taurocholate- histaminein dosesthat suppressedhistamine-induced acid secretionin pylorus-ligated rats. The H2-antagonistalso prevented gastric mucosal lesions induced by taurocholate-serotonin,iodoacetamide, acidified aspirin and acidifiedethanol. Cimeti- dine, pirenzepineand cetraxateshowed the inhibitoryeffects on almostall types of the gastric lesions,but their inhibitoryeffects were much less potent than those of famotidine.On the other hand, famotidineinhibited the decreasesof gastricmucosal blood flow inducedby acidifiedethanol and the mucosalcontents of glycoprotein in- ducedby waterimmersion restraint stress. In addition,famotidine increased the trans- gastricpotential difference (PD) and promotedthe recoveryof decreasedtransgastric PD induced by acidifiedethanol in rats. These resultssuggest that the preventive effect of famotidineon gastriclesions is attributablenot only to suppression of acid secretionbut to activationof the gastricmucosal defensive mechanisms. Histamine H2-receptor antagonists, famoti- ity. dine, cimetidine and ranitidine, have been Famotidine has been reported to be a po- shown to be effective in preventing the forma- tent H2-receptor antagonist in vitro (10-12) tion of gastric mucosal lesions in rats (1-3) and in vivo (4, 13) with greater antisecretory and in promoting the healing in rat (2, 4) and activity than cimetidine and ranitidine (3, 14, human ulcers (5 -7).