Phytomedicines Used for Diabetes Mellitus in Ghana: a Systematic Search and Review of Preclinical and Clinical Evidence
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
The Mechanisms of Action of Ppars
12 Dec 2001 8:6 AR AR149-24.tex AR149-24.SGM LaTeX2e(2001/05/10) P1: GSR Annu. Rev. Med. 2002. 53:409–35 Copyright c 2002 by Annual Reviews. All rights reserved THE MECHANISMS OF ACTION OF PPARS Joel Berger and David E. Moller Department of Molecular Endocrinology, Merck Research Laboratories, P.O. Box 2000, Rahway, New Jersey 07065; e-mail: joel [email protected]; david [email protected] Key Words PPAR, nuclear receptors, diabetes, dyslipidemia ■ Abstract The peroxisome proliferator-activated receptors (PPARs) are a group of three nuclear receptor isoforms, PPAR ,PPAR, and PPAR, encoded by different genes. PPARs are ligand-regulated transcription factors that control gene expression by binding to specific response elements (PPREs) within promoters. PPARs bind as heterodimers with a retinoid X receptor and, upon binding agonist, interact with co- factors such that the rate of transcription initiation is increased. The PPARs play a critical physiological role as lipid sensors and regulators of lipid metabolism. Fatty acids and eicosanoids have been identified as natural ligands for the PPARs. More potent synthetic PPAR ligands, including the fibrates and thiazolidinediones, have proven effective in the treatment of dyslipidemia and diabetes. Use of such ligands has allowed researchers to unveil many potential roles for the PPARs in pathological states including atherosclerosis, inflammation, cancer, infertility, and demyelination. Here, we present the current state of knowledge regarding the molecular mechanisms of PPAR action and the involvement of the PPARs in the etiology and treatment of several chronic diseases. INTRODUCTION The peroxisome proliferator-activated receptors (PPARs) form a subfamily of the nuclear receptor superfamily. -
(12) United States Patent (10) Patent No.: US 7,700,128 B2 Doken Et Al
US007700128B2 (12) United States Patent (10) Patent No.: US 7,700,128 B2 Doken et al. (45) Date of Patent: Apr. 20, 2010 (54) SOLID PREPARATION COMPRISING AN 5,726,201 A * 3/1998 Fekete et al. ................ 514,471 INSULIN SENSITIZER, AN INSULIN 6,599,529 B1* 7/2003 Skinha et al. .... ... 424/458 SECRETAGOGUE ANDA 2003/0147952 A1* 8, 2003 Lim et al. ................... 424/468 POLYOXYETHYLENE SORBITAN EATTY 2003. O180352 A1 9, 2003 Patel et al. ACD ESTER 2004/O147564 A1 7/2004 Rao et al. 2004/0175421 A1* 9, 2004 Gidwani et al. ............. 424/465 (75) Inventors: Kazuhiro Doken, Osaka (JP); Tetsuya FOREIGN PATENT DOCUMENTS Kawano, Osaka (JP); Hiroyoshi EP O749751 A2 12/1996 Koyama, Osaka (JP): Naoru FR 2758461 7, 1998 Hamaguchi, Osaka (JP) GB 23990 15 9, 2004 JP 58065213 * 4f1983 (73) Assignee: Takeda Pharmaceutical Company WO WO95/12385 5, 1995 Limited, Osaka (JP) WO WO98, 11.884 3, 1998 WO WO 98,31360 7, 1998 (*) Notice: Subject to any disclaimer, the term of this WO WO 98/36755 8, 1998 patent is extended or adjusted under 35 WO WO98,57649 12/1998 U.S.C. 154(b) by 711 days. WO WO99.03476 1, 1999 WO WO99.03477 1, 1999 (21) Appl. No.: 10/544,581 WO WO99.03478 1, 1999 WO WOOO,274O1 5, 2000 WO WOOO.28989 5, 2000 (22) PCT Filed: Oct. 21, 2004 WO WOO1? 41737 A2 6, 2001 WO WOO1, 51463 T 2001 (86). PCT No.: PCT/UP2004/O15958 WO WOO2,04024 1, 2002 WO WO O2/O55009 T 2002 S371 (c)(1), WO WO 03/066028 A1 8, 2003 (2), (4) Date: Apr. -
WO 2016/118476 Al 28 July 2016 (28.07.2016) W P O P C T
(12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date WO 2016/118476 Al 28 July 2016 (28.07.2016) W P O P C T (51) International Patent Classification: DO, DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, A61K 38/46 (2006.01) HN, HR, HU, ID, IL, IN, IR, IS, JP, KE, KG, KN, KP, KR, KZ, LA, LC, LK, LR, LS, LU, LY, MA, MD, ME, MG, (21) International Application Number: MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, OM, PCT/US2016/013847 PA, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SA, SC, (22) International Filing Date: SD, SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, TN, 19 January 2016 (19.01 .2016) TR, TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW. (25) Filing Language: English (84) Designated States (unless otherwise indicated, for every kind of regional protection available): ARIPO (BW, GH, (26) Publication Language: English GM, KE, LR, LS, MW, MZ, NA, RW, SD, SL, ST, SZ, (30) Priority Data: TZ, UG, ZM, ZW), Eurasian (AM, AZ, BY, KG, KZ, RU, 62/105,342 20 January 2015 (20.01.2015) US TJ, TM), European (AL, AT, BE, BG, CH, CY, CZ, DE, DK, EE, ES, FI, FR, GB, GR, HR, HU, IE, IS, IT, LT, LU, (71) Applicant: THE CHILDREN'S MEDICAL CENTER LV, MC, MK, MT, NL, NO, PL, PT, RO, RS, SE, SI, SK, CORPORATION [US/US]; 300 Longwood Avenue, Bo SM, TR), OAPI (BF, BJ, CF, CG, CI, CM, GA, GN, GQ, ston, Massachusetts 021 15-5724 (US). -
Diabetes-Related Biomarkers and Methods of Use Thereof
(19) TZZ _ _T (11) EP 2 541 254 B1 (12) EUROPEAN PATENT SPECIFICATION (45) Date of publication and mention (51) Int Cl.: of the grant of the patent: G01N 21/76 (2006.01) G01N 21/64 (2006.01) 12.11.2014 Bulletin 2014/46 G01N 33/66 (2006.01) G01N 33/74 (2006.01) G01N 33/68 (2006.01) (21) Application number: 12175286.9 (22) Date of filing: 18.04.2008 (54) Diabetes-related biomarkers and methods of use thereof Diabetesassoziierte Biomarker und Verfahren zur deren Verwendung dafür Biomarqueurs associés aux diabètes et procédés d’utilisation correspondants (84) Designated Contracting States: • HANLEY ANTHONY J G ET AL: "Metabolic and AT BE BG CH CY CZ DE DK EE ES FI FR GB GR inflammation variable clusters and prediction of HR HU IE IS IT LI LT LU LV MC MT NL NO PL PT type 2 diabetes: factor analysis using directly RO SE SI SK TR measured insulin sensitivity.", DIABETES JUL 2004, vol. 53, no. 7, July 2004 (2004-07), pages (30) Priority: 18.04.2007 US 788260 1773-1781, XP002486180, ISSN: 0012-1797 08.11.2007 US 2609 P • EDELMAN DAVID ET AL: "Utility of hemoglobin A1c in predicting diabetes risk", JOURNAL OF (43) Date of publication of application: GENERAL INTERNAL MEDICINE, vol. 19, no. 12, 02.01.2013 Bulletin 2013/01 December 2004 (2004-12), pages 1175-1180, XP002502995, ISSN: 0884-8734 (62) Document number(s) of the earlier application(s) in • INOUE ET AL: "The combination of fasting accordance with Art. 76 EPC: plasma glucose and glycosylated hemoglobin 08746276.8 / 2 147 315 predicts type 2 diabetes in Japanese workers", DIABETES RESEARCH AND CLINICAL (73) Proprietor: Health Diagnostic Laboratory, Inc. -
203313Orig1s000 203314Orig1s000
CENTER FOR DRUG EVALUATION AND RESEARCH APPLICATION NUMBER: 203313Orig1s000 203314Orig1s000 PROPRIETARY NAME REVIEW(S) PROPRIETARY NAME MEMORANDUM Division of Medication Error Prevention and Analysis (DMEPA) Office of Medication Error Prevention and Risk Management (OMEPRM) Office of Surveillance and Epidemiology (OSE) Center for Drug Evaluation and Research (CDER) *** This document contains proprietary information that cannot be released to the public*** Date of This Review: September 1, 2015 Application Type and Number: NDA 203313 Product Name and Strength: Ryzodeg 70/30 (insulin degludec and insulin aspart) injection, 100 units/mL Product Type: Combination (Drug + Device) Rx or OTC: Rx Applicant/Sponsor Name: Novo Nordisk Panorama #: 2015-1341036 DMEPA Primary Reviewer: Sarah K. Vee, PharmD DMEPA Team Leader: Yelena Maslov, PharmD Reference ID: 3813971 1 INTRODUCTION The Applicant submitted the proposed proprietary name, Ryzodeg on March 26, 2015 (b) (4) Division of Medication Error Prevention and Analysis (DMEPA) found the name conditionally acceptable in our previous review1 . On August 19, 2015, the Agency recommended that the Applicant consider including the modifier “70/30” to the proposed proprietary name to indicate the concentrations of the two insulins in the formulation. Since Ryzodeg is a mixed insulin formulation containing 70 % insulin degludec and 30 % insulin aspart, the addition of the modifier 70/30 would be consistent with current naming approach for mixed insulins. Thus, the Applicant submitted the name, Ryzodeg 70/30, for review on August 21, 2015. We note that the product characteristics are the same. This memorandum is to communicate that DMEPA finds the proposed proprietary name, Ryzodeg 70/30 (b) (4) is acceptable from both a misbranding and safety perspective. -
Englitazone Administration to Late Pregnant Rats Produces Delayed Body Growth and Insulin Resistance in Their Fetuses and Neonates
Biochem. J. (2005) 389, 913–918 (Printed in Great Britain) 913 Englitazone administration to late pregnant rats produces delayed body growth and insulin resistance in their fetuses and neonates Julio SEVILLANO, Inmaculada C. LOPEZ-P´ EREZ,´ Emilio HERRERA, Mar´ıa DEL PILAR RAMOS and Carlos BOCOS1 Facultad de Farmacia, Universidad San Pablo-CEU, Montepr´ıncipe, Ctra. Boadilla del Monte Km 5.300, E-28668 Boadilla del Monte (Madrid), Spain The level of maternal circulating triacylglycerols during late preg- pregnant rats was corroborated, since they showed higher plasma nancy has been correlated with the mass of newborns. PPARγ NEFA [non-esterified (‘free’) fatty acid] levels, ketonaemia and (peroxisome-proliferator-activated receptor γ ) ligands, such as liver LPL (lipoprotein lipase) activity and lower plasma IGF-I TZDs (thiazolidinediones), have been shown to reduce triacyl- (type 1 insulin-like growth factor) levels, in comparison with glycerolaemia and have also been implicated in the inhibition those from control mothers. Moreover, at the molecular level, an of tissue growth and the promotion of cell differentiation. increase in Akt phosphorylation was found in the liver of neonates Therefore TZDs might control cell proliferation during late fetal from EZ-treated mothers, which confirms that the insulin pathway development and, by extension, body mass of pups. To investigate was negatively affected. Thus the response of fetuses and neonates the response to EZ (englitazone), a TZD, on perinatal develop- to maternal antidiabetic drug treatment is the opposite of what ment, 0 or 50 mg of englitazone/kg of body mass was given as an would be expected, and can be justified by the scarce amount of oral dose to pregnant rats daily from day 16 of gestation until either adipose tissue impeding a normal response to PPARγ ligands and day 20 for the study of their fetuses, or until day 21 of gestation by hyperinsulinaemia as being responsible for a major insulin- for the study of neonates. -
Possible Role of Rivoglitazone Thiazolidine Class of Drug As Dual
Medical Hypotheses 131 (2019) 109305 Contents lists available at ScienceDirect Medical Hypotheses journal homepage: www.elsevier.com/locate/mehy Possible role of rivoglitazone thiazolidine class of drug as dual-target therapeutic agent for bacterial infections: An in silico study T ⁎ Vidyasrilekha Yele , Niladri Saha, Afzal Azam Md Department of Pharmaceutical Chemistry, JSS College of Pharmacy, Ootacamund, JSS Academy of Higher Education & Research, Mysuru 643001, India ARTICLE INFO ABSTRACT Keywords: Infections due to resistant bacteria are the life-threatening and leading cause of mortality worldwide. The Rivoglitazone current therapy for bacterial infections includes treatment with various drugs and antibiotics. The misuse and ParE over usage of these antibiotics leads to bacterial resistance. There are several mechanisms by which bacteria MurE exhibit resistance to some antibiotics. These include drug inactivation or modification, elimination of antibiotics Docking through efflux pumps, drug target alteration, and modification of metabolic pathway. However, it is difficult to MM-GBSA treat infections caused by resistant bacteria by conventional existing therapy. In the present study binding af- Molecular dynamic simulations fi Anti-bacterial agent nities of some glitazones against ParE and MurE bacterial enzymes are investigated by in silico methods. As evident by extra-precision docking and binding free energy calculation (MM-GBSA) results, rivoglitazone ex- hibited higher binding affinity against both ParE and MurE enzymes compared to all other selected compounds. Further molecular dynamic (MD) simulations were performed to validate the stability of rivoglitazone/4MOT and rivoglitazone/4C13 complexes and to get insight into the binding mode of inhibitor. Thus, we hypothesize that structural modifications of the rivoglitazone scaffold can be useful for the development of an effective antibacterial agent. -
Curriculum Vitae: Marc Stephen Rendell, Md
P a g e | 1 CURRICULUM VITAE: MARC STEPHEN RENDELL, M.D. ADDRESS: The Rose Salter Medical Research Foundation 34 Versailles Newport Coast, CA 92657-0065 clinic office 355 Placentia Avenue, Suite 308b Newport Beach, CA 92663 TELEPHONE: 402 -578-1580 HOSPITAL AND FACULTY APPOINTMENTS: 12/1977-6/1983 Active Staff and Assistant Professor Division of Endocrinology Department of Medicine The Johns Hopkins Hospital Baltimore, Maryland 6/1980-6/1983 Assistant Professor Division of Nuclear Medicine Department of Radiology The Johns Hopkins University School of Medicine Baltimore, Maryland 12/1977-6/1983 Chief, Endocrinology Director, Radioimmunoassay Laboratory The US Public Health Service Hospital Baltimore, Maryland 7/1983-11/1984 Director, Diabetes Institute City of Faith Medical and Research Center Associate Professor, Medicine and Pathology ORU School of Medicine Tulsa, Oklahoma 2/1985- 9/2016 Director, Creighton Diabetes Center Associate Professor of Medicine Associate Professor of Biomedical Sciences (1993-1995) P a g e | 2 Professor of Medicine and Biomedical Sciences (1996-2016 ) Creighton University School of Medicine Omaha, Nebraska 3/1999- Medical Director: Rose Salter Medical Research Foundation Baltimore, Maryland, Omaha, Nebraska, Newport Beach, California CLINICAL PRACTICE 12/1977-6/1983 Active Staff Division of Endocrinology Department of Medicine The Johns Hopkins Hospital Baltimore, Maryland 12/1977-6/1983 Chief, Endocrinology Director, Radioimmunoassay Laboratory The US Public Health Service Hospital Baltimore, Maryland 7/1983-11/1984 Director, Diabetes Institute City of Faith Medical and Research Center ORU School of Medicine Tulsa, Oklahoma 2/1985- 9/2016 Director, Creighton Diabetes Center Creighton University Medical Center Omaha, Nebraska 9/2016- Medical Director: Rose Salter Diabetes Center Newport Beach, California 1/2017- Telemedicine Physician Teladoc and MDLive EDUCATION: 9/1964-6/1968 B.S. -
Sugar-Lowering Drugs for Type 2 Diabetes Mellitus and Metabolic Syndrome—Review of Classical and New Compounds: Part-I
pharmaceuticals Review Sugar-Lowering Drugs for Type 2 Diabetes Mellitus and Metabolic Syndrome—Review of Classical and New Compounds: Part-I Raquel Vieira 1 , Selma B. Souto 2, Elena Sánchez-López 3,4 , Ana López Machado 4, Patricia Severino 5,6 , Sajan Jose 7 , Antonello Santini 8 , Ana Fortuna 9,10, Maria Luisa García 3,4, Amelia M. Silva 11,12 and Eliana B. Souto 1,13,* 1 Department of Pharmaceutical Technology, Faculty of Pharmacy, University of Coimbra (FFUC), Pólo das Ciências da Saúde, 3000-548 Coimbra, Portugal; [email protected] 2 Department of Endocrinology, Hospital São João, Prof. Alameda Hernâni Monteiro, 4200-319 Porto, Portugal; [email protected] 3 Department of Pharmacy, Pharmaceutical Technology and Physical Chemistry, Faculty of Pharmacy and Food Sciences, University of Barcelona, Institute of Nanoscience and Nanotechnology (IN2UB), 08028 Barcelona, Spain; [email protected] (E.S.-L.); [email protected] (M.L.G.) 4 Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), University of Barcelona, 08028 Barcelona, Spain; [email protected] 5 Laboratory of Nanotechnology and Nanomedicine (LNMED), Institute of Technology and Research (ITP), Av. Murilo Dantas, 300, Aracaju 49010-390, Brazil; [email protected] 6 University of Tiradentes (UNIT), Industrial Biotechnology Program, Av. Murilo Dantas 300, Aracaju 49032-490, Brazil 7 Department of Pharmaceutical Sciences, Mahatma Gandhi University, Cheruvandoor Campus, Ettumanoor, Kerala 686631, India; [email protected] 8 -
Pancreatic Hormones and Antidiabetic Drugs. In
Chapter 41 Pancreatic Hormones & Antidiabetic Drugs Contents Pancreatic Hormones & Antidiabetic Drugs The endocrine pancreas Antidiabetic Drugs The Pancreas An organ that makes insulin and enzymes for digestion. Both endocrine system and digestive system (exocrine). Function of the hormones Insulin: the storage and anabolic hormone of the body (glyco-metabolism) Amylin: modulates appetite, gastric emptying, and glucagon and insulin secretion Glucagon: the hyperglycemic factor that mobilizes glycogen stores Disorders of the Pancreas: Diabetes Mellitus Caused by: Insufficient secretion of insulin Resistance of body cells to the effects of insulin Diabetes Mellitus Type1 Type2 Type3 Type4 Insulin- Noninsulin- Gestational Diabetes Other dependent dependent specific diabetes diabetes Mellitus (GDM) types elevated blood glucose Type Ⅰ Diabetes --- develops suddenly, usually before age 15 results in insulin dependence severe or absolute insulin deficiency In response to high levels of glucose in the blood, the insulin-producing cells in the pancreas secrete the hormone insulin. Type I diabetes occurs when these cells are destroyed by the body’s own immune system. Treatment of Type Ⅰ Diabetes Injection of insulin Surgery: replacing the pancreas or just the beta cells pancreas-kidney transplant Stem cell research Type Ⅱ Diabetes --- adult onset, usually occurs after age 40 Etiology: Insulin resistance; relative deficiency in insulin secretion. blood glucose levels rise due to : 1) Lack of insulin production 2) Insufficient insulin -
(12) Patent Application Publication (10) Pub. No.: US 2007/0191611 A1 Rao Et Al
US 2007.019 1611A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2007/0191611 A1 Rao et al. (43) Pub. Date: Aug. 16, 2007 (54) SYNTHESIS OF ANTIDIABETIC Publication Classification ROSGLTAZONE DERVATIVES (51) Int. Cl. (75) Inventors: Dharmaraj Ramachandra Rao, C07D 417/02 (2006.01) Maharashtra (IN); Rajendra C07D 213/72 (2006.01) Narayanrao Kankan, Maharashtra (IN) (52) U.S. Cl. ......................................... 546/269.7: 546/304 Correspondence Address: (57) ABSTRACT CONLEY ROSE, PC. A process of preparing rosiglitaZone, or a pharmaceutically 5700 GRANITE PARKWAY, SUITE 330 acceptable salt thereof, which process employs an interme PLANO, TX 75024 (US) diate metabisulphite complex of 4-2-(N-methyl-N-(2-py ridyl)amino) ethoxybenzaldehyde, which metabisulphite (73) Assignee: CIPLA LIMITED, MAHARASHA- complex is represented by following formula (III); where X TRA, INDIA (IN) represents an alkali metal. The present invention further provides rosiglitaZone, or a pharmaceutically acceptable salt (21) Appl. No.: 11/568,610 thereof, prepared by the above process. (22) PCT Filed: May 3, 2005 (III) (86). PCT No.: PCT/GBOS/O1671 N OH S 371(c)(1), O SOX (2), (4) Date: Jan. 11, 2007 4. 1N1 3 (30) Foreign Application Priority Data hi, H May 5, 2004 (GB)......................................... O41OO13.7 US 2007/019 1611 A1 Aug. 16, 2007 SYNTHESIS OF ANTDABETIC ROSIGLTAZONE thiazolidine-2,4-dione, which is then reduced with Pd/C to DERVATIVES obtain rosiglitazone free base. We have now developed an improved synthesis of rosiglitaZone, or a pharmaceutically 0001. The present invention describes a novel process for the synthesis of the antidiabetic compound, 5-4-2-(N- acceptable salt thereof, which alleviates many problems methyl-N-(2-pyridyl)amino)ethoxybenzyl)thiazolidine-2, associated with the prior art preparation of rosiglitaZone 4-dione, namely rosiglitaZone, especially as the maleate salt substantially as hereinafter described in greater detail. -
George Grunberger, M.D., F.A.C.P., F.A.C.E
GEORGE GRUNBERGER, M.D., F.A.C.P., F.A.C.E. Chairman, Grunberger Diabetes Institute Clinical Professor, Department of Internal Medicine Clinical Professor, Center for Molecular Medicine & Genetics Wayne State University School of Medicine Professor, Department of Internal Medicine Oakland University William Beaumont School of Medicine Visiting Professor, First Faculty of Medicine Charles University, Prague (Czech Republic) Phone: (248) 335-7740 43494 Woodward Ave, ste 208, Bloomfield Hills, MI 48302 Fax: (248) 338-7979 e-mail: [email protected] EDUCATION 1973 BA degree (Biochemistry), Columbia College, New York, NY 1977 MD degree, New York University School of Medicine, New York, NY TRAINING 1977-1980 Residency, Internal Medicine Case Western Reserve University University Hospitals of Cleveland, Cleveland, Ohio 1980-1983 Fellowship (clinical and basic research), Endocrinology and Metabolism, Diabetes Branch, National Institute of Arthritis, Diabetes, Digestive and Kidney Diseases National Institutes of Health, Bethesda, Maryland FACULTY APPOINTMENTS, Wayne State University, Detroit, Michigan 1986-1992 Associate Professor (tenured), Department of Internal Medicine Associate Professor (tenured), Department of Molecular Biology and Genetics 1992-2002 Professor (tenured), Department of Internal Medicine 1995-1996 Interim Chairman, Department of Internal Medicine 1992-1994 Professor (tenured), Department of Molecular Biology & Genetics 1994-present Professor (tenured), Center for Molecular Medicine & Genetics 1986-present Regular member