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NO-1886 Decreases Ectopic Lipid Deposition and Protects Pancreatic Cells in Diet-Induced Diabetic Swine
399 NO-1886 decreases ectopic lipid deposition and protects pancreatic cells in diet-induced diabetic swine W Yin*,1,2,5, D Liao*,1,2, M Kusunoki6,SXi1, K Tsutsumi3, Z Wang1, X Lian1, T Koike4, J Fan4, Y Yang5 and C Tang5 1Department of Biochemistry and Biotechnology, Nanhua University School of Life Sciences and Technology, Hengyang, Hunan 421001, China 2Department of Pathophysiology, Central South University Xiangya Medical College, Changsha, Hunan, China 3Research and Development, Otsuka Pharmaceutical Factory Inc., Tokushima, Japan 4Laboratory of Cardiovascular Disease, Department of Pathology, Institute of Basic Medical Sciences, University of Tsukuba, Tsukuba 305-8575, Japan 5Institute of Cardiovascular Research, Nanhua University Medical School, Hengyang, Hunan 421001, China 6Department of Internal Medicine, Faculty of Medicine, Aichi Medical University, Nagakute-cho, Aichigunte, Aichi 480-11, Japan (Requests for offprints should be addressed to W Yin, Department of Biochemistry and Molecular Biology, Nanhua University School of Life Sciences and Technology, Hengyang, Hunan 421001, China; Email: [email protected]) *W Yin and D Liao contributed equally to this paper Abstract The synthetic compound NO-1886 (ibrolipim) is a lipo- skeletal muscle, liver and pancreas, and also caused pan- protein lipase activator that has been proven to be highly creatic cell damage. However, supplementing 1% NO- effective in lowering plasma triglycerides. Recently, we 1886 (200 mg/kg per day) into the high-fat/high-sucrose found that NO-1886 also reduced plasma free fatty acids diet decreased ectopic lipid deposition, improved insulin and glucose in high-fat/high-sucrose diet-induced dia- resistance, and alleviated the cell damage. These results betic rabbits. -
Stems for Nonproprietary Drug Names
USAN STEM LIST STEM DEFINITION EXAMPLES -abine (see -arabine, -citabine) -ac anti-inflammatory agents (acetic acid derivatives) bromfenac dexpemedolac -acetam (see -racetam) -adol or analgesics (mixed opiate receptor agonists/ tazadolene -adol- antagonists) spiradolene levonantradol -adox antibacterials (quinoline dioxide derivatives) carbadox -afenone antiarrhythmics (propafenone derivatives) alprafenone diprafenonex -afil PDE5 inhibitors tadalafil -aj- antiarrhythmics (ajmaline derivatives) lorajmine -aldrate antacid aluminum salts magaldrate -algron alpha1 - and alpha2 - adrenoreceptor agonists dabuzalgron -alol combined alpha and beta blockers labetalol medroxalol -amidis antimyloidotics tafamidis -amivir (see -vir) -ampa ionotropic non-NMDA glutamate receptors (AMPA and/or KA receptors) subgroup: -ampanel antagonists becampanel -ampator modulators forampator -anib angiogenesis inhibitors pegaptanib cediranib 1 subgroup: -siranib siRNA bevasiranib -andr- androgens nandrolone -anserin serotonin 5-HT2 receptor antagonists altanserin tropanserin adatanserin -antel anthelmintics (undefined group) carbantel subgroup: -quantel 2-deoxoparaherquamide A derivatives derquantel -antrone antineoplastics; anthraquinone derivatives pixantrone -apsel P-selectin antagonists torapsel -arabine antineoplastics (arabinofuranosyl derivatives) fazarabine fludarabine aril-, -aril, -aril- antiviral (arildone derivatives) pleconaril arildone fosarilate -arit antirheumatics (lobenzarit type) lobenzarit clobuzarit -arol anticoagulants (dicumarol type) dicumarol -
Lipoprotein Lipase As an Attractive Target for Correcting Dyslipidemia and Reduction of Cvd Residual Risk
ISSN 2311-715X УКРАЇНСЬКИЙ БІОФАРМАЦЕВТИЧНИЙ ЖУРНАЛ, № 4 (45) 2016 UDC 577.125.8:616.005 National University of Pharmacy D. A. Dorovsky, A. L. Zagayko LIPOPROTEIN LIPASE AS AN ATTRACTIVE TARGET FOR CORRECTING DYSLIPIDEMIA AND REDUCTION OF CVD RESIDUAL RISK Lipoprotein lipase has long been known to hydrolyse triglycerides from triglycerides-rich lipoproteins. It also the ability to promote the binding of lipoproteins to the wide variation of lipoprotein receptors. There are some studies that suggest the possible atherogenic role of lipoprotein lipase. In theory, lipoprotein lipase deficiency should help to clarify this question. However, the rarity of this condition means that it has not been possible to conduct epidemiological studies. During the last decade it became obvious that elevated plasma TG and low HDL-cholesterol are part of CVD residual risk. Thus LPL is an attractive target for correcting dyslipidemia and reduction of CVD residual risk. Key words: Lipoprotein lipase; atherosclerosis; lipoproteins INTRODUCTION differences in M expression of LPL contributed to diffe- Lipoprotein lipase (LPL) is synthesized and secreted rences in the development of atherosclerotic plaque for- in several tissues, such as skeletal muscle, adipose tissue, mation. Concentrations of LPL protein, activity and mRNA cardiac muscle and macrophages (M), binding to the in atherosclerosis-prone mice were found to be seve- vascular endothelial cell surface of the capillary through- ral-fold higher than in atherosclerosis-resistant counter- heparan sulphate. parts. Ichikawa et al. compared atherosclerotic lesions in Lipoprotein lipase (LPL) plays a central role in lipo wild-type strains with lesions in rabbits with over-exp- protein metabolism by catalyzing hydrolysis of triglyce- ressed M-specific human lipoprotein lipase, after giving rides (TG) in very low-density lipoprotein (VLDL) partic- both groups food containing 0.3 % cholesterol. -
(12) United States Patent (10) Patent No.: US 8,486,621 B2 Luo Et Al
USOO8486.621B2 (12) United States Patent (10) Patent No.: US 8,486,621 B2 Luo et al. (45) Date of Patent: Jul. 16, 2013 (54) NUCLEICACID-BASED MATRIXES 2005. O130180 A1 6/2005 Luo et al. 2006/0084607 A1 4/2006 Spirio et al. (75) Inventors: ity, N. (US); Soong Ho 2007/01482462007/0048759 A1 3/20076/2007 Luo et al. m, Ithaca, NY (US) 2008.0167454 A1 7, 2008 Luo et al. 2010, O136614 A1 6, 2010 Luo et al. (73) Assignee: Cornell Research Foundation, Inc., 2012/0022244 A1 1, 2012 Yin Ithaca, NY (US) FOREIGN PATENT DOCUMENTS (*) Notice: Subject to any disclaimer, the term of this WO WO 2004/057023 A1 T 2004 patent is extended or adjusted under 35 U.S.C. 154(b) by 808 days. OTHER PUBLICATIONS Lin et al. (J Biomech Eng. Feb. 2004;126(1):104-10).* (21) Appl. No.: 11/464,184 Li et al. (Nat Mater. Jan. 2004:3(1):38-42. Epub Dec. 21, 2003).* Ma et al. (Nucleic Acids Res. Dec. 22, 1986;14(24):9745-53).* (22) Filed: Aug. 11, 2006 Matsuura, et al. Nucleo-nanocages: designed ternary oligodeoxyribonucleotides spontaneously form nanosized DNA (65) Prior Publication Data cages. Chem Commun (Camb). 2003; (3):376-7. Li, et al. Multiplexed detection of pathogen DNA with DNA-based US 2007/01 17177 A1 May 24, 2007 fluorescence nanobarcodes. Nat Biotechnol. 2005; 23(7): 885-9. Lund, et al. Self-assembling a molecular pegboard. JAm ChemSoc. Related U.S. Application Data 2005; 127(50): 17606-7. (60) Provisional application No. 60/722,032, filed on Sep. -
The Use of Stems in the Selection of International Nonproprietary Names (INN) for Pharmaceutical Substances
WHO/PSM/QSM/2006.3 The use of stems in the selection of International Nonproprietary Names (INN) for pharmaceutical substances 2006 Programme on International Nonproprietary Names (INN) Quality Assurance and Safety: Medicines Medicines Policy and Standards The use of stems in the selection of International Nonproprietary Names (INN) for pharmaceutical substances FORMER DOCUMENT NUMBER: WHO/PHARM S/NOM 15 © World Health Organization 2006 All rights reserved. Publications of the World Health Organization can be obtained from WHO Press, World Health Organization, 20 Avenue Appia, 1211 Geneva 27, Switzerland (tel.: +41 22 791 3264; fax: +41 22 791 4857; e-mail: [email protected]). Requests for permission to reproduce or translate WHO publications – whether for sale or for noncommercial distribution – should be addressed to WHO Press, at the above address (fax: +41 22 791 4806; e-mail: [email protected]). 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 World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent approximate border lines for which there may not yet be full agreement. The mention of specific companies or of certain manufacturers’ products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned. Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters. -
WO 2013/037390 Al R
(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 2013/037390 Al 21 March 2013 (21.03.2013) P O P C T (51) International Patent Classification: (74) Agent: WINGEFELD, Renate; c/o Sanofi-Aventis C07D 471/04 (2006.01) A61P 9/00 (2006.01) Deutschland GmbH, Patents Germany, Industriepark A61K 31/437 (2006.01) A61P 25/00 (2006.01) Hochst, Geb. K 801, 65926 Frankfurt (DE). A61P 3/10 (2006.01) A61P 35/00 (2006.01) (81) Designated States (unless otherwise indicated, for every (21) International Application Number: kind of national protection available): AE, AG, AL, AM, PCT/EP201 1/065715 AO, AT, AU, AZ, BA, BB, BG, BH, BR, BW, BY, BZ, CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, DO, (22) International Filing Date: DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, HN, 12 September 201 1 (12.09.201 1) HR, HU, ID, IL, IN, IS, JP, KE, KG, KM, KN, KP, KR, (25) Filing Language: English KZ, LA, LC, LK, LR, LS, LT, LU, LY, MA, MD, ME, MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, (26) Publication Language: English OM, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SC, SD, (71) Applicant (for all designated States except US): SANOFI SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, TN, TR, [FR/FR]; 54, rue de la Boetie, F-75008 Paris (FR). TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW. -
Sympathoadrenergic Modulation of Hematopoiesis: a Review of Available Evidence and of Therapeutic Perspectives
REVIEW published: 05 August 2015 doi: 10.3389/fncel.2015.00302 Sympathoadrenergic modulation of hematopoiesis: a review of available evidence and of therapeutic perspectives Marco Cosentino*, Franca Marino and Georges J. M. Maestroni Center for Research in Medical Pharmacology, University of Insubria, Varese, Italy Innervation of the bone marrow (BM) has been described more than one century ago, however the first in vivo evidence that sympathoadrenergic fibers have a role in hematopoiesis dates back to less than 25 years ago. Evidence has since increased showing that adrenergic nerves in the BM release noradrenaline and possibly also dopamine, which act on adrenoceptors and dopaminergic receptors (DR) expressed on hematopoietic cells and affect cell survival, proliferation, migration and engraftment ability. Remarkably, dysregulation of adrenergic fibers to the BM is associated with hematopoietic disturbances and myeloproliferative disease. Several adrenergic and dopaminergic agents are already in clinical use for non-hematological indications and with a usually favorable risk-benefit profile, and are therefore potential candidates for Edited by: non-conventional modulation of hematopoiesis. Wanda Lattanzi, Università Cattolica del Sacro Cuore, Keywords: dopamine, noradrenaline, adrenaline, adrenoceptors, dopaminergic receptors, hematopoiesis, Italy neuroimmune phamacology, drug repurposing Reviewed by: Sujit Basu, Introduction Ohio State University, USA Tsvee Lapidot, Weizmann Institute of Science, Israel The term ‘‘niche’’, derived from the Latin word ‘‘mytilus’’ (mussel), has eventually come to designate a shallow recess in a wall, as for a statue or other decorative object, in view of the *Correspondence: similarity with the shape of a seashell, and broadly a place suitable or appropriate for a person or Marco Cosentino, Center for Research in Medical thing. -
GPCR/G Protein
Inhibitors, Agonists, Screening Libraries www.MedChemExpress.com GPCR/G Protein G Protein Coupled Receptors (GPCRs) perceive many extracellular signals and transduce them to heterotrimeric G proteins, which further transduce these signals intracellular to appropriate downstream effectors and thereby play an important role in various signaling pathways. G proteins are specialized proteins with the ability to bind the nucleotides guanosine triphosphate (GTP) and guanosine diphosphate (GDP). In unstimulated cells, the state of G alpha is defined by its interaction with GDP, G beta-gamma, and a GPCR. Upon receptor stimulation by a ligand, G alpha dissociates from the receptor and G beta-gamma, and GTP is exchanged for the bound GDP, which leads to G alpha activation. G alpha then goes on to activate other molecules in the cell. These effects include activating the MAPK and PI3K pathways, as well as inhibition of the Na+/H+ exchanger in the plasma membrane, and the lowering of intracellular Ca2+ levels. Most human GPCRs can be grouped into five main families named; Glutamate, Rhodopsin, Adhesion, Frizzled/Taste2, and Secretin, forming the GRAFS classification system. A series of studies showed that aberrant GPCR Signaling including those for GPCR-PCa, PSGR2, CaSR, GPR30, and GPR39 are associated with tumorigenesis or metastasis, thus interfering with these receptors and their downstream targets might provide an opportunity for the development of new strategies for cancer diagnosis, prevention and treatment. At present, modulators of GPCRs form a key area for the pharmaceutical industry, representing approximately 27% of all FDA-approved drugs. References: [1] Moreira IS. Biochim Biophys Acta. 2014 Jan;1840(1):16-33. -
Research Article Hepatic Gene Expression Profiles Are Altered by Dietary Unsalted Korean Fermented Soybean
Hindawi Publishing Corporation Journal of Nutrition and Metabolism Volume 2011, Article ID 260214, 10 pages doi:10.1155/2011/260214 Research Article Hepatic Gene Expression Profiles Are Altered by Dietary Unsalted Korean Fermented Soybean (Chongkukjang) Consumption in Mice with Diet-Induced Obesity JuRyoun Soh,1 Dae Young Kwon,2 and Youn-Soo Cha1 1 Department of Food Science and Human Nutrition, and Research Institute of Human Ecology, Chonbuk National University, 664-14 Dukjin-Dong 1-Ga, Jeonju 561-756, Republic of Korea 2 Food Functional Research Division, Korean Food Research Institutes, San 46-1, Baekhyun-dong, Bundang-gu, Sungnam-si, Gyeonggi-do 463-746, Republic of Korea Correspondence should be addressed to Youn-Soo Cha, [email protected] Received 30 August 2010; Revised 1 December 2010; Accepted 3 January 2011 Academic Editor: Phillip B. Hylemon Copyright © 2011 JuRyoun Soh et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. We found that Chongkukjang, traditional unsalted fermented soybean, has an antiobesity effect in mice with diet-induced obesity and examined the changes in hepatic transcriptional profiles using cDNA microarray. High-fat diet-induced obese C57BL/6J mice were divided into three groups: normal-diet control group (NDcon, 10% of total energy from fat), high-fat diet control group (HDcon, 45% of total energy from fat), and HDcon plus 40% Chongkukjang (HDC) and were fed for 9 weeks. The HDC group mice were pair-fed (isocalorie) with mice in the HDcon group. -
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 . -
Downloaded from Survive Nursing | Survivenursing.Com V20110426
Generic Stem Stem Definition Examples -abine (see -arabine, -citabine) decitabine -ac Anti-inflammatory agents (acetic acid derivatives) bromfenac; dexpemedolac -acetam See -racetam -actide Synthetic corticotropins seractide -adol or -aldol- Analgesics (mixed opiate receptor agonists/ antagonists) tazadolene; spiradolene; levonantradol -adox Antibacterials (quinoline dioxide derivatives) carbadox -afenone Antiarrhythmics (propafenone derivatives) alprafenone; diprafenone -afil PDE5 inhibitors tadalafil -aj- Antiarrhythmics (ajmaline derivatives) lorajmine -aldrate Antacid aluminum salts magaldrate -algron Alpha1 - and alpha2 - adrenoreceptor agonists dabuzalgron -alol Combined alpha and beta blockers labetalol; medroxalol -amivir (see -vir) -ampa Ionotropic non-NMDA glutamate receptors (AMPA and/or KA receptors) -ampanel Ionotropic non-NMDA glutamate receptors (AMPA and/or KA receptors) ; becampanel antagonists -ampator Ionotropic non-NMDA glutamate receptors (AMPA and/or KA receptors) ; forampator modulators -andr- Androgens nandrolone -anib Angiogenesis inhibitors semaxanib -anserin Serotonin 5-HT2 receptor antagonists altanserin; tropanserin; adatanserin -antel Anthelmintics (undefined group) carbantel -antrone Antineoplastics; anthraquinone derivatives pixantrone -apsel P-selectin antagonists torapsel -arabine Antineoplastics (arabinofuranosyl derivatives) fazarabine; fludarabine aril-, -aril, -aril- Antiviral (arildone derivatives) pleconaril; arildone; fosarilate -arit Antirheumatics (lobenzarit type) lobenzarit; clobuzarit -arol -
Lipoprotein Lipase and Obesity
Vol.4, No.12A, 1405-1412 (2012) Health http://dx.doi.org/10.4236/health.2012.412A203 Lipoprotein lipase and obesity Masataka Kusunoki1*, Kazuhiko Tsutsumi2, Daisuke Sato3, Takao Nakamura3 1Department of Internal Medicine, Medical Clinic, Aichi Medical University, Nagoya, Japan; *Corresponding Author: [email protected] 2Okinaka Memorial Institute for Medical Research, Tokyo, Japan 3Department of Biomedical Information Engineering, Graduate School of Medical Science, Yamagata University, Yamagata, Japan Received 11 October 2012; revised 11 November 2012; accepted 24 November 2012 ABSTRACT stored in adipose tissue. The balance between these competing effects could determine whether increased Obesity is one of the fast-growing major dis- LPL activity will lead to a reduced rate of weight gain or eases in developed and developing countries. to increased adiposity through increased rates of adipose As has been persuasively argued, long-term tissue storage of TG. An imbalance of LPL activity may imbalance between intake and expenditure of fat alter the partitions of plasma TG between muscle and is a central factor in the etiology of obesity. adipose tissue, and thus influence insulin resistance and Obesity aggravates insulin resistance and pro- obesity. motes cardiovascular diseases and atheroscle- Institute of Otsuka Pharmaceutical Factory, Inc. syn- rosis. We hypothesized that elevating lipopro- thesized the LPL activator NO-1886 ([4-(4-bromo-2- tein lipase (LPL) activity in skeletal muscle cyano-phenylcarbamoyl)-benzyl]-phosphonic acid diethyl would cause an improvement of obesity. To test ester, CAS no.: 133208-93-2, generic name: ibrolipim). this hypothesis, we studied the effects of the Hara et al. reported that LPL activator NO-1886 LPL activator NO-1886 in obese animals.