DOCSLIB.ORG

Amgen and UCB Push Forward with Bone-Building Antibody

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Amgen and UCB Push Forward with Bone-Building Antibody April 04, 2012 Amgen and UCB push forward with bone-building antibody Jonathan Gardner Promising mid-stage results for what could be the first bone-building antibody to treat osteoporosis have encouraged two companies that could use a little help from their pipelines to initiate a phase III trial. Amgen the world’s biggest biotech and UCB the Belgian specialty pharma company today announced plans to test AMG 785 (CDP7851) in 5,000 women in a trial that should report in 2015, and show whether the therapy can reduce the incidence of fractures. Introducing an expensive biological into what will be a very genercised market – even Eli Lilly’s bone-building incumbent Forteo will be nearing the end of its market exclusivity by the time the Amgen/UCB antibody can reach prescribing physicians – will be a big ask. Still, Forteo, itself a biological, has been able to carve out blockbuster sales even going up against off-patent drugs by targeting high-risk patients and those intolerant to bisphosphonates, suggesting there is still a place for new treatments. Building bone Bisphosphonates have shown themselves able to improve bone mineral density and reduce the risk of fractures by preventing bone resorption, the process by which mature tissue is removed from the skeleton. By contrast, AMG 785 aims to stimulate bone formation; it does so by inhibiting the action of sclerostin, a protein that inhibits bone formation, on bone morphogenetic proteins. Sclerostin levels are low in patients with sclerosteosis, a disease characterised by excessive bone growth. Likewise, Forteo, or teriparatide, a recombinant form of parathyroid hormone, increases the number and action of bone-building osteoblasts. However, as a more costly once-daily injectable biological, it is indicated in patients with a high risk of fracture, meaning those with multiple risk factors - past fractures or signs of vertebral fractures as well as those who are unable to take other osteoporosis medications. Whilst a largely safe drug, bisphosphonates do have side effects such as oesophagitis, which have raised concerns about the possibility of oesophageal cancer. Forteo itself has a black-box warning for risk of osteosarcoma. Whether AMG 785 will have similar problems is a question that the Amgen/UCB antibody will need to answer among other matters, in a long-term trial. Clarity needed So far, AMG 785 has shown promising data in a six-month phase I/II study, which was associated with a 5% improvement in spinal bone mineral density over six months. In a March 14 note, analysts from Deutsche Bank wrote that based on phase I/II trial results a 10% improvement in bone mineral density could be expected over one year. Comparative numbers are 6-8% per year for Forteo, 2-5% a year for bisphosphonates and 3-5% a year with Amgen’s marketed anti-osteoporosis antibody Prolia. Additionally, Amgen and UCB announced success in a phase II trial a year ago, which pitted the antibody dosed once monthly and once every three months against placebo, Forteo and Fosamax, over one year. The companies announced significant increases in bone mineral density when compared to placebo and that the antibody “compared positively” with the two active treatment arms. No specific numbers have been disclosed yet, however – more detail is expected at the American Society of Bone Mineral Research in October, giving observers few clues as to the efficacy. Mark Schoenebaum, an analyst with ISI Group, noted today that the phase III trial design is for two years of treatment versus three years for Prolia, indicating the companies may be confident of a “giant” benefit in fracture reduction, on a par with Forteo’s 65% reduction. Reinforcing his belief of the confidence that the companies have in AMG 785, Mr Schoenebaum also said it is much smaller than Merck’s trial for bone drug odanacatib, which is enrolling 17,000 (Merck’s odanacatib has high hurdles to clear, September 20, 2011). Should it succeed in the clinic and with regulators, obanacatib probably will not launch until 2015, giving it about two years’ head start on AMG 785. Given its 2015 reporting date, few analysts are willing to attach forecast numbers to the antibody – none of the banks that cover Amgen have sales estimates, and of UCB analysts Morgan Stanley forecasts $295m and Barclays Capital $299m in 2018. The two companies have a worldwide profit-sharing deal. Thus much mystery still surrounds the molecule; its promise may become clearer when data from the 12- month phase II trial is released. Despite the competition and the unknowns, AMG 785 remains one to watch. More from Evaluate Vantage Evaluate HQ 44-(0)20-7377-0800 Evaluate Americas +1-617-573-9450 Evaluate APAC +81-(0)80-1164-4754 © Copyright 2021 Evaluate Ltd..
Load more

Recommended publications
  • We Need Drugs That…
    7/5/2016 Disclosures New Osteoporosis Treatments Mary L. Bouxsein, PhD Advisory Board: Merck, Eli Lilly, Radius Department of Orthopedic Surgery Harvard Medical School, Boston, MA Research funding: Merck, Amgen Consulting fees: Acceleron Pharma, Agnovos What we have today We need drugs that… • Treatments that reduce the risk of vertebral • Maintain or promote bone formation fractures by 50 to 80% • Strengthen cortical bone —> reduce Non‐VFx • Treatments that reduce the risk of non‐vertebral fractures by 20‐25% – Non‐vertebral fracture remain major source of disability • Are convenient for patient • Are cost‐effective % of days of disability due to different • Are safe types of fractures Results from FIT II Cummings et al, JAMA 2006 1 7/5/2016 New treatments, new mechanisms of action Cathepsin K and Bone Resorption • CatK is a lysosomal protease highly expressed in osteoclasts, where it is • Cathepsin K inhibitors released during bone resorption Odanacatib (ODN) • CatK is the major protease responsible for degradation of type I collagen • Anti‐sclerostin antibody Romozosumab • Novel PTH Analogs Abaloparitide (BA‐058) Rodan SB et al. IBMS BoneKey. 2008;5:16–24. Global deletion of Cathepsin K in mice decreases bone resorption but increases bone formation Distal femur Serum CTx WT How can cathepsin K inhibition lead to increased bone formation? WT KO Revisiting the ‘coupled’ process of BFR/BS KO bone remodeling WT KO Pennypacker B. et al., Bone, 2009 2 7/5/2016 Coupling of bone formation & resorption Genetic deletion of CatK in osteoclasts Bone mass Bone resorption OPG “Clastokines” Bone formation RANKL Osteoclast # CON OC CatK KO ) * 2 # Oc MDGFs BFR * (IGF1, TGFß) BFR/TV (%/year) Image courtesy of R.
    [Show full text]
  • Targeting Cathepsin K for the Treatment of Osteoporosis – Focus
    Drugs or :he Future 2010, 35(8): 643-,;49 THOMSON Rf.CJTfRS \' (opvtlght ~ lOIO Prous Sd1.?no:•, SA U. <11 it~ lir.f:>nsor!=. At~ right~ r~~Q1~d CCC: 0.377-Lll82/W10 001: 10 1353/~of.2010 35 8 .152~'l'.2 F{E\/!EW J\f<TICLE TARGETING CATHEPSIN K FOR THE TREATMENT OF OSTEOPOROSIS: FOCUS ON ODANACATIB E.M. Lewiecki New Mexico Clinical Research & Osteoporosis Center, Albuquerque, New Mexico, USA CONTENTS density (BMD) and bone strength are stable. II bone resorption SummJry .......... ....... .. , . .... ..... • ...... ... .643 exceeds bone formation, as occurs in postmenopausat estrogen· deficient women, there is a net loss of bone over time that may ulti· Introduction ........ ........ • .. .... .. • ..... ..... .. .643 mately result in osteoporosis and increased risk of fractures (1) . Cathepsin K inhibitors .......... .. ...... .. .... ... .... .645 Osteoporosis is a common disease associated with increased Conclusions ....... ....... .. .. .. ...... ....... .648 morbidity, increased mortality and high henlthcare costs due to frac­ Referencr.s .......... ..•. .. .... ... • . ... • .. .. , .. .648 tures (2). Bone resorption requires the attachment of an osteoclast to the bone surface by means of a "sealing zone" in order to create a self· SUMMARY contained compartment between the bone surface and the adjacent Cathepsin K is a lysosomal cysteine protease expressed by osteoclasts ruffled border of the osteoclast (3). The acidic microenvironment that degrades type I collagen during the process of bone remodeling. beneath the osteoclast demineralizes the bone and exposes the Postmenopovsal osteoporosis (PMO) is a disease of excessive bone underlylng matrix, which is then degraded through the action of cys­ tvrnover, wit/1 an imbalance between bone resorption and bone formo - teine proteases (4). Since cathepsin K is the most abundant cysteine tion that covses loss of bone strength and increased risk of fractures.
    [Show full text]
  • 10 Jahre UNIVERSUM INNERE MEDIZIN Liebe
    P.b.b. GZ02Z031655M, Benachrichtigungspostamt 1070 Wien unDie Fachzeitschrift versum der Österreichischen Gesellschaft für Innere Medizin InnereMedizinInnereMedizin Sonderausgabe aus Anlass des 10-jährigen Bestehens von UNIVERSUM INNERE MEDIZIN Österreichische Gesellschaft für Innere Medizin www.oegim.at 1010 Jahre Jahre InnereInnere MedizinMedizin FortschritteFortschritte undund KontroversenKontroversen ausaus derder Jubiläums-PerspektiveJubiläums-Perspektive MedMedia Falls unzustellbar,Falls bitte retour an:Verlag, MEDMEDIA 1.1, Seidengasse 9/Top Wien 1070 Verlags Ges.m.b.H. Fachkurzinformation siehe Seite 68 GRUSSWORT DES HERAUSGEBERS o. Univ.-Prof. Dr. Günter j. Krejs Herausgeber Universum Innere Medizin 10 Jahre UNIVERSUM INNERE MEDIZIN Relevanz und Aktualität zu bieten. Dafür danken wir ganz diese 10 Jahre, die hinter uns liegen, und helfen Sie mit, herzlich allen unseren vielen Autoren. dass UNIVERSUM INNERE MEDIZIN auch in der Zukunft Es ist ein besonderer Anlass und es erfüllt uns mit Freude, In dieser Jubiläumsausgabe haben Sie einen breiten Quer- erfolgreich sein wird. dass wir auf den Erfolg dieser letzten Jahre zurückblicken schnitt dessen, was wir in den verschiedensten Sparten dürfen. Eine große Zahl von Ärzten und Spezialisten aus den publiziert haben. Ich bin sicher, Sie werden diese Ihr verschiedensten Bereichen haben dazu beigetragen, Sie Jubiläumsausgabe mit Vergnügen lesen. Sie kommt auch immer sehr prompt über neueste Entwicklungen und neue- rechtzeitig zur 40. Jahrestagung der Österreichischen ste Diagnostik und Therapie zu informieren. Die kurze Zeit Gesellschaft für Innere Medizin, für die UNIVERSUM INNERE vom Erstellen der Manuskripte bis zum Druck (durch- MEDIZIN ein Eckpfeiler der Publikationen der Gesellschaft schnittlich 6 Wochen) erlaubt es, Information von größter wurde. Autoren und Leser, freuen Sie sich mit uns über o.
    [Show full text]
  • Efficacy of a Cathepsin K Inhibitor in a Preclinical Model for Prevention and Treatment of Breast Cancer Bone Metastasis
    Author Manuscript Published OnlineFirst on September 23, 2014; DOI: 10.1158/1535-7163.MCT-14-0253 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Efficacy of a Cathepsin K Inhibitor in a Preclinical Model for Prevention and Treatment of Breast Cancer Bone Metastasis Le T. Duong1, Gregg A. Wesolowski, Patrick Leung, Renata Oballa*, Maureen Pickarski Merck & Co. Inc., Whitehouse Station, NJ, USA. Running Title: Cathepsin K inhibitor for metastatic bone disease Keywords: Cathepsin K inhibitor, osteoclast, metastatic bone disease, osteolysis, breast cancer. 1Author for correspondence: Le T. Duong, Ph.D. Bone Biology Merck & Co., Inc. 770 Sumneytown Pike West Point, PA 19486, USA Tel. 215-652-7574 Fax: 215-652-4328 E-mail: [email protected] Funding Statement - This study was funded by Merck & Co., Whitehouse Station, NJ, USA Downloaded from mct.aacrjournals.org on September 27, 2021. © 2014 American Association for Cancer Research. Author Manuscript Published OnlineFirst on September 23, 2014; DOI: 10.1158/1535-7163.MCT-14-0253 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Cathepsin K inhibitor for metastatic bone disease Le T. Duong Bone Biology Merck & Co., Inc. 770 Sumneytown Pike West Point, PA 19486, USA Tel. 215-652-7574 Fax: 215-652-4328 E-mail: [email protected] Gregg A. Wesolowski Bone Biology Merck & Co., Inc. 770 Sumneytown Pike West Point, PA 19486, USA E-mail: [email protected] Patrick Leung Bone Biology Merck & Co., Inc. 770 Sumneytown Pike West Point, PA 19486, USA E-mail: [email protected] *Renata Oballa Inception Sciences Canada Inc.
    [Show full text]
  • Odanacatib: a Possible New Therapeutic Option for the Treatment of Osteoporosis
    Drug Evaluation Odanacatib: a possible new therapeutic option for the treatment of osteoporosis Cathepsin K is a protease released by osteoclasts, which is involved in the destruction of collagen fibers that form the organic phase of the bone matrix, and plays a key role in bone resorption. Odanacatib is a selective inhibitor of cathepsin K, which blocks bone remodeling by inhibiting resorption. Phase II trials have shown that odanacatib is a potent antiresorptive agent and does not significantly reduce biochemical markers of bone formation during long-term treatment of postmenopausal women. This increases the bone mineral density that is comparable with the most powerful antiresorptive agents. Odanacatib has a generally favorable tolerability and safety profile. Currently, only Phase II studies have been reported and its efficacy in reducing fractures has not been demonstrated. The adverse effects are reversible and disappear after discontinuation. If this antifracture efficacy can be shown, odanacatib could be a safe, efficacious option for the treatment of osteoporosis. KEYWORDS: cathepsin K n odanacatib n osteoclast n osteoporosis José Luis Pérez-Castrillón*1,2, Florentino Pinacho3, Throughout life, bone remodeling maintains the gene that codes for cathepsin K, causing an Marta Ruiz-Mambrilla4 the structure of bone tissue, leading to changes increase in BMD, low stature, cranial deformi- & Antonio Dueñas Laita3 in bone density, shape and strength that allow ties and acroosteolysis of the distal phalanges 1Internal Medicine Department, it to adapt to biomechanical circumstances at [4]. In addition to osteoclasts, osteocytes secrete Rio Hortega University Hospital, Faculty of Medicine, Valladolid, Spain any given time. This remodeling occurs both in cathepsin K, although their function remains 2Institute of Endocrinology & Nutrition cortical bone, which is responsible for load bear- unknown.
    [Show full text]
  • Odanacatib, a Cathepsin K Inhibitor for the Treatment of Osteoporosis and Other Skeletal Disorders Associated with Excessive Bone Remodeling E Michael Lewiecki
    !Drugs 200912(12):7~()-809 (~ Tliornso11 Reuters (Scientific) ltd ISSN 2040· 3410 DRUC PROFILE Odanacatib, a cathepsin K inhibitor for the treatment of osteoporosis and other skeletal disorders associated with excessive bone remodeling E Michael Lewiecki Address New Mexico Clinic.ii Research & Osteoporosis Center, 300 Oak Street NE, Albuquerque, NM 87106, USA !:mail: lewiecki@aolcorn Odanacatib (MK·0822, MK-822) is an orally administered cathepsin K inhibitor being developed by Merck & Co Inc, under license from Ce/era Croup, for the treatment of osteoporosis and bone metastases. Cathepsin K, a lysosomol cysteine protease that is expressed by osteoclasts during the process of bone resorption, acts as the major col/agenase responsible for the degradation of the organic bone matrix during the bone remodeling process. Because excessive bone remodeling is a key element in the pathogenesis of postmenopousal osteoporosis and other skeletal disorders, cathepsin K is a potential target for therapeutic intervention. In a phase II clinical trial, weekly doses of odanacatib increased bone mineral density (BMD) and reduced bone turnover markers in postmenopausol women with low BMD. No tolerability concerns or evidence of skeletol toxicity were reported. Phase Ill trials, including a trial to evaluate the effects of odanocatib on froctt1re risk in up to 20,000 women with postmenopausol osteoporosis, were ongoing or recruiting participants at the time of publication. Odanacatib is a promising agent for the management of postmenopausal osteoporosis and other skeletal disorders associated with excessive bone remade/Ing. Introduction Therapeutic Odanacatib Osteoporosis is a common skeletal disease characterized by low bone mineral density (BMD) and poor bone quality Originator Celera Group that reduces bone strength and increases the risk of fractures [506066].
    [Show full text]
  • Der Einfluss Der VO (EG) 1901/2006 Auf Den Off-Label Use in Der Neonatologie“
    DIPLOMARBEIT / DIPLOMA THESIS Titel der Diplomarbeit / Title of the Diploma Thesis „Der Einfluss der VO (EG) 1901/2006 auf den Off-Label Use in der Neonatologie“ verfasst von / submitted by Stefanie Bub angestrebter akademischer Grad / in partial fulfilment of the requirements for the degree of Magistra der Pharmazie (Mag.pharm.) Wien, 2016 / Vienna, 2016 Studienkennzahl lt. Studienblatt / A 449 degree programme code as it appears on the student record sheet: Studienrichtung lt. Studienblatt / Diplomstudium Pharmazie degree programme as it appears on the student record sheet: Betreut von / Supervisor: Ao. Univ.-Prof. Mag. Dr. Rosa Lemmens Danksagung Als erstes möchte ich mich bei Frau Prof. Dr. Rosa Lemmens für die Betreuung meiner Diplomarbeit bedanken. Durch sie war es mir erst möglich, dieses Thema zu behandeln und meine Interessen zu verwirklichen. Ganz besonders möchte ich auch Dr. Andreas Doschek für seine jahrelange Unterstützung in diesem Studium danken. Abgesehen von den abertausenden Kopien und Ausdrucken, die er mir und meinen MitstudentInnen zur Verfügung gestellt hat, hat er mir vor jeder Prüfung den Rücken freigehalten, mich abgeprüft und mir so das Studium sehr erleichtert. Ihm habe ich auch das Interesse für die Materie des Arzneimittelrechts zu verdanken, weswegen ich mich für dieses Thema in meiner Abschlußarbeit entschieden habe. Meiner Familie und meinen Freunden danke ich für die Motivation und die guten Ratschläge und meinen MitstudentInnen für eine wundervolle Zeit. Danke! Wien, September 2016 I II Inhaltsverzeichnis Seite 1. Einführung 1 2. Grundlagen der zulassungsüberschreitenden Arzneimittelanwendung 4 2.1. Begriffsdefinitionen 4 2.1.1. Random controlled trial (RCT) 4 2.1.2. Pharmakokinetik-Studien 4 2.1.3.
    [Show full text]
  • Richard Eastell1, Eric Vittinghoff2, Li-Yung Lui3, Charles E
    Surrogate threshold effect: a novel approach for potential approval of new osteoporosis treatments using change in BMD. Study-level analysis from the FNIH Bone Quality Project • Richard Eastell1, Eric Vittinghoff2, Li-Yung Lui3, Charles E. McCulloch2, Fernando Marin4, Anne de Papp5, Arkadi Chines6, Sundeep Khosla7, Jane A. Cauley8, Douglas C. Bauer2, Mary Bouxsein9, Dennis M. Black2 For the FNIH Bone Quality Project 1 University of Sheffield, 2 University of California, San Francisco, 3 California Pacific Medical Center, 4 Eli Lilly and Co., 5 Merck & Co., Inc., Kenilworth, NJ USA, 6 Amgen Inc., Thousand Oaks, CA, 7 Mayo Clinic Center for Clinical and Translational Science, 8 Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, 9 Center for Advanced Orthopedic Studies, Beth Israel Deaconess Medical Center and Harvard Medical School. Disclosures • Consultancy funding from IDS, Roche Diagnostics, GSK Nutrition, Mereo, Lilly, Sandoz, Nittobo, Abbvie, Samsung, Haoma Medica, CL Bio, and Viking • Grant funding from Nittobo, IDS, Roche, Amgen and Alexion Background • Change in dual-energy X-ray absorptiometry (DXA) bone mineral density (BMD) o May be a useful surrogate for fracture endpoints o Could enable much smaller and shorter clinical trials for new drug approvals in osteoporosis • The difference in the change in total hip BMD between active and placebo groups is strongly related to fracture risk reduction with osteoporosis treatments (1) • What BMD increase would predict a fracture benefit? o Such knowledge
    [Show full text]
  • A Selective Cathepsin K Inhibitor for the Treatment of Osteoporosis
    DiscoveryDiscovery andand developmentdevelopment ofof odanacatib:odanacatib: AA selectiveselective cathepsincathepsin KK inhibitorinhibitor forfor thethe treatmenttreatment ofof osteoporosisosteoporosis Shawn J. Stachel On behalf of the odanacatib discovery and product development teams Merck Research Laboratories 8th RSC-SCI Symposium on Proteinase Inhibitor Design April 16, 2013 1 AcknowledgementsAcknowledgements Biology Chemistry Process Chemistry Bone Biology (WP) Christine Brideau Kevin Bateman Paul O’Shea Don Kimmel Wanda Cromlish Christopher Bayly Dean Bender Sevgi Rodan Sylvie Desmarais Cameron Black Mirlinda Biba Gideon Rodan Jean-Pierre Falgueyret Michael Boyd Jennifer Chilenski Le Duong Louis-Jacques Fortin Nathalie Chauret Jimmy DaSilva Pat Masarachia Sonia Lamontagne Sheldon Crane Rich Desmond Brenda Pennypacker France Landry Stephen Day Paul Devine Maureen Pickarski Frederic Masse Jacques Yves Gauthier Pete Dormer Gregg Wesolowski Dave Percival Robert Houle Bruce Foster Ya Zhuo Denis Riendeau Elise Isabel Don Guathier Pharmaceutical R&D Paul Tawa C.K. Lau Danny Gauvreau Cynthia Bazin Jennifer Wang Serge Leger Francis Gosselin Sophie-Dorothee Clas Comp. Med. Tammy LeRiche Derek Henderson Elizabeth Kwong Stephanie Alleyn Jean-Francois Levesque Greg Hughes Pauline Luk Liette Belair Chun-Sing Li John Leazer Rafik Naccache Joel Bosquet Christophe Mellon Bill Leonard Wayne Parent Carl Brière Renata Oballa John Limanto Suzanne Spagnoli Nancy Kelly Joel Robichaud Christian Nadeau Dendi Susanto Gayle Lapointe Bruno Roy Thorsten Rosner Hongshi Yu Mira Lavoie John Scheigetz Kara Rubin Safety Assessment Sonia Lesvesque Carmai Seto Ali Shafiee Laura Gumprecht Denis Normandin Michel Therien Veena Upadhyay Cindy Fishman Karen Ortega Laird Trimble Chris Welch Pharmacology Roberta Rasori Jean-Francois Truchon Clinical Development Sylvie Toulmond Josianne Rozon Vouy-Linh Truong Aubrey Stoch Tony Lombardi Wayne Sturkenboom Qingping Wang Deborah Miller Albert Leung Celera Simon Wong 2 Osteoporosis:Osteoporosis: AA ContinuingContinuing DiseaseDisease BurdenBurden .
    [Show full text]
  • 507 Update 8/25/2018
    1 Legacy Biomarker Qualification Project Status Update Administrative Information Requesting Organization Name: Biomarkers Consortium, Foundation for the National Institutes of Health (FNIH) Address: 11400 Rockville Pike, Suite 600, North Bethesda, MD 20852 Phone: (301) 402-5311 Email: [email protected] Website: https://fnih.org/what-we-do/biomarkers-consortium Primary Contact Name: Tania Kamphaus, PhD – Scientific Program Manager, Metabolic Disorders; and Joseph Menetski, PhD – Associate Vice President of Research Partnerships Address: 11400 Rockville Pike, Suite 600, North Bethesda, MD 20852 Phone (301) 435-6247; (301) 594-6596 Email: [email protected]; [email protected] Alternate Contact Name: Dennis Black, PhD Address: Department of Epidemiology and Biostatistics, UCSF; 550 16th St., San Francisco, CA 94158 Phone: (415) 378-7144 Email: [email protected] Submission Date (MM/DD/YYYY): ____________________4/26/16____________________________ 1 The content you provide in this completed Status Update will be publicly posted as part of the section 507 transparency provisions. 1 I. Context of Use A. Biomarker Category Proportional change in dual-energy x-ray absorptiometry (DXA) bone mineral density (BMD) can be used to predict outcomes of hip fracture. We propose that results from DXA BMD scans in subjects at risk for hip and non-vertebral fracture can be a quantitative surrogate endpoint for response to investigational anti-osteoporosis drug treatments. B. Intended Use in Drug Development In order to facilitate development of additional
    [Show full text]
  • Management of Osteoporosis in Postmenopausal Women: 2010 Position Statement of the North American Menopause Society
    Menopause: The Journal of The North American Menopause Society Vol. 17, No. 1, pp. 23/24 DOI: 10.1097/gme.0b013e3181cdd4a7 * 2010 by The North American Menopause Society 5 Text printed on acid-free paper NAMS continuing medical education activity Management of osteoporosis in postmenopausal women: 2010 position statement of The North American Menopause Society This position statement, which begins on page 25, has been COMMERCIAL SUPPORT designated a continuing medical education (CME) activity from The CME activity is supported by an unrestricted educa- The North American Menopause Society (NAMS). tional grant from the Alliance for Better Bone Health, a collaboration between Warner Chilcott plc and its affiliates GOAL and sanofi-aventis (US). To demonstrate an increase in, or affirmation of, current knowledge regarding the management of osteoporosis in ACKNOWLEDGMENTS postmenopausal women. NAMS appreciates the contributions of the following members of the Osteoporosis Editorial Board: Sydney L. Bonnick, MD, FACP, LEARNING OBJECTIVES Medical Director, Clinical Research Center of North Texas, Adjunct After reading this position statement, participants should Professor, Departments of Biology and Kinesiology, University of be able to: North Texas, Denton, TX; Steven T. Harris, MD, FACP, Clinical Professor of Medicine, University of California, San Francisco, San & Describe the effect of menopause and aging on bone Francisco, CA; David L. Kendler, MD, FRCPC, Associate Professor health. of Medicine, University of British Columbia, Vancouver, BC, Canada; Michael R. McClung, MD, Director, Oregon Osteoporosis & Identify risk factors that contribute to fracture risk. Center, Portland, OR; and Stuart L. Silverman, MD, FACP, FACR, & Discuss the assessments of risk factors for fracture and Attending Physician, Cedars-Sinai Medical Center, Clinical Professor how to rule out secondary causes of osteoporosis.
    [Show full text]
  • The Development of Molecular Biology of Osteoporosis
    International Journal of Molecular Sciences Review The Development of Molecular Biology of Osteoporosis Yongguang Gao 1,*,† , Suryaji Patil 2,† and Jingxian Jia 1 1 Tangshan Key Laboratory of Green Speciality Chemicals, Department of Chemistry, Tangshan Normal University, Tangshan 063000, China; [email protected] 2 Lab for Bone Metabolism, School of Life Sciences, Northwestern Polytechnical University, Xi’an 710072, China; [email protected] * Correspondence: [email protected]; Tel.: +86-18189262029 † These authors contributed equally to this work. Abstract: Osteoporosis is one of the major bone disorders that affects both women and men, and causes bone deterioration and bone strength. Bone remodeling maintains bone mass and mineral homeostasis through the balanced action of osteoblasts and osteoclasts, which are responsible for bone formation and bone resorption, respectively. The imbalance in bone remodeling is known to be the main cause of osteoporosis. The imbalance can be the result of the action of various molecules produced by one bone cell that acts on other bone cells and influence cell activity. The understanding of the effect of these molecules on bone can help identify new targets and therapeutics to prevent and treat bone disorders. In this article, we have focused on molecules that are produced by osteoblasts, osteocytes, and osteoclasts and their mechanism of action on these cells. We have also summarized the different pharmacological osteoporosis treatments that target different molecular aspects of these bone cells to minimize osteoporosis. Keywords: osteoporosis; bone remodeling; osteoblasts; osteocytes; osteoclasts; bone therapeutics Citation: Gao, Y.; Patil, S.; Jia, J. The Development of Molecular Biology of Osteoporosis. Int.
    [Show full text]