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LHRH) Antagonist Cetrorelix and LHRH Agonist Triptorelin on the Gene Expression of Pituitary LHRH Receptors in Rats
Comparison of mechanisms of action of luteinizing hormone-releasing hormone (LHRH) antagonist cetrorelix and LHRH agonist triptorelin on the gene expression of pituitary LHRH receptors in rats Magdolna Kovacs*†‡ and Andrew V. Schally*†§ *Endocrine, Polypeptide, and Cancer Institute, Veterans Affairs Medical Center, New Orleans, LA 70112; and †Section of Experimental Medicine, Department of Medicine, Tulane University School of Medicine, New Orleans, LA 70112 Contributed by Andrew V. Schally, August 21, 2001 The mechanisms through which luteinizing hormone (LH)-releasing however, are different. LHRH agonists achieve the inhibition of hormone (LHRH) antagonists suppress pituitary gonadotroph func- gonadotropin secretion after a period of continuous exposure (1, tions and LHRH-receptor (LHRH-R) expression are incompletely un- 2, 11–14). In contrast, antagonists of LHRH produce a compet- derstood. Consequently, we investigated the direct effect of LHRH itive blockade of LHRH-R and cause an immediate cessation of antagonist cetrorelix in vitro on the expression of the pituitary the release of gonadotropins and sex steroids, reducing the time LHRH-R gene and its ability to counteract the exogenous LHRH and of the onset of therapeutic effects as compared with the agonists the agonist triptorelin in the regulation of this gene. We also com- (1, 2, 15–17). LHRH agonists such as triptorelin, leuprolide, pared the effects of chronic administration of cetrorelix and triptore- buserelin, or goserelin (1, 2, 14) have been used worldwide for lin on the LHRH-R mRNA level and gonadotropin secretion in ovari- nearly two decades, but LHRH antagonists such as cetrorelix, ectomized (OVX) and normal female rats. The exposure of pituitary ganirelix, and Abarelix have been introduced into the clinical cells in vitro to 3-min pulses of 1 nM LHRH or 0.1 nM triptorelin for 5 h practice relatively recently (1, 2, 15, 16). -
Degarelix for Treating Advanced Hormone- Dependent Prostate Cancer
CONFIDENTIAL UNTIL PUBLISHED NATIONAL INSTITUTE FOR HEALTH AND CARE EXCELLENCE Final appraisal determination Degarelix for treating advanced hormone- dependent prostate cancer This guidance was developed using the single technology appraisal (STA) process 1 Guidance 1.1 Degarelix is recommended as an option for treating advanced hormone-dependent prostate cancer, only in adults with spinal metastases who present with signs or symptoms of spinal cord compression. 1.2 People currently receiving treatment initiated within the NHS with degarelix that is not recommended for them by NICE in this guidance should be able to continue treatment until they and their NHS clinician consider it appropriate to stop. 2 The technology 2.1 Degarelix (Firmagon, Ferring Pharmaceuticals) is a selective gonadotrophin-releasing hormone antagonist that reduces the release of gonadotrophins by the pituitary, which in turn reduces the secretion of testosterone by the testes. Gonadotrophin- releasing hormone is also known as luteinising hormone-releasing hormone (LHRH). Because gonadotrophin-releasing hormone antagonists do not produce a rise in hormone levels at the start of treatment, there is no initial testosterone surge or tumour stimulation, and therefore no potential for symptomatic flares. National Institute for Health and Care Excellence Page 1 of 71 Final appraisal determination – Degarelix for treating advanced hormone-dependent prostate cancer Issue date: April 2014 CONFIDENTIAL UNTIL PUBLISHED Degarelix has a UK marketing authorisation for the ‘treatment of adult male patients with advanced hormone-dependent prostate cancer’. It is administered as a subcutaneous injection. 2.2 The most common adverse reactions with degarelix are related to the effects of testosterone suppression, including hot flushes and weight increase, or injection site reactions (such as pain and erythema). -
Degarelix Acetate (Firmagon) Reference Number: PA.CP.PHAR.170 Effective Date: 01/18 Last Review Date: 10/18 Revision Log
Clinical Policy: Degarelix Acetate (Firmagon) Reference Number: PA.CP.PHAR.170 Effective Date: 01/18 Last Review Date: 10/18 Revision Log Description The intent of the criteria is to ensure that patients follow selection elements established by Pennsylvania Health and Wellness® clinical policy for the use of Degarelix Acetate (Firmagon®). FDA Approved Indication(s) Firmagon is indicated for treatment of advanced prostate cancer. Policy/Criteria It is the policy of Pennsylvania Health and Wellness that Firmagon is medically necessary when the following criteria are met: I. Initial Approval Criteria A. Prostate Cancer (must meet all): 1. Diagnosis of prostate cancer; 2. Prescribed by or in consultation with an oncologist; 3. Request meets one of the following (a, b or c): a. Starting dose does not exceed 240 mg given as two injections of 120 mg each; b. Maintenance dose does not exceed 80 mg as a single injection per 28 days; c. Dose is supported by practice guidelines or peer-reviewed literature for the relevant off- label use (prescriber must submit supporting evidence). Approval duration: 12 months B. Other diagnoses/indications: Refer to PA.CP.PMN.53 1. The following NCCN recommended uses for Firmagon, meeting NCCN categories 1, 2a, or 2b, are approved per the PA.CP.PMN.53: II. Continued Approval A. Prostate Cancer (must meet all): 1. Currently receiving medication via Pennsylvania Health and Wellness benefit or member has previously met approval criteria or the Continuity of Care policy (PA.LTSS.PHAR.01) applies; 2. Member is responding positively to therapy; 3. If request is for a dose increase, request meets one of the following: a. -
Follicular and Endocrine Profiles Associated with Different Gnrh
Reproductive BioMedicine Online (2012) 24, 153– 162 www.sciencedirect.com www.rbmonline.com ARTICLE Follicular and endocrine profiles associated with different GnRH-antagonist regimens: a randomized controlled trial Juan Antonio Garcı´a-Velasco a, Sanja Kupesic b, Antonio Pellicer c, Claire Bourgain d, Carlos Simo´n e, Milan Mrazek f, Paul Devroey g, Joan-Carles Arce h,* a IVI Foundation, Reproductive Endocrinology, Madrid, Spain; b Texas Tech University Health Sciences Center, Department of Obstetrics and Gynecology, El Paso, TX, USA; c IVI Foundation, Reproductive Endocrinology, Valencia, Spain; d UZ Brussel, Department of Pathology, Brussels, Belgium; e IVI Foundation, Research Department, Valencia, Spain; f ISCARE IVF a.s., Lighthouse, Prague, Czech Republic; g UZ Brussel, Centre for Reproductive Medicine, Brussels, Belgium; h Reproductive Health, Global Clinical and Non-Clinical R & D, Ferring Pharmaceuticals, Copenhagen, Denmark * Corresponding author. E-mail address: [email protected] (J.-C. Arce). Dr Juan Garcı´a-Velasco did his training in obstetrics and gynaecology at Madrid Autonoma University, and then his reproductive endocrinology and infertility fellowship at Yale University, USA (1997–1998). He is now Director of IVI-Madrid and Associate Professor at Rey Juan Carlos University. He has published over 100 peer- reviewed articles. He is an ad-hoc reviewer for the main journals in the field and serves on the editorial board of Reproductive BioMedicine Online. His main research interests are endometriosis, ovarian hyperstimulation syndrome, low responders and human implantation. Abstract This trial assessed the impact of early initiation of gonadotrophin-releasing hormone (GnRH) antagonist on follicular and endocrine profiles compared with the fixed GnRH-antagonist protocol. -
Gnrh Antagonists Have Direct Inhibitory Effects on Castration-Resistant Prostate
Author Manuscript Published OnlineFirst on July 24, 2019; DOI: 10.1158/1535-7163.MCT-18-1337 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. GnRH antagonists have direct inhibitory effects on castration-resistant prostate cancer via intracrine androgen and AR-V7 expression. Vito Cucchiara1*, Joy C. Yang1*, Chengfei Liu1, Hans H. Adomat2, Emma S. Tomlinson Guns2, Martin E. Gleave2, Allen C. Gao1,3, Christopher P. Evans1,3 1Department of Urologic Surgery, University of California at Davis, Sacramento, California. 2Vancouver Prostate Centre, University of British Columbia, Vancouver, BC, Canada 3UC Davis Comprehensive Cancer Center, University of California Davis, California. Running title: GnRH antagonist inhibits intracrine androgen and AR-V7 Keywords: Prostate Cancer, ADT, GnRH antagonist, intracrine androgen Financial Support: This work is supported in part by grants DOD PC150040P1 and Ferring Pharmaceuticals to CP Evans. Conflicts of Interest: Research support from Ferring to CPE and JCY. All other authors have no conflicts of interest. Corresponding Author: Christopher P. Evans, MD, FACS Professor and Chairman, Department of Urology Urologic Surgical Oncology University of California, Davis, School of Medicine 4860 Y St., Suite 3500 Sacramento, CA 95817 academic office tel # (916)734-7520 academic office fax # (916)734-8094 email: [email protected] *These authors contributed equally to this work Downloaded from mct.aacrjournals.org on October 6, 2021. © 2019 American Association for Cancer Research. Author Manuscript Published OnlineFirst on July 24, 2019; DOI: 10.1158/1535-7163.MCT-18-1337 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. -
WO 2009/137104 Al
(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 12 November 2009 (12.11.2009) WO 2009/137104 Al (51) International Patent Classification: (81) Designated States (unless otherwise indicated, for every A61K 31/137 (2006.01) A61K 31/5685 (2006.01) kind of national protection available): AE, AG, AL, AM, A61K 31/138 (2006.01) A61P 35/00 (2006.01) AO, AT, AU, AZ, BA, BB, BG, BH, BR, BW, BY, BZ, A61K 31/4196 (2006.01) CA, CH, CN, CO, CR, CU, CZ, DE, DK, DM, DO, DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, HN, (21) International Application Number: HR, HU, ID, IL, IN, IS, JP, KE, KG, KM, KN, KP, KR, PCT/US2009/002885 KZ, LA, LC, LK, LR, LS, LT, LU, LY, MA, MD, ME, (22) International Filing Date: MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, 7 May 2009 (07.05.2009) NZ, OM, PG, PH, PL, PT, RO, RS, RU, SC, SD, SE, SG, SK, SL, SM, ST, SV, SY, TJ, TM, TN, TR, TT, TZ, UA, (25) Filing Language: English UG, US, UZ, VC, VN, ZA, ZM, ZW. (26) Publication Language: English (84) Designated States (unless otherwise indicated, for every (30) Priority Data: kind of regional protection available): ARIPO (BW, GH, 61/127,025 9 May 2008 (09.05.2008) US GM, KE, LS, MW, MZ, NA, SD, SL, SZ, TZ, UG, ZM, ZW), Eurasian (AM, AZ, BY, KG, KZ, MD, RU, TJ, (71) Applicant (for all designated States except US): RA¬ TM), European (AT, BE, BG, CH, CY, CZ, DE, DK, EE, DIUS HEALTH, INC. -
April 16,2004 Steve E. Phurrough, MD, MPA Office of Clinical Standards & Quality Centers for Medicare and Medicaid Services
April 16,2004 Steve E. Phurrough, MD, MPA Office of Clinical Standards & Quality Centers for Medicare and Medicaid Services 7500 Security Boulevard Mail Stop C1-09-06 Baltimore, MD 21244-1850 Dear Dr. Phurrough: This is a formal request for a national coverage determination ("NCD") on the use of Plenaxis™ (abarelix for injectable suspension) under the Medicare program. This request is being made pursuant to NCD development Track #1 - Requests for New National Coverage Determinations Initiated by Any Party, Including Beneficiaries, Manufacturers, Providers, or Suppliers. We believe that Plenaxis meets the qualifications for coverage in the Medicare benefit category of "drugs or biologicals," as defined under § 1861(t)(1) of the Social Security Act. Plenaxis (abarelix for injectable suspension) is a synthetic decapeptide with potent antagonistic activity against naturally occurring gonadotropin releasing-hormones (GnRH). It is the only GnRH antagonist ever to have been approved by the Food and Drug Administration ("FDA") as a treatment for prostate cancer. Specifically, Plenaxis was first approved by FDA on November 25, 2003 for the palliative treatment of men with advanced symptomatic prostate cancer, in whom LHRH agonist therapy is not appropriate and who refuse surgical castration, and have one or more of the following: (1) risk of neurological compromise due to metastases, (2) ureteral or bladder outlet obstruction due to local encroachment or metastatic disease, or (3) severe bone pain from skeletal metastases persisting on narcotic analgesia. On March 31, 2004, Plenaxis was approved for inclusion in the United States Pharmacopeia Drug Information.® Enclosed you will find three copies of a two compact disc ("CD") set containing the supporting documentation for this NCD request. -
214621Orig1s000
CENTER FOR DRUG EVALUATION AND RESEARCH APPLICATION NUMBER: 214621Orig1s000 MULTI-DISCIPLINE REVIEW Summary Review Office Director Cross Discipline Team Leader Review Clinical Review Non-Clinical Review Statistical Review Clinical Pharmacology Review NDA/BLA Multi-disciplinary Review and Evaluation: NDA 214, 621 Relugolix NDA/BLA Multi-disciplinary Review and Evaluation Disclaimer: In this document, the sections labeled as “The Applicant’s Position” are completed by the Applicant, which do not necessarily reflect the positions of the FDA. Application Type NDA Application Number(s) NDA 214621 Priority or Standard Priority Submit Date(s) April 20, 2020 Received Date(s) April 20, 2020 PDUFA Goal Date December 20, 2020 Division/Office OND/CDER/OOD/DO1 Review Completion Date Established Name Relugolix (b) (4) (Proposed) Trade Name Pharmacologic Class Gonadotropin-releasing hormone (GnRH) receptor antagonist Code name TAK-385 Applicant Myovant Sciences, Inc. Formulation(s) oral tablet Dosing Regimen One time loading dose of 360 mg followed by 120 mg daily Applicant Proposed RELUGOLIX is a gonadotropin-releasing hormone Indication(s)/Population(s) (GnRH) antagonist indicated for the treatment of patients with advanced prostate cancer. Recommendation on Regular approval Regulatory Action Recommended RELUGOLIX is a gonadotropin-releasing hormone Indication(s)/Population(s) (GnRH) antagonist indicated for the treatment of (if applicable) patients with advanced prostate cancer. 1 Version date: January 2020 (ALL NDA/ BLA reviews) Disclaimer: In this document, the sections labeled as “The Applicant’s Position” are completed by the Applicant and do not necessarily reflect the positions of the FDA. Reference ID: 4719259 NDA/BLA Multi-disciplinary Review and Evaluation: NDA 214, 621 Relugolix Table of Contents Reviewers of Multi-Disciplinary Review and Evaluation .................................................. -
LHRH Analogues and Degarelix for Treatment of Prostate Cancer – Sorted by Drug
LHRH analogues and degarelix for treatment of prostate cancer – sorted by drug Drug Degarelix Goserelin Leuprorelin Triptorelin Drug & Dose Degarelix Goserelin Goserelin Leuprorelin Leuprorelin Leuprorelin Leuprorelin Triptorelin Triptorelin Triptorelin Triptorelin 80mg 3.6mg 10.8mg 3.75mg 3.75mg 11.25mg 22.5mg 3mg 3.75mg 11.25mg 22.5mg Administration Monthly 28 days 12 weekly Monthly Monthly 3 monthly 3 monthly 28 days 4 weekly 3 monthly 6 monthly interval Brand Name Firmagon Zoladex Zoladex Lutrate Prostap SR Prostap 3 Lutrate 3 Decapeptyl Gonapeptyl Decapeptyl Decapeptyl LA Depot DCS DCS month SR Depot SR SR 3.75mg Depot Form Powder with Implant in Implant in Powder for Powder plus Powder plus Powder for Powder for Powder for Powder for Powder for a prefilled prefilled prefilled suspension solvent in solvent in suspension suspension suspension suspension suspension syringe syringe syringe with diluent prefilled prefilled with diluent with diluent with vehicle with diluent with diluent containing in syringe syringe syringe syringe (in ampoule) filled (in ampoule) (in solvent. syringe ampoule) Administration Monthly 28 days 12 weekly Monthly Monthly 3 monthly 3 monthly 28 days 4 weekly 3 monthly 6 monthly interval Needle safety No Yes Yes Yes Yes Yes No No No No No device Needle size 25 gauge 16 gauge 14 gauge 20 gauge 23 gauge 23 gauge 20 gauge 20 gauge 21 gauge 20 gauge 20 gauge Injection route Deep S/C S/C S/C I/M S/C or I/M S/C I/M I/M S/C or I/M I/M I/M Injection site Abdomen Anterior Anterior Upper outer Arm, thigh Arm, thigh Upper outer Buttock SC (e.g. -
The Role of the FSH System in the Development and Progression of Prostate Cancer
· PROSTATE CANCER · The Role of the FSH System in the Development and Progression of Prostate Cancer E. David Crawford, MD, Kyle O. Rove, MD, Andrew V. Schally, PhD, MDhc (Multi), DSc,hc, Ferenc G. Rick, MD, PhD, Norman L. Block, MD, Thomas J.R. Beveridge, PhD, David N. Dahdal, PhD, and Dennis C. Marshall, RN, MS, PhD Abstract the term FSH system to encompass all aspects of FSH, including This article describes relationships between follicle- the synthesis, release, and circulating levels of FSH itself, as well stimulating hormone (FSH), vascular endothelial growth as its receptor and receptor signaling. factor (VEGF), and other modulators of prostatic cancer, in order to help optimize treatment decisions. A com- prehensive literature search of PubMed and relevant Follicle-Stimulating Hormone congress abstract databases was conducted using FSH is a 30 kDa heterodimeric glycoprotein that belongs to a combinations of the key words prostate cancer, follicle- class of proteins that includes luteinizing hormone (LH), thy- stimulating hormone, vascular endothelial growth fac- roid-stimulating hormone, and human chorionic gonadotropin. tor, inhibins/activins, gonadotropin-releasing hormone (GnRH)/luteinizing hormone-releasing hormone (LHRH) Structurally, these glycoproteins share a common alpha subunit, receptor agonists/antagonists, and angiogenesis/neo- but have unique beta subunits that confer receptor specificity.6 genesis. This was followed by a consensus meeting of FSH binds to the FSH receptor, which belongs to the G-protein prostate cancer experts to discuss current knowledge coupled superfamily characterized by their 7 hydrophobic trans- surrounding FSH and the relevant evidence for its role in the development and progression of prostate cancer. -
Firmagon®) SMC No
degarelix 120mg and 80mg powder and solvent for solution for injection (Firmagon®) SMC No. (560/09) Ferring Pharmaceuticals Ltd 17 December 2010 The Scottish Medicines Consortium (SMC) has completed its assessment of the above product and advises NHS Boards and Area Drug and Therapeutic Committees (ADTCs) on its use in NHS Scotland. The advice is summarised as follows: ADVICE: following a resubmission degarelix (Firmagon®) is accepted for use within NHS Scotland. Indication under review: degarelix is a gonadotropin-releasing hormone (GnRH) antagonist indicated for the treatment of adult male patients with advanced hormone-dependent prostate cancer. In one study that included patients with all stages of prostate cancer, degarelix was shown to be non-inferior to a luteinising hormone releasing hormone (LHRH) agonist in suppressing testosterone levels over a one year treatment period without an initial testosterone flare. This SMC advice takes account of the benefits of a patient access scheme (PAS) that improves the cost-effectiveness of degarelix. This SMC advice is contingent upon the continuing availability of the patient access scheme in NHS Scotland. Overleaf is the detailed advice on this product. Chairman, Scottish Medicines Consortium Published 17 January, 2011 1 Indication Degarelix is a gonadotropin-releasing hormone (GnRH) antagonist indicated for the treatment of adult male patients with advanced hormone-dependent prostate cancer. Dosing Information Starting dose: 240mg (administered as two 120mg/3mL subcutaneous injections). Maintenance dose: 80mg/4mL administered as one subcutaneous injection every month. Product availability date 5 May 2009 Summary of evidence on comparative efficacy Degarelix is a novel testosterone ablating therapy that acts as an antagonist at the gonadatropin releasing hormone (GnRH) receptor. -
Mellon CV 7-15-20
Pamela L. Mellon, Ph.D. Vice-Chair for Research, Department of Obstetrics, Gynecology, and Reproductive Sciences Distinguished Professor, Department of Obstetrics, Gynecology, and Reproductive Sciences and Department of Neurosciences Director, Center for Reproductive Science and Medicine University of California, San Diego, School of Medicine 3A14 Leichtag Biomedical Research Building 9500 Gilman Drive, La Jolla, CA 92093-0674 (858) 534-1312, Fax (858) 534-1438, e-mail: [email protected] Departmental Web page: http://repromed.ucsd.edu/faculty/Faculty_Mellon.shtml Laboratory Web Page: http://repro.ucsd.edu/Mellon/SitePages/Home.aspx ORCID 0000-0002-8856-0410 EDUCATION B.A., 1975, University of California at Santa Cruz Degrees in both Biology and Chemistry with Highest Honors Ph.D., 1979, University of California at Berkeley Department of Molecular Biology Dissertation: Two Transforming Genes and Three Replicative Genes of Avian RNA Tumor Viruses: Identification, Gene Order, and Gene Expression APPOINTMENTS Research Associate, 1975, University of California at Berkeley Department of Molecular Biology with Dr. Harrison Echols Postdoctoral Fellow with Dr. Tom Maniatis 1979-1980, California Institute of Technology, Division of Biology 1980-1984, Harvard University, Department of Biochemistry and Molecular Biology Assistant Professor 1984-1990, The Salk Institute for Biological Studies, Regulatory Biology Laboratory Assistant Adjunct Professor 1988-1991, University of California, San Diego Associate Professor 1990-1991, The Salk Institute