Biopharmaceutical Pharmacy Program

Total Page:16

File Type:pdf, Size:1020Kb

Biopharmaceutical Pharmacy Program BIOPHARMACEUTICAL PHARMACY PROGRAM bsolute Total Care provides a number of biopharmaceutical products through the Biopharmaceutical Pharmacy Program. The program helps deliver medications to members or A provider offices that are not traditionally found at a local pharmacy. Most biopharmaceuticals and injectables billed for more than $250 require a prior authorization (PA) to be approved for payment by Absolute Total Care; however, PA requirements are programmed specific to the drug as indicated in the table below. Since the list of drugs requiring PA changes over time, due to new drug arrivals and other market conditions, the $250 amount is used as a reference gauge to help in determining whether to apply for PA. Some of these products can be delivered to the member or directly to the provider’s location for office administration through Acaria Health. Prescribers can submit requests for biopharmaceutical products to Absolute Total Care by filling out the Absolute Total Care Specialty Medications Prior Authorization Form that is available on the Coordinated Care website at www.absolutetotalcare.com. Fax the Absolute Total Care Specialty Medications Prior Authorization Form to 1-855-865-9469 or call Absolute Total Care at 1-866-433-6041 ext. 64455. If approved, Acaria Health Specialty Pharmacy will contact the member and/or the provider for delivery confirmation. Updated PA Requirement Trade Name (if Additional (PL Codes) HCPCS Code applicable) HCPCS Desription Information Auth required for all GENERAL 90281 GLOBULIN, IMMUNE providers Auth required for all GENERAL 90283 GLOBULIN, IMMUNE providers GLOBULIN, IMMUNE SC Auth required for all GENERAL 90284 (ZLB BEHRING) providers GLOBULIN, IMMUNE SC Auth required for all GENERAL 90291 (ZLB BEHRING) providers Auth required for all GENERAL 90378 Synagis PALIVIZUMAB providers Auth required for all providers except HEM/ONC A9542 Zevalin IBRITUMOMAB TIUXETAN hospital, hematology, or oncology providers. Auth required for all providers except IODINE I 131 HEM/ONC A9545 Bexxar hospital, TOSITUMOMAB hematology, or oncology providers. Page 1 of 24 *As of 06/2015 BIOPHARMACEUTICAL PHARMACY PROGRAM Updated PA Requirement Trade Name (if Additional (PL Codes) HCPCS Code applicable) HCPCS Desription Information Auth required for all HEM/ONC J9035 Avastin BEVACIZUMAB providers Auth required for all GENERAL J0485 Nulojix BELATACEPT providers Auth required for all providers except HEM/ONC J9042 Adcetris BRENTUXIMAB VEDOTIN hospital, hematology, or oncology providers. Auth required for all MISC C9399 MISC MISC CODES providers Auth required for all providers except HEM/ONC G3001 Bexxar TOSITUMOMAB hospital, hematology, or oncology providers. Auth required for all GENERAL J0129 Orencia ABATACEPT providers Auth required for all GENERAL J0135 Humira ADALIMUMAB providers Auth required for all GENERAL J0180 Fabrazyme AGALSIDASE BETA providers Auth required for all GENERAL J0205 Ceredase ALGLUCERASE providers Auth required for all GENERAL J0207 Ethyol AMIFOSTINE providers Auth required for all GENERAL J0215 Amevive ALEFACEPT providers Auth required for all GENERAL J0220 Myozyme ALGLUCOSIDASE ALFA providers Auth required for all GENERAL J0221 Lumizyme ALGLUCOSIDASE ALFA providers Prolastin; PROTEINASE INHIBITOR Auth required for all GENERAL J0256 Zemira (HUMAN) providers Updated PA Requirement Trade Name (if Additional (PL Codes) HCPCS Code applicable) HCPCS Desription Information Page 2 of 24 *As of 06/2015 BIOPHARMACEUTICAL PHARMACY PROGRAM ALPHA 1 PROTEINASE Auth required for all GENERAL J0257 Glassia INHIBITOR (HUMAN) providers APOMORPHINE Auth required for all GENERAL J0364 Apokyn HYDROCHLORIDE providers Auth required for all GENERAL J0480 Simulect BASILIXIMAB providers Auth required for all GENERAL J0490 Benlysta BELIMUMAB providers CLOSTRIDIUM Auth required for all GENERAL J0585 Botox BOTULINUM TOXIN TYPE providers A Auth required for all GENERAL J0586 Dysport ABOBOTULINUMTOXINA providers CLOSTRIDIUM Auth required for all GENERAL J0587 Myobloc BOTULINUM TOXIN TYPE providers B INCOBOTULINUMTOXIN Auth required for all GENERAL J0588 Xeomin A providers Auth required for all providers except HEM/ONC J0594 Busulfex BUSULFAN hospital, hematology, or oncology providers. Auth required for all GENERAL J0597 Berinert C 1 ESTERASE, BERINERT providers Auth required for all GENERAL J0598 Cinryze C1 INHIBITOR (HUMAN) providers Auth required for all GENERAL J0638 Ilaris CANAKINUMAB providers LEVOLEUCOVORIN Auth required for all GENERAL J0641 Fusilev CALCIUM providers COLLAGENASE, CLOST Auth required for all GENERAL J0775 Xiaflex HIST providers Auth required for all GENERAL J0800 HP Acthar Gel CORTICOTROPIN providers Updated PA Requirement Trade Name (if Additional (PL Codes) HCPCS Code applicable) HCPCS Desription Information Page 3 of 24 *As of 06/2015 BIOPHARMACEUTICAL PHARMACY PROGRAM CYTOMEGALOVIRUS Auth required for all GENERAL J0850 CytoGam IMMUNE GLOBULIN providers Aranesp (non Auth required for all GENERAL J0881 DARBEPOETIN ALFA ESRD) providers Auth required for all GENERAL J0882 Aranesp (ESRD) DARBEPOETIN ALFA providers Epogen; Procrit Auth required for all GENERAL J0885 EPOETIN ALFA (non ESRD) providers Epogen; Procrit Auth required for all GENERAL J0886 EPOETIN ALFA (ESRD) providers Auth required for all providers except HEM/ONC J0894 Dacogen DECITABINE hospital, hematology, or oncology providers. DEFEROXAMINE Auth required for all GENERAL J0895 Desferal MESYLATE providers Auth required for all GENERAL J0897 Prolia; Xgeva DENOSUMAB INJECTION providers Auth required for all GENERAL J1190 Zinecard DEXRAZOXANE providers Auth required for all GENERAL J1290 Kalbitor ECALLANTIDE providers Auth required for all GENERAL J1300 Soliris ECULIZUMAB providers Auth required for all GENERAL J1324 Fuzeon ENFUVIRTIDE providers Auth required for all GENERAL J1325 Flolan EPOPROSTENOL SODIUM providers Auth required for all GENERAL J1438 Enbrel ETANERCEPT providers Neupogen Auth required for all GENERAL J1442 300mcg & FILGRASTIM providers 480mcg Updated PA Requirement Trade Name (if Additional (PL Codes) HCPCS Code applicable) HCPCS Desription Information Auth required for all GENERAL J1458 Naglazyme GALSULFASE providers Page 4 of 24 *As of 06/2015 BIOPHARMACEUTICAL PHARMACY PROGRAM GLOBULIN, IMMUNE IV Auth required for all GENERAL J1459 Privigen (BAXTER/AM RED CROS) providers Auth required for all GENERAL J1460 GamaSTAN S/D GLOBULIN, IMMUNE providers Auth required for all GENERAL J1557 Gammaplex GLOBULIN, IMMUNE providers Auth required for all GENERAL J1559 Hizentra HIZENTRA providers Auth required for all GENERAL J1560 GamaSTAN S/D GLOBULIN, IMMUNE providers GLOBULIN, IMMUNE IV Auth required for all GENERAL J1561 Gamunex (TALECRIS) providers GLOBULIN, IMMUNE SC Auth required for all GENERAL J1562 Vivaglobin (ZLB BEHRING) providers Auth required for all GENERAL J1566 Carimune GLOBULIN, IMMUNE providers GLOBULIN, IMMUNE IV Auth required for all GENERAL J1568 Octagam (OCTAPHARM) providers Gammagard GLOBULIN, IMMUNE IV Auth required for all GENERAL J1569 Liquid (BAXTER/AM RED CROS) providers Auth required for all GENERAL J1572 Febogamma GLOBULIN, IMMUNE providers Auth required for all GENERAL J1595 Copaxone GLATIRAMER ACETATE providers IVIG NON LYOPHILIZED, Auth required for all MISC J1599 MISC NOS providers Auth required for all GENERAL J1640 Panhematin HEMIN providers Auth required for all GENERAL J1645 Fragmin DALTEPARIN SODIUM providers Auth required for all GENERAL J1650 Lovenox ENOXAPARIN SODIUM providers Updated PA Requirement Trade Name (if Additional (PL Codes) HCPCS Code applicable) HCPCS Desription Information Auth required for all GENERAL J1652 Arixtra FONDAPARINUX SODIUM providers Auth required for all GENERAL J1655 Innohep TINZAPARIN SODIUM providers Page 5 of 24 *As of 06/2015 BIOPHARMACEUTICAL PHARMACY PROGRAM FIBRINOGEN Auth required for all GENERAL J7178 RiaSTAP CONCENTRATE (HUMAN) providers HYDROXYPROGESTERONE Auth required for all GENERAL J1725 Makena CAPROATE providers Auth required for all GENERAL J1740 Boniva IBANDRONATE SODIUM providers Auth required for all GENERAL J1743 Elaprase IDURSULFASE providers Auth required for all GENERAL J1745 Remicade INFLIXIMAB providers Auth required for all GENERAL J1786 Cerezyme IMUGLUCERASE providers Auth required for all GENERAL J1826 Avonex INTERFERON BETA 1A providers Auth required for all GENERAL J1830 Betaseron INTERFERON BETA 1B providers Auth required for all GENERAL J1930 Somatuline LANREOTIDE ACETATE providers Auth required for all GENERAL J1931 Aldurazyme LARONIDASE providers Eliguard; Lupron; Lupron Auth required for all GENERAL J1950 LEUPROLIDE ACETATE 3; Lupron 4; providers Lupron Depot Auth required for all GENERAL J2170 Iplex; Increlex MECASERMIN providers Auth required for all GENERAL J2278 Prialt ZICONOTIDE ACETATE providers Auth required for all GENERAL J2315 Vivitrol NALTREXONE providers Updated PA Requirement Trade Name (if Additional (PL Codes) HCPCS Code applicable) HCPCS Desription Information Auth required for all GENERAL J2323 Tysabri NATALIZUMAB providers Auth required for all GENERAL J2325 Natrecor NESIRITIDE providers Page 6 of 24 *As of 06/2015 BIOPHARMACEUTICAL PHARMACY PROGRAM Sandostatin Auth required for all GENERAL J2353 OCTREOTIDE ACETATE LAR providers Auth required for all GENERAL J2354 Sandostatin OCTREOTIDE ACETATE providers Auth required for all GENERAL J2355 Neumega OPRELVEKIN providers Auth required for all GENERAL J2357 Xolair OMALIZUMAB providers Zyprexa OLANZAPINE LONG Auth required for all GENERAL J2358 Relprevv ACTING
Recommended publications
  • Why and How to Perform Therapeutic Drug Monitoring for Mycophenolate Mofetil
    Trends in Transplantation 2007;12007;1:24-34 Why and How to Perform Therapeutic Drug Monitoring for Mycophenolate Mofetil Brenda de Winter and Teun van Gelder Department of Hospital Pharmacy, Clinical Pharmacology Unit, Erasmus Medical Centre, Rotterdam, the Netherlands Abstract The introduction of the immunosuppressive agent mycophenolate mofetil as a standard-dose drug has resulted in a reduced risk of rejection after renal transplantation and improved graft survival compared to azathioprine. The favorable balance between efficacy and safety has made mycophenolate mofetil a cornerstone immunosuppressive drug, and the vast majority of newly transplanted patients are now started on mycophenolate mofetil therapy. Despite the obvious success of mycophenolate mofetil as a standard-dose drug, there is reason to believe that the “one size fits all” approach is not optimal. Recent studies have shown that the pharmacokinetics of mycophenolic acid are influenced by patient charac- teristics such as gender, time after transplantation, serum albumin concentration, renal function, co-medication, and pharmacogenetic factors. As a result, with standard-dose therapy there is wide between-patient variability in exposure of mycophenolic acid. This variability is of clinical relevance because it has repeatedly been shown that exposure to the active metabolite mycophenolic acid is correlated with the risk of developing acute rejection. Especially with the increasing popularity of immunosuppressive regimens in which the concomitant immunosuppression is reduced or eliminated, ensuring an appropri- ate level of immunosuppression afforded by mycophenolic acid is of utmost importance. By introducing therapeutic drug monitoring, mycophenolic acid exposure can be targeted to the widely accepted therapeutic window (mycophenolic acid AUC0-12 between 30 and 60 mg·h/l).
    [Show full text]
  • WO 2018/223101 Al 06 December 2018 (06.12.2018) W !P O PCT
    (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 2018/223101 Al 06 December 2018 (06.12.2018) W !P O PCT (51) International Patent Classification: (71) Applicant: JUNO THERAPEUTICS, INC. [US/US]; 400 A 61K 35/1 7 (20 15.0 1) A 61P 35/00 (2006 .0 1) Dexter Ave. N., Suite 1200, Seattle, WA 98109 (US). (21) International Application Number: (72) Inventor: ALBERTSON, Tina; 400 Dexter Ave. N., Suite PCT/US2018/035755 1200, Seattle, WA 98109 (US). (22) International Filing Date: (74) Agent: AHN, Sejin et al; Morrison & Foerster LLP, 1253 1 0 1 June 2018 (01 .06.2018) High Bluff Drive, Suite 100, San Diego, CA 92130-2040 (US). (25) Filing Language: English (81) Designated States (unless otherwise indicated, for every (26) Publication Language: English kind of national protection available): AE, AG, AL, AM, (30) Priority Data: AO, AT, AU, AZ, BA, BB, BG, BH, BN, BR, BW, BY, BZ, 62/5 14,774 02 June 2017 (02.06.2017) US CA, CH, CL, CN, CO, CR, CU, CZ, DE, DJ, DK, DM, DO, 62/5 15,530 05 June 2017 (05.06.2017) US DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, HN, 62/521,366 16 June 2017 (16.06.2017) u s HR, HU, ID, IL, IN, IR, IS, JO, JP, KE, KG, KH, KN, KP, 62/527,000 29 June 2017 (29.06.2017) u s KR, KW, KZ, LA, LC, LK, LR, LS, LU, LY, MA, MD, ME, 62/549,938 24 August 2017 (24.08.2017) u s MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, 62/580,425 0 1 November 2017 (01 .11.2017) u s OM, PA, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SA, 62/593,871 0 1 December 2017 (01 .12.2017) u s SC, SD, SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, TN, 62/596,764 08 December 2017 (08.12.2017) u s TR, TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW.
    [Show full text]
  • Advances in Immunosuppression for Renal Transplantation Antoine Durrbach, Helene Francois, Severine Beaudreuil, Antoine Jacquet and Bernard Charpentier
    REVIEWS Advances in immunosuppression for renal transplantation Antoine Durrbach, Helene Francois, Severine Beaudreuil, Antoine Jacquet and Bernard Charpentier Abstract | The development of immunosuppressants with minimal adverse and nephrotoxic effects is important to improve outcomes, such as acute and chronic antibody-mediated rejection, after organ transplantation. In addition, the application of expanded criteria for donors and transplantation in immunized patients necessitates the development of new therapies. Drug development over the past 10 years has generally been disappointing, but several new promising compounds have been or are being developed to prevent acute and chronic transplant rejection. In this Review, we report on several compounds that have been developed to remove allogenic T cells and/or to inhibit T-cell activation. We also discuss compounds that interfere with antibody-mediated rejection. Durrbach, A. et al. Nat. Rev. Nephrol. 6, 160–167 (2010); published online 2 February 2010; doi:10.1038/nrneph.2009.233 Introduction Renal transplantation has specific features that make or as a result of previous transplantation, has increased it different from transplantation procedures for other over the past decade. In addition, ABO­incompatible organs. For example, outcomes can be affected by grafts are becoming more frequently used. Together, these common states, such as donor and/or recipient age, high factors have led to a rise in the number of ‘immuno logically blood pressure, diabetes mellitus, metabolic disturbances at­risk’ kidney transplantations. Few immunosuppressants (such as high LDL cholesterol) and abnormalities in fluid targeted to B cells have, however, been available to control and electrolyte balance. The kidney is also very sensitive the antibody­mediated response.
    [Show full text]
  • Biologic Armamentarium in Psoriasis
    Vol 9, Issue 1, 2016 ISSN - 0974-2441 Review Article BIOLOGIC ARMAMENTARIUM IN PSORIASIS GANESH PAI1*, NITHIN SASHIDHARAN2 1Medical Director, Derma-Care ‘The Trade Centre’, Mangalore - 575 003, Karnataka, India. 2Consultant Clinical Pharmacologist, Derma-Care ‘The Trade Centre’, Mangalore - 575 003, Karnataka, India. Email: [email protected] Received: 14 July 2015, Revised and Accepted: 24 August 2015 ABSTRACT Psoriasis is an autoimmune disease and further classed as a chronic inflammatory skin condition serving as a global burden. A moderate to severe psoriasis can be treated with conventional therapies. Less efficacy, poor patient compliance, and toxicity issues were the major problems associated with conventional therapies. The introduction of biologic therapy has a great impression on psoriatic treatment duration and enhanced quality of life in psoriasis patients. The new biologic therapies are tailor-made medications with the goal of more specific and effective treatment; less toxicity. The biologic therapy is aimed to target antigen presentation and co-stimulation, T-cell activation, and leukocyte adhesion; and pro-inflammatory cascade. They act as effective and safer substitute to traditional therapy. Secukinumab, certolizumab, itolizumab, golimumab, ustekinumab, adalimumab, infliximab etanercept, alefacept, etc. are the approved biologic with the global market. This review briefs about psoriasis pathogenesis, traditional treatments, and biologic therapies potential. Keywords: Psoriasis, Biologic, Non-biologic treatment. INTRODUCTION migration, potentiation of Th1 type of response, angiogenesis, and epidermal hyperplasia [7]. Psoriasis is an autoimmune disease and further classed as a chronic inflammatory skin condition with prevalence ranging 1-3% in the TNF- is plays vital role in the pathogenesis of psoriasis. It acts by world [1].
    [Show full text]
  • (12) Patent Application Publication (10) Pub. No.: US 2017/0209462 A1 Bilotti Et Al
    US 20170209462A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2017/0209462 A1 Bilotti et al. (43) Pub. Date: Jul. 27, 2017 (54) BTK INHIBITOR COMBINATIONS FOR Publication Classification TREATING MULTIPLE MYELOMA (51) Int. Cl. (71) Applicant: Pharmacyclics LLC, Sunnyvale, CA A 6LX 3/573 (2006.01) A69/20 (2006.01) (US) A6IR 9/00 (2006.01) (72) Inventors: Elizabeth Bilotti, Sunnyvale, CA (US); A69/48 (2006.01) Thorsten Graef, Los Altos Hills, CA A 6LX 3/59 (2006.01) (US) A63L/454 (2006.01) (52) U.S. Cl. CPC .......... A61 K3I/573 (2013.01); A61K 3 1/519 (21) Appl. No.: 15/252,385 (2013.01); A61 K3I/454 (2013.01); A61 K 9/0053 (2013.01); A61K 9/48 (2013.01); A61 K (22) Filed: Aug. 31, 2016 9/20 (2013.01) (57) ABSTRACT Disclosed herein are pharmaceutical combinations, dosing Related U.S. Application Data regimen, and methods of administering a combination of a (60) Provisional application No. 62/212.518, filed on Aug. BTK inhibitor (e.g., ibrutinib), an immunomodulatory agent, 31, 2015. and a steroid for the treatment of a hematologic malignancy. US 2017/0209462 A1 Jul. 27, 2017 BTK INHIBITOR COMBINATIONS FOR Subject in need thereof comprising administering pomalido TREATING MULTIPLE MYELOMA mide, ibrutinib, and dexamethasone, wherein pomalido mide, ibrutinib, and dexamethasone are administered con CROSS-REFERENCE TO RELATED currently, simulataneously, and/or co-administered. APPLICATION 0008. In some aspects, provided herein is a method of treating a hematologic malignancy in a subject in need 0001. This application claims the benefit of U.S.
    [Show full text]
  • Challenges and Approaches for the Development of Safer Immunomodulatory Biologics
    REVIEWS Challenges and approaches for the development of safer immunomodulatory biologics Jean G. Sathish1*, Swaminathan Sethu1*, Marie-Christine Bielsky2, Lolke de Haan3, Neil S. French1, Karthik Govindappa1, James Green4, Christopher E. M. Griffiths5, Stephen Holgate6, David Jones2, Ian Kimber7, Jonathan Moggs8, Dean J. Naisbitt1, Munir Pirmohamed1, Gabriele Reichmann9, Jennifer Sims10, Meena Subramanyam11, Marque D. Todd12, Jan Willem Van Der Laan13, Richard J. Weaver14 and B. Kevin Park1 Abstract | Immunomodulatory biologics, which render their therapeutic effects by modulating or harnessing immune responses, have proven their therapeutic utility in several complex conditions including cancer and autoimmune diseases. However, unwanted adverse reactions — including serious infections, malignancy, cytokine release syndrome, anaphylaxis and hypersensitivity as well as immunogenicity — pose a challenge to the development of new (and safer) immunomodulatory biologics. In this article, we assess the safety issues associated with immunomodulatory biologics and discuss the current approaches for predicting and mitigating adverse reactions associated with their use. We also outline how these approaches can inform the development of safer immunomodulatory biologics. Immunomodulatory Biologics currently represent more than 30% of licensed The high specificity of the interactions of immu- biologics pharmaceutical products and have expanded the thera- nomodulatory biologics with their relevant immune Biotechnology-derived peutic options available
    [Show full text]
  • Alefacept for Severe Alopecia Areata a Randomized, Double-Blind, Placebo-Controlled Study
    STUDY Alefacept for Severe Alopecia Areata A Randomized, Double-blind, Placebo-Controlled Study Bruce E. Strober, MD, PhD; Kavita Menon, MD; Amy McMichael, MD; Maria Hordinsky, MD; Gerald Krueger, MD; Jackie Panko, MD; Kimberly Siu, MD; Jonathan L. Lustgarten, PhD; Elizabeth K. Ross, MD; Jerry Shapiro, MD Objective: To assess the efficacy of alefacept for the treat- istration–approved T-cell biologic inhibitor for the treat- ment of severe alopecia areata (AA). ment of moderate to severe plaque psoriasis. Design: Multicenter, double-blind, randomized, placebo- Main Outcome Measure: Improved Severity of Alo- controlled clinical trial. pecia Tool (SALT) score over 24 weeks. Results: Participants receiving alefacept for 12 consecu- Setting: Academic departments of dermatology in the tive weeks demonstrated no statistically significant im- United States. provement in AA when compared with a well-matched placebo-receiving group (P =.70). Participants: Forty-five individuals with chronic and severe AA affecting 50% to 95% of the scalp hair and re- Conclusion: Alefacept is ineffective for the treatment of sistant to previous therapies. severe AA. Intervention: Alefacept, a US Food and Drug Admin- Arch Dermatol. 2009;145(11):1262-1266 LOPECIA AREATA (AA) IS A lesions of AA are transplanted into mice chronic, potentially revers- with severe combined immunodefi- ible autoimmune skin dis- ciency that lack T lymphocytes, hair ease characterized by non- growth may resume, further confirming scarring patchy hair loss the potential pathogenic role of T lym- Ainvolving any hair-bearing surface.1 Alo- phocytes.8 pecia areata often causes considerable emo- Treatment options for more severe pre- tional distress and has limited treatment sentations of AA are limited, and neither Author Affiliations: options.
    [Show full text]
  • Tanibirumab (CUI C3490677) Add to Cart
    5/17/2018 NCI Metathesaurus Contains Exact Match Begins With Name Code Property Relationship Source ALL Advanced Search NCIm Version: 201706 Version 2.8 (using LexEVS 6.5) Home | NCIt Hierarchy | Sources | Help Suggest changes to this concept Tanibirumab (CUI C3490677) Add to Cart Table of Contents Terms & Properties Synonym Details Relationships By Source Terms & Properties Concept Unique Identifier (CUI): C3490677 NCI Thesaurus Code: C102877 (see NCI Thesaurus info) Semantic Type: Immunologic Factor Semantic Type: Amino Acid, Peptide, or Protein Semantic Type: Pharmacologic Substance NCIt Definition: A fully human monoclonal antibody targeting the vascular endothelial growth factor receptor 2 (VEGFR2), with potential antiangiogenic activity. Upon administration, tanibirumab specifically binds to VEGFR2, thereby preventing the binding of its ligand VEGF. This may result in the inhibition of tumor angiogenesis and a decrease in tumor nutrient supply. VEGFR2 is a pro-angiogenic growth factor receptor tyrosine kinase expressed by endothelial cells, while VEGF is overexpressed in many tumors and is correlated to tumor progression. PDQ Definition: A fully human monoclonal antibody targeting the vascular endothelial growth factor receptor 2 (VEGFR2), with potential antiangiogenic activity. Upon administration, tanibirumab specifically binds to VEGFR2, thereby preventing the binding of its ligand VEGF. This may result in the inhibition of tumor angiogenesis and a decrease in tumor nutrient supply. VEGFR2 is a pro-angiogenic growth factor receptor
    [Show full text]
  • Comparative Effectiveness of Immunosuppressive Drugs and Corticosteroids for Lupus Nephritis: a Systematic Review and Network Meta-Analysis Jasvinder A
    Singh et al. Systematic Reviews (2016) 5:155 DOI 10.1186/s13643-016-0328-z RESEARCH Open Access Comparative effectiveness of immunosuppressive drugs and corticosteroids for lupus nephritis: a systematic review and network meta-analysis Jasvinder A. Singh1,2,3*, Alomgir Hossain4, Ahmed Kotb4 and George A. Wells4 Abstract Background: There is a lack of high-quality meta-analyses and network meta-analyses of immunosuppressive drugs for lupus nephritis. Our objective was to assess the comparative benefits and harms of immunosuppressive drugs and corticosteroids in lupus nephritis. Methods: We conducted a systematic review and network meta-analysis (NMA) of trials of immunosuppressive drugs and corticosteroids in patients with lupus nephritis. We calculated odds ratios (OR) and 95 % credible intervals (CrI). Results: Sixty-five studies that met inclusion and exclusion criteria; data were analyzed for renal remission/response (37 trials; 2697 patients), renal relapse/flare (13 studies; 1108 patients), amenorrhea/ovarian failure (eight trials; 839 patients) and cytopenia (16 trials; 2257 patients). Cyclophosphamide [CYC] low dose (LD) and CYC high-dose (HD) were less likely than mycophenolate mofetil [MMF] and azathioprine [AZA], CYC LD, CYC HD and plasmapharesis less likely than cyclosporine [CSA] to achieve renal remission/response. Tacrolimus [TAC] was more likely than CYC LD to achieve renal remission/response. MMF and CYC were associated with a lower odds of renal relapse/flare compared to PRED and MMF was associated with a lower rate of renal relapse/flare than AZA. CYC was more likely than MMF and PRED to be associated with amenorrhea/ovarian failure. Compared to MMF, CYC, AZA, CYC LD, and CYC HD were associated with a higher risk of cytopenia.
    [Show full text]
  • Cytokine and CAM Antagonists and Related Agents Review 01/22/2010
    Cytokine and CAM Antagonists and Related Agents Review 01/22/2010 Copyright © 2005 - 2010 by Provider Synergies, L.L.C. All rights reserved. Printed in the United States of America. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, digital scanning, or via any information storage and retrieval system without the express written consent of Provider Synergies, L.L.C. All requests for permission should be mailed to: Attention: Copyright Administrator Intellectual Property Department Provider Synergies, L.L.C. 10101 Alliance Rd, Ste 201 Cincinnati, Ohio 45242 The materials contained herein represent the opinions of the collective authors and editors and should not be construed to be the official representation of any professional organization or group, any state Pharmacy and Therapeutics committee, any state Medicaid Agency, or any other clinical committee. This material is not intended to be relied upon as medical advice for specific medical cases and nothing contained herein should be relied upon by any patient, medical professional or layperson seeking information about a specific course of treatment for a specific medical condition. All readers of this material are responsible for independently obtaining medical advice and guidance from their own physician and/or other medical professional in regard to the best course of treatment for their specific medical condition. This publication, inclusive of all forms contained herein, is intended to be educational in nature and is intended to be used for informational purposes only. Email comments and suggestions to [email protected].
    [Show full text]
  • Recent Topics on the Mechanisms of Immunosuppressive Therapy-Related Neurotoxicities
    Preprints (www.preprints.org) | NOT PEER-REVIEWED | Posted: 29 May 2019 doi:10.20944/preprints201905.0358.v1 Peer-reviewed version available at Int. J. Mol. Sci. 2019, 20, 3210; doi:10.3390/ijms20133210 1 of 39 1 Review 2 Recent topics on the mechanisms of 3 immunosuppressive therapy-related neurotoxicities 4 Wei Zhang 1, Nobuaki Egashira 1,2,* and Satohiro Masuda 1,2 5 1 Department of Clinical Pharmacology and Biopharmaceutics, Graduate School of Pharmaceutical Sciences, 6 Kyushu University, Fukuoka 812-8582, Japan 7 2 Department of Pharmacy, Kyushu University Hospital, Fukuoka 812-8582, Japan 8 * Correspondence: [email protected], Tel.: 81-92-642-5920 9 Abstract: Although transplantation procedures have been developed for patients with end-stagec 10 hepatic insufficiency or other diseases, allograft rejection still threatens patient health and lifespan. 11 Over the last few decades, the emergence of immunosuppressive agents, such as calcineurin 12 inhibitors (CNIs) and mammalian target of rapamycin (mTOR) inhibitors, have strikingly 13 increased graft survival. Unfortunately, immunosuppressive agent-related neurotoxicity is 14 commonly occurred in clinical situations, with the majority of neurotoxicity cases caused by CNIs. 15 The possible mechanisms whereby CNIs cause neurotoxicity include: increasing the permeability 16 or injury of the blood-brain barrier, alterations of mitochondrial function, and alterations in 17 electrophysiological state. Other immunosuppressants can also induce neuropsychiatric 18 complications. For example, mTOR inhibitors induce seizures; mycophenolate mofetil induces 19 depression and headache; methotrexate affects the central nervous system; mouse monoclonal 20 immunoglobulin G2 antibody against cluster of differentiation 3 also induces headache; and 21 patients using corticosteroids usually experience cognitive alteration.
    [Show full text]
  • Eisai Submits Marketing Authorization Application in Japan
    N o. 20-15 March 26, 2020 Eisai Co., Ltd. EISAI SUBMITS MARKETING AUTHORIZATION APPLICATION IN JAPAN FOR ANTICANCER AGENT DENILEUKIN DIFTITOX (GENETIC RECOMBINANT) FOR CUTANEOUS T-CELL LYMPHOMA AND PERIPHERAL T-CELL LYMPHOMA Eisai Co., Ltd. (Headquarters: Tokyo, CEO: Haruo Naito, “Eisai”) announced today that it has submitted in Japan a marketing authorization application of the anticancer agent denileukin diftitox (genetic recombinant) (generic name, development code: E7777) for relapsed or refractory Cutaneous T-cell Lymphoma (CTCL) and Peripheral T-cell Lymphoma (PTCL). This application is based on data from a multicenter, open-label, single-arm Phase II clinical study (study 205) conducted in Japan for patients with relapsed or refractory CTCL or PTCL to evaluate the efficacy and safety of this agent. This study achieved the primary endpoint and exceeded a predetermined threshold with statistical significance: the objective response rate (ORR) of CTCL and PTCL patients in total (n=36) was 36.1% (95% confidence interval (CI): 20.8-53.8). The ORRs of each subtype were 31.6% (95% CI:12.6-56.6) for CTCL (n=19) and 41.2% (95%CI: 18.4-67.1) for PTCL (n=17). The five most frequent adverse events observed in this study were increased aspartate aminotransferase (AST) (89.2%), increased alanine aminotransferase (ALT) (86.5%), hypoalbuminaemia (70.3%), lymphopenia (70.3%), and pyrexia (51.4%). Denileukin diftitox (genetic recombinant) is a fusion protein of the receptor-binding portion of interleukin-2 (IL-2) and diphtheria toxin that specifically binds to the IL-2 receptor on the surface of tumoral lymphocyte.
    [Show full text]