Vincristine (Conventional): Drug Information
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Hodgkin Lymphoma Treatment Regimens
HODGKIN LYMPHOMA TREATMENT REGIMENS (Part 1 of 5) Clinical Trials: The National Comprehensive Cancer Network recommends cancer patient participation in clinical trials as the gold standard for treatment. Cancer therapy selection, dosing, administration, and the management of related adverse events can be a complex process that should be handled by an experienced health care team. Clinicians must choose and verify treatment options based on the individual patient; drug dose modifications and supportive care interventions should be administered accordingly. The cancer treatment regimens below may include both U.S. Food and Drug Administration-approved and unapproved indications/regimens. These regimens are provided only to supplement the latest treatment strategies. These Guidelines are a work in progress that may be refined as often as new significant data become available. The NCCN Guidelines® are a consensus statement of its authors regarding their views of currently accepted approaches to treatment. Any clinician seeking to apply or consult any NCCN Guidelines® is expected to use independent medical judgment in the context of individual clinical circumstances to determine any patient’s care or treatment. The NCCN makes no warranties of any kind whatsoever regarding their content, use, or application and disclaims any responsibility for their application or use in any way. Classical Hodgkin Lymphoma1 Note: All recommendations are Category 2A unless otherwise indicated. Primary Treatment Stage IA, IIA Favorable (No Bulky Disease, <3 Sites of Disease, ESR <50, and No E-lesions) REGIMEN DOSING Doxorubicin + Bleomycin + Days 1 and 15: Doxorubicin 25mg/m2 IV push + bleomycin 10units/m2 IV push + Vinblastine + Dacarbazine vinblastine 6mg/m2 IV over 5–10 minutes + dacarbazine 375mg/m2 IV over (ABVD) (Category 1)2-5 60 minutes. -
HODGKIN LYMPHOMA TREATMENT REGIMENS (Part 1 of 2)
HODGKIN LYMPHOMA TREATMENT REGIMENS (Part 1 of 2) The selection, dosing, and administration of anticancer agents and the management of associated toxicities are complex. Drug dose modifications and schedule and initiation of supportive care interventions are often necessary because of expected toxicities and because of individual patient variability, prior treatment, and comorbidities. Thus, the optimal delivery of anticancer agents requires a healthcare delivery team experienced in the use of such agents and the management of associated toxicities in patients with cancer. The cancer treatment regimens below may include both FDA-approved and unapproved uses/regimens and are provided as references only to the latest treatment strategies. Clinicians must choose and verify treatment options based on the individual patient. NOTE: GREY SHADED BOXES CONTAIN UPDATED REGIMENS. REGIMEN DOSING Classical Hodgkin Lymphoma—First-Line Treatment General treatment note: Routine use of growth factors is not recommended. Leukopenia is not a factor for treatment delay or dose reduction (except for escalated BEACOPP).1 CR=complete response IPS=International Prognostic Score PD=progressive disease PFTs=pulmonary function tests PR=partial response RT=radiation therapy SD=stable disease Stage IA, IIA Favorable ABVD (doxorubicin [Adriamycin] Days 1 and 15: Doxorubicin 25mg/m2 IV + bleomycin 10mg/m2 IV + vinblastine + bleomycin + vinblastine + 6mg/m2 IV + dacarbazine 375mg/m2 IV. dacarbazine [DTIC-Dome]) + Repeat cycle every 4 weeks for 2–4 cycles. involved-field radiotherapy (IFRT)1–4 Follow with IFRT after completion of chemotherapy. Abbreviated Stanford V Weeks 1, 3, 5 and 7: Vinblastine 6mg/m2 IV + doxorubicin 25mg/m2 IV. (doxorubicin + vinblastine + Weeks 1 and 5: Mechlorethamine 6mg/m2. -
Effect of Human Fibroblast Interferon on the Antiviral Activity of Mammalian Cells Treated with Bleomycin, Vincristine, Or Mitomycin C1
[CANCER RESEARCH 43, 5462-5466. November 1983] Effect of Human Fibroblast Interferon on the Antiviral Activity of Mammalian Cells Treated with Bleomycin, Vincristine, or Mitomycin C1 Robert J. Suhadolnik,2 Yosuke Sawada,3 Maryann B. Flick, Nancy L. Reichenbach, and Joseph D. Mosca3 Department of Biochemistry, Temple University School of Medicine, Philadelphia, Pennsylvania 19140 ABSTRACT protein kinase (2,9,28,34,36). In addition to the use of interferon in the treatment of cancer (1, 11, 12, 29, 34), combination Bleomycin, vincristine, or mitomycin C, when added to HeLa chemotherapy of interferon and methotrexate, c/s-platinum diam- cells simultaneously with human fibroblast interferon (IFN-0), minedichloride, cyclophosphamide, or 1,3-bis(/i-chloroethyl)-1- caused a decrease in cell density and inhibited DMA synthesis nitrosourea on either tumor cells in culture or in leukemic mice compared with HeLa cells treated with IFN-/3 alone. However, has been reported (5, 7, 10, 25). Furthermore, Stolfi ef al. (37) the IFN-0-induced antiviral processes were unaffected by the reported recently that the administration of mouse interferon to presence of these drugs as determined by in vitro enzyme assays mice following the administration of 5-fluorouracil protected the and the development of the antiviral state in the intact HeLa cell. mice from mortality. Because it is possible to selectively inhibit HeLa cells treated with IFN-/Õalone or with IFN-/3 in combination proliferation of tumor cells with chemotherapeutic drugs, we with bleomycin, vincristine, or mitomycin C were able to induce reasoned that the ability of the normal cell to maintain the antiviral the double-stranded RNA-dependent adenosine triphos- phate:2',5'-oligoadenylic acid adenyltransferase (EC 2.2.2.-) and state might be adversely affected by such drugs and that the antiproliferative action of interferons might affect the activity of the double-stranded RNA-dependent protein kinase. -
Highlights from the Pan Pacific Lymphoma Conference
October 2011 A SPECIAL MEETING REVIEW EDITION Volume 9, Issue 10, Supplement 24 Highlights From the Pan Pacific Lymphoma Conference August 15–19, 2011 Kauai, Hawaii Special Reporting on: • Aggressive T-Cell Lymphomas • Novel Agents With Activity in CLL/SLL • PTCL—Update on Novel Therapies • Agents Targeting the Stromal Elements of the Lymph Node • Inducing Apoptosis in Lymphoma Cells Through Novel Agents With Expert Commentary by: Bruce D. Cheson, MD Deputy Chief Division of Hematology-Oncology Head of Hematology Lombardi Comprehensive Cancer Center Georgetown University Hospital Washington, DC Eb: E W Th O N www.clinicaladvances.com ENGINEERING T H E N E X T GENERATION OF ANTIBODY-DRUG CONJUGATES 003203_sgncor_adcadvcaho_fa4.indd 2 8/25/11 11:13 AM An innovative approach to improving outcomes in patients with cancer Antibody-drug conjugates (ADCs) use a conditionally stable linker to combine the targeting specificity of monoclonal antibodies with the tumor-killing power of potent cytotoxic agents.1,2 This could allow potent drugs to be delivered directly to tumor cells with minimal systemic toxicity. Optimizing the parameters for clinical success Scientists at Seattle Genetics are focused on parameters critical to the effective performance of ADCs, including target antigen selection,3,4 linker stability5-7 and potent cytotoxic agents.4,7,8 Elements of an antibody-drug conjugate Linker ADCs link precision and Antibody attaches the cytotoxic agent to specific for a tumor-associated the antibody. Newer linker potency for greater activity -
Eliminating Vincristine Administration Events
Issue 37 October 2017 Eliminating vincristine administration events Issue: Despite the usually deadly consequences of accidentally administering the chemotherapy drug vincristine intrathecally, adverse events still occur, typically because some organizations still administer vincristine via syringe. The good news is that these events are happening less in the United States, mostly because of the efforts of leading national organizations to promote an effective prevention strategy that assures a mechanical barrier to intrathecal administration (into the subarachnoid space). The strategy involves diluting intravenous vincristine or other vinca alkaloids in a minibag that contains a volume that is too large for intrathecal administration (e.g., 25 mL for pediatric patients and 50 mL for adults), making it mechanically difficult to accidentally administer intrathecally.1 Vinca alkaloids (vinblastine, vinorelbine, vincristine, and vincristine liposomal) are chemotherapy drugs that are intended to be administered intravenously. If given intrathecally, vincristine is nearly always fatal and associated with an irreversible, painful ascending paralysis.2 When vinca alkaloids are injected intrathecally, destruction of the central nervous system occurs, radiating out from the injection site. The few survivors of this adverse event experienced devastating neurological damage.1 Part of the problem stems from ordering intravenous vincristine in conjunction with medications that are administered intrathecally via a syringe, such as methotrexate, cytarabine and hydrocortisone. In some adverse events, vincristine was mistakenly injected into the cerebrospinal fluid (CSF) of patients when the intent was to inject another intrathecal chemotherapy agent, such as methotrexate or cytarabine.3 Intravenous vincristine and other vinca alkaloids are dispensed from the pharmacy with explicit warning labels about their lethality if given intrathecally. -
Vincristine Archive File
Vincristine archive file Vincristine is a vinakaloid, which was first discovered 1958 in the tropical plant Catharanthus roseus, native in Madagascar. Its ability to inhibit the metaphase of the mitosis by suppressing the polymerization of the microtubule makes it very important as a chemotherapeutic agent, especially against non-Hodgkin lymphomas and Wilms' tumor. History: Vinblastine and Vincristine are bisindole alkaloids and both widely known for their use as antitumor drugs. In former times they were isolated in trace quantities from the leaves of Catharanthus roseus. Because of their importance in the medical field numerous researches were examining the structure, use and synthesis of Vinblastine, Vincristine and their derivates. Their biological effect to inhibit the microtubule formation and mitosis was and still is a very important part of medical cancer therapy. They were both among the first natural products whose structures were identified by X-ray crystallography and among the first for which X-ray analysis of a heavy atom derivative was used to establish their absolute configuration. ( 2) Timeline: 1958 Vinblastine was first discovered as an unexpected myelosuppressive agent by Noble, R. L., C. T. Beer, and J. H. Cutts during the search for an antidiabetic agent in Catharanthus roseus (myelosupression decreased activity of the bone marrow) 1959 independendently researchers from Eli Lilly (Johnson, I. S., J. G. Armstrong, M. Gorman, and J. P. Burnett, Jr.)discovered that the extracts of C. roseus Possesses activity against -
Differential Activity of Vincristine and Vinblastine Against Cultured Cells1 ;
[CANCER RESEARCH 44, 3307-3312, August 1984] Differential Activity of Vincristine and Vinblastine against Cultured Cells1 ; Peter J. Ferguson,2 J. Robert Phillips, Milada Seiner, and Carol E. Cass3 Cancer Research Group (McEachern Laboratory) [P. J. F., J. Ft. P., M. S., C. E. C.] and Department of Biochemistry [P. J. F., C. E. C.¡,University of Alberta, Edmonton, Alberta, Canada T6G 2H7 ABSTRACT determine if differential activity is related to differences in uptake4 or release of drug. Included were cells from these established Vincristine and vinblastine exhibit differential activity against lines: mouse neuroblastoma; mouse leukemia L1210; mouse tumors and normal tissues. In this work, a number of cultured lymphoma S49; HeLa; and human promyelocytic leukemia HL- cell lines were assayed for their sensitivity to the antiproliferative 60. Drug sensitivity in each cell line was determined by assaying and cytotoxic effects of the two drugs following short-term (4 hr) inhibition of proliferation during a continuous exposure to either or during continuous exposures. Differential activity was not drug or by assaying colony formation following a 24-hr exposure. seen when cells were subjected to continuous exposures. The Because of rapid loss of Vinca alkaloids from human serum concentrations of Vincristine and vinblastine, respectively, that following an i.v. bolus injection (11, 12,14, 17), the sensitivity of inhibited growth rates by 50% were: mouse leukemia L1210 cells to short-term (1- and 4-hr) exposures was also determined cells, 4.4 and 4.0 nw; mouse lymphoma S49 cells, 5 and 3.5 nM; for both drugs. Although there were differences in sensitivity to mouse neuroblastoma cells, 33 and 15 nw; HeLa cells, 1.4 and vincristine and vinblastine between cell lines, there was little or 2.6 nw; and human leukemia HL-60 cells, 4.1 and 5.3 nM. -
Etoposide Compared with the Combination of Vincristine, Doxorubicin, and Cyclophosphamide in the Treatment of Small Cell Lung Cancer
Thorax 1989;44:215-219 Thorax: first published as 10.1136/thx.44.3.215 on 1 March 1989. Downloaded from Etoposide compared with the combination of vincristine, doxorubicin, and cyclophosphamide in the treatment of small cell lung cancer M B McILLMURRAY, R J BIBBY, BE TAYLOR, L P ORMEROD, J R EDGE, R J WOLSTENHOLME, R F WILLEY, J F O'REILLY, N HORSFIELD, C E JOHNSON, C P MUSTCHIN, D BRISCOE From the Royal Lancaster Infirmary, Lancaster; Victoria Hospital, Blackpool; Royal Preston Hospital, Preston; Blackburn Royal Infirmary, Blackburn; Marsden Hospital, Burnley; Furness General Hospital, Cumbria; Cumberland Infirmary, Carlisle; and Royal Albert Edward Infirmary, Wigan ABSTRACT One hundred and three patients with small cell lung carcinoma were stratified according to stage ofdisese (47 limited disease, 56 extensive disease) and then randomised to receive etoposide 300 mg/m2 alone for two days or a combination (VAC) of vincristine 1 mg/m2, doxorubicin (Adriamycin) 50 mg/m2, and cyclophosphamide 1000 mg/m2. The drugs were given at three week intervals. Patients were assessed after three cycles of treatment and continued with the same regimen ifin complete remission and with the alternative regimen ifin partial remission; they were withdrawn if the disease had progressed. Twenty four patients (23%) achieved complete remission and this copyright. occurred more often when patients were receiving VAC (19 of82) than etoposide (5 of75). There was no difference, however, in overall survival between those initially treated with etoposide and those having combination chemotherapy, whether for limited disease (both 8 months) or extensive disease (7 and 5 5 months). -
Frontline Paid New York, Ny a Lymphoma Rounds Publication Permit #370
Lymphoma Rounds Leadership Chicago - Loyola University Chicago New England - Baystate Medical MD, PhD; Francesca Montanari, Anna Niewiarowska, MD - Scott Smith, MD, PhD, FACP; Center - Armen Asik, MD; Beth MD; Hackensack University Medical Patrick Stiff, MD; Northwestern Israel Deaconess Medical Center Center - Andre Goy, MD, MS; Icahn Seattle - Kaiser Permanente University - Leo Gordon, MD, - Jon Arnason, MD; Robin Joyce, School of Medicine at Mount Sinai - Washington - Eric Chen, MD, PhD; FACP; Reem Karmali, MD, MS MD; Boston University School of Joshua Brody, MD; Memorial Sloan The Polyclinic - Sherry Hu, MD, (chair); Jane Winter, MD; Rush Medicine - J. Mark Sloan, MD; Kettering Cancer Center - Anthony PhD; Swedish Medical Center - University Medical Center - Jerome Brown University School of Medicine Mato, MD, MSCE; David Straus, Hank Kaplan, MD; John Pagel, Loew, MD; Sunita Nathan, MD; - Adam Olszewski, MD; Dana- MD (chair); NYU Langone Medical MD, PhD, DSc (chair); University of Parameswaran Venugopal, MD; Farber Cancer Institute - Jorge Center - Catherine Diefenbach, Washington - Paul S. Martin, MD; The University of Chicago - Sonali Castillo, MD; Ann LaCasce, MD, MD; Rutgers Cancer Institute of The University of Washington/Fred Smith, MD; Girish Venkataraman, MSc; Dartmouth-Hitchcock Medical New Jersey - Joseph Bertino, MD; Hutchinson Cancer Research Center MD; University of Illinois at Chicago Center - Elizabeth Bengtson, Andrew Evens, DO, MSc, FACP; - Stephen Smith, MD; Virginia - Frederick Behm, MD; David MD; Erick Lansigan, MD; Lahey Weill Cornell Medicine - Koen van Mason Medical Center - David Peace, MD Hospital and Medical Center - Tarun Besien, MD, PhD; Ethel Cesarman, Aboulafia, MD Kewalramani, MD; Massachusetts MD, PhD; Amy Chadburn, MD; Los Angeles - Cedars-Sinai Medical General Hospital Cancer Center- Morton Coleman, MD Washington, D.C. -
Adcetris, INN-Brentuximab Vedotin
19 July 2012 EMA/702390/2012 Committee for Medicinal Products for Human Use (CHMP) Assessment report Adcetris International non-proprietary name: brentuximab vedotin Procedure No. EMEA/H/C/002455 Note Assessment report as adopted by the CHMP with all information of a commercially confidential nature deleted. 7 Westferry Circus ● Canary Wharf ● London E14 4HB ● United Kingdom Telephone +44 (0)20 7418 8400 Facsimile +44 (0)20 7523 7455 E -mail [email protected] Website www.ema.europa.eu An agency of the European Union Product information Name of the medicinal product: Adcetris Applicant: Takeda Global Research and Development Centre (Europe) Ltd. 61 Aldwych London WC2B 4AE United Kingdom Active substance: brentuximab vedotin International Nonproprietary Name/Common Name: brentuximab vedotin Pharmaco-therapeutic group Monoclonal antibodies (ATC Code): (L01XC12) ADCETRIS is indicated for the treatment of adult Therapeutic indication(s): patients with relapsed or refractory CD30+ Hodgkin lymphoma (HL): 1. following autologous stem cell transplant (ASCT) or 2. following at least two prior therapies when ASCT or multi-agent chemotherpay are not a treatment option ADCETRIS is indicated for the treatment of adult patients with relapsed or refractory systemic anaplastic large cell lymphoma (sALCL). Pharmaceutical form(s): Powder for concentrate for solution for infusion Strength(s): 50 mg Route(s) of administration: Intravenous use Packaging: vial (glass) Package size(s): 1 vial Adcetris CHMP assessment report Page 2/102 Rev10.11 Table of contents 1. Background information on the procedure .............................................. 9 1.1. Submission of the dossier ...................................................................................... 9 1.2. Steps taken for the assessment of the product ....................................................... 10 2. Scientific discussion ............................................................................. -
(12) United States Patent (10) Patent No.: US 9,545.449 B2 Krantz (45) Date of Patent: Jan
USOO9545449B2 (12) United States Patent (10) Patent No.: US 9,545.449 B2 Krantz (45) Date of Patent: Jan. 17, 2017 (54) SITE-SPECIFIC LABELING AND TARGETED 8,030.459 B2 10/2011 Papisov et al. DELIVERY OF PROTEINS FOR THE 8,927.485 B2 1/2015 Krantz et al. 2003/0215877 A1 11/2003 Love et al. TREATMENT OF CANCER 2005, 00792O8 A1 4/2005 Albani 2007, 0123465 A1 5/2007 Adermann et al. (71) Applicant: Advanced Proteome Therapeutics 2010.0099649 A1* 4/2010 Krantz et al. ................. 514f131 Inc., Boston, MA (US) 2011 0002978 A1 1/2011 Harrison 2011/0263832 A1 10/2011 Krantz et al. (72) Inventor: Alexander Krantz, Boston, MA (US) 2013,0165382 A1 6/2013 Krantz et al. (73) Assignee: Advanced Proteone Therapeutics Inc., FOREIGN PATENT DOCUMENTS Boston, MA (US) WO WO-89/11867 A1 12/1989 WO WO-02/42427 A2 5, 2002 (*) Notice: Subject to any disclaimer, the term of this WO WO-O2/O87497 A2 11/2002 patent is extended or adjusted under 35 WO WO-03/093478 A1 11, 2003 U.S.C. 154(b) by 0 days. WO WO-2007 112362 A2 10, 2007 WO WO-2010, 140886 A1 12/2010 (21) Appl. No.: 14/400,190 WO WO-2011, 153250 A2 12/2011 (22) PCT Filed: May 13, 2013 OTHER PUBLICATIONS (86). PCT No.: PCT/US2O13/040823 Yu et al. Site-specific crosslinking of annexin proteins by 1.4- benzoquinone: a novel crosslinker for the formation of protein S 371 (c)(1), dimers and diverse protein conjugates (Org. Biomol. Chem..., 2012, (2) Date: Nov. -
Brentuximab Vedotin: First-Line Agent for Advanced Hodgkin Lymphoma
ANTICANCER RESEARCH 33: 3879-3886 (2013) Brentuximab Vedotin: First-line Agent for Advanced Hodgkin Lymphoma HUYNH CAO1, KENNETH YAMAMOTO1, LI-XI YANG1,2 and ROBERT WEBER1 1St. Mary’s Medical Center, San Francisco, CA, U.S.A.; 2Radiobiology Laboratory, California Pacific Medical Center Research Institute, San Francisco, CA, U.S.A. Abstract. Hodgkin lymphoma (HL) is characterized by The mortality rate of Hodgkin lymphoma (HL) has fallen malignant Reed-Sternberg cells which express CD30. rapidly in the United States in the past five decades due to Current National Comprehensive Cancer Network guidelines the development of multiagent therapies. Among adults, for patients with advanced HL (stage III/IV disease) there are about 9,060 new cases with a reported death of recommend adriamycin, bleomycin, vinblastine, and 1,190 in 2012 (1). Current standard first-line regimens dacarbazine (ABVD), or escalated bleomycin, etoposide, include adriamycin, bleomycin, vinblastine, dacarbazine adriamycin, cyclophosphamide, vincristine, procarbazine, (ABVD), bleomycin, etoposide, adriamycin, cyclo- and prednisone (BEACOPP) as first-line regimens. ABVD phosphamide, vincristine, procarbazine, prednisone appears to be as effective, with fewer side effects, as (BEACOPP) and Stanford V. Brentuximab vedotin, the first escalated BEACOPP. Escalated BEACOPP leads to a Food and Drug Administration (FDA)-approved agent for the greater progression-free survival but no difference in overall treatment of HL in over three decades, has been well-studied survival. Recent advancements in technology have enabled in many trials as a second-line agent after prior failed an exciting shift to molecular-targeted cancer therapy. chemotherapies. However, through our comprehensive Brentuximab vedotin, a CD30-directed antibody conjugate, literature research we did not find any study that reported the specifically targets malignant HL cells.