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A Systematic Review of the Effectiveness of Docetaxel and Mitoxantrone for the Treatment of Metastatic Hormone-Refractory Prostate Cancer
British Journal of Cancer (2006) 95, 457 – 462 & 2006 Cancer Research UK All rights reserved 0007 – 0920/06 $30.00 www.bjcancer.com A systematic review of the effectiveness of docetaxel and mitoxantrone for the treatment of metastatic hormone-refractory prostate cancer *,1 1 1 1 2 3 4 5 R Collins , R Trowman , G Norman , K Light , A Birtle , E Fenwick , S Palmer and R Riemsma 1 2 Centre for Reviews and Dissemination, University of York, Heslington, York YO10 5DD, UK; Rosemere Cancer Centre, Royal Preston Hospital, Sharoe 3 Green Lane North, Fulwood, Preston PR2 9HT, UK; Public Health & Health Policy, Division of Community Based Sciences, University of Glasgow, 4 5 1 Lilybank Gardens, Glasgow G12 8RZ, UK; Centre for Health Economics, University of York, Heslington, York YO10 5DD, UK; Kleijnen Systematic Reviews Ltd, Westminster Business Centre, 10 Great North Way, Nether Poppleton, York YO26 6RB, UK Clinical Studies A systematic review was performed to evaluate the clinical effectiveness of docetaxel in combination with prednisolone (docetaxel is licensed in the UK for use in combination with prednisone or prednisolone for the treatment of patients with metastatic hormone- refractory prostate cancer. Prednisone is not used in the UK, but it is reasonable to use docetaxel plus prednisone data in this review of docetaxel plus prednisolone) for the treatment of metastatic hormone-refractory prostate cancer. A scoping search identified a trial of docetaxel plus prednisone vs mitoxantrone plus prednisone, but did not identify any trials comparing docetaxel plus prednisolone/prednisone with any other treatments. Therefore, we considered additional indirect evidence that would enable a comparison of docetaxel plus prednisolone/prednisone with other chemotherapy regimens and active supportive care. -
Idamycin PFS® Idarubicin Hydrochloride Injection
Idamycin PFS® idarubicin hydrochloride injection Rx only FOR INTRAVENOUS USE ONLY WARNINGS 1. IDAMYCIN PFS Injection should be given slowly into a freely flowing intravenous infusion. It must never be given intramuscularly or subcutaneously. Severe local tissue necrosis can occur if there is extravasation during administration. 2. As is the case with other anthracyclines the use of IDAMYCIN PFS can cause myocardial toxicity leading to congestive heart failure. Cardiac toxicity is more common in patients who have received prior anthracyclines or who have pre- existing cardiac disease. 3. As is usual with antileukemic agents, severe myelosuppression occurs when IDAMYCIN PFS is used at effective therapeutic doses. 4. It is recommended that IDAMYCIN PFS be administered only under the supervision of a physician who is experienced in leukemia chemotherapy and in facilities with laboratory and supportive resources adequate to monitor drug tolerance and protect and maintain a patient compromised by drug toxicity. The physician and institution must be capable of responding rapidly and completely to severe hemorrhagic conditions and/or overwhelming infection. 5. Dosage should be reduced in patients with impaired hepatic or renal function. (See DOSAGE AND ADMINISTRATION.) DESCRIPTION IDAMYCIN PFS Injection contains idarubicin hydrochloride and is a sterile, semi- synthetic, preservative-free solution (PFS) antineoplastic anthracycline for intravenous use. Chemically, idarubicin hydrochloride is 5, 12-Naphthacenedione, 9-acetyl-7-[(3- amino-2,3,6-trideoxy-α-L-lyxo-hexopyranosyl)oxy]-7,8,9,10-tetrahydro-6,9,11- trihydroxyhydrochloride, (7S-cis). The structural formula is as follows: C26 H27 NO9 .HCL M.W. 533.96 1 Reference ID: 3668307 IDAMYCIN PFS is a sterile, red-orange, isotonic parenteral preservative-free solution, available in 5 mL (5 mg), 10 mL (10 mg) and 20 mL (20 mg) single-use-only vials. -
NOVANTRONE (Mitoxantrone for Injection Concentrate) in Patients with Hepatic Insufficiency Is Not Established (See CLINICAL PHARMACOLOGY)
NOVANTRONE® mitoXANTRONE for injection concentrate WARNING NOVANTRONE® (mitoxantrone for injection concentrate) should be administered under the supervision of a physician experienced in the use of cytotoxic chemotherapy agents. NOVANTRONE® should be given slowly into a freely flowing intravenous infusion. It must never be given subcutaneously, intramuscularly, or intra-arterially. Severe local tissue damage may occur if there is extravasation during administration. (See ADVERSE REACTIONS, General, Cutaneous and DOSAGE AND ADMINISTRATION, Preparation and Administration Precautions). NOT FOR INTRATHECAL USE. Severe injury with permanent sequelae can result from intrathecal administration. (See WARNINGS, General) Except for the treatment of acute nonlymphocytic leukemia, NOVANTRONE® therapy generally should not be given to patients with baseline neutrophil counts of less than 1,500 cells/mm3. In order to monitor the occurrence of bone marrow suppression, primarily neutropenia, which may be severe and result in infection, it is recommended that frequent peripheral blood cell counts be performed on all patients receiving NOVANTRONE®. Cardiotoxicity: Congestive heart failure (CHF), potentially fatal, may occur either during therapy with NOVANTRONE® or months to years after termination of therapy. Cardiotoxicity risk increases with cumulative NOVANTRONE dose and may occur whether or not cardiac risk factors are present. Presence or history of cardiovascular disease, radiotherapy to the mediastinal/pericardial area, previous therapy with other anthracyclines or anthracenediones, or use of other cardiotoxic drugs may increase this risk. In cancer patients, the risk of symptomatic CHF was estimated to be 2.6% for patients receiving up to a cumulative dose of 140 mg/m2. To mitigate the cardiotoxicity risk with NOVANTRONE, prescribers should consider the following: NOVANTRONE mitoXANTRONE for injection 1 All Patients: - All patients should be assessed for cardiac signs and symptoms by history, physical examination, and ECG prior to start of NOVANTRONE® therapy. -
Idarubicin.Pdf
PRODUCT MONOGRAPH INCLUDING PATIENT MEDICATION INFORMATION PrIDARUBICIN idarubicin hydrochloride injection Preservative Free Solution, 1 mg/mL, intravenous injection Antineoplastic Agent Pfizer Canada ULC Date of Initial Authorization: 17,300 Trans-Canada Highway July 30, 2013 Kirkland, Quebec, H9J 2M5 Date of Revision: September 14, 2021 Submission Control Number: 255782 ©Pfizer Canada ULC, 2021 IDARUBICIN (idarubicin hydrochloride injection) Page 1 of 31 RECENT MAJOR LABEL CHANGES 7 Warnings and Precautions, Cardiovascular JA/2021 TABLE OF CONTENTS Sections or subsections that are not applicable at the time of authorization are not listed. RECENT MAJOR LABEL CHANGES ..........................................................................................2 TABLE OF CONTENTS ............................................................................................................2 1 INDICATIONS.............................................................................................................4 1.1 Pediatrics .................................................................................................................4 1.2 Geriatrics..................................................................................................................4 2 CONTRAINDICATIONS................................................................................................4 3 SERIOUS WARNINGS AND PRECAUTIONS BOX ...........................................................5 4 DOSAGE AND ADMINISTRATION................................................................................5 -
Summary Attachment for Eudract
Avenue E. Mounier 83/11 1200 Brussels Belgium Tel: +32 2 774 1611 Email: [email protected] www.eortc.org Summary Attachment for EudraCT Name of Individual study Table Referring to Part of the Dossier (For National Authority Use Sponsor/Company: Only) EORTC Name of the Volume: finished product Name of Active Page Ingredients: Clofarabine Cytarabine Idarubicin Title of the Study Clofarabine in combination with a standard remissioninduction regimen (AraC and idarubicin) in patients 18-60 years old with previously untreated intermediate and bad risk acute myelogenous leukemia (AML) or high risk myelodysplasia (MDS) : a phase I-II study of the EORTC-LG and GIMEMA (AML-14A trial) Investigators & Study Centers Number of Country City patients Belgium 4 101.Hopital Jules Bordet (BE) Brussels 1 109.A.Z. St Jan (BE) Brugge 3 Italy 28 3931.Tor Vergata Roma (IT) Roma 12 733.La Sapienza Ematologia (IT) Roma 16 Netherlands 43 304.RU Nijmegen (NL) Nijmegen 24 310.Univ Med Ctr Leiden (NL) Leiden 13 22.J Bosch 'S Hertogenb (NL) 's-Hertogenbosch 6 Grand Total 75 ST-006-AF-01 Page 1 of 4 Template version 2 Short Study Report for Health Authorities EORTC Name of Individual study Table Referring to Part of the Dossier (For National Authority Use Sponsor/Company: Only) EORTC Name of the Volume: finished product Name of Active Page Ingredients: Clofarabine Cytarabine Idarubicin Publication Willemze R, Suciu S, Muus P, Halkes CJ, Meloni G, Meert L, Karrasch M, Rapion J, (reference) Vignetti M, Amadori S, de Witte T, Marie JP.Clofarabine in combination with a standard remission induction regimen (cytosine arabinoside and idarubicin) in patients with previously untreated intermediate and bad-risk acute myelogenous leukemia (AML) or high-risk myelodysplastic syndrome (HR-MDS): phase I results of an ongoing phase I/II study of the leukemia groups of EORTC and GIMEMA (EORTC GIMEMA 06061/AML-14A trial). -
BC Cancer Benefit Drug List September 2021
Page 1 of 65 BC Cancer Benefit Drug List September 2021 DEFINITIONS Class I Reimbursed for active cancer or approved treatment or approved indication only. Reimbursed for approved indications only. Completion of the BC Cancer Compassionate Access Program Application (formerly Undesignated Indication Form) is necessary to Restricted Funding (R) provide the appropriate clinical information for each patient. NOTES 1. BC Cancer will reimburse, to the Communities Oncology Network hospital pharmacy, the actual acquisition cost of a Benefit Drug, up to the maximum price as determined by BC Cancer, based on the current brand and contract price. Please contact the OSCAR Hotline at 1-888-355-0355 if more information is required. 2. Not Otherwise Specified (NOS) code only applicable to Class I drugs where indicated. 3. Intrahepatic use of chemotherapy drugs is not reimbursable unless specified. 4. For queries regarding other indications not specified, please contact the BC Cancer Compassionate Access Program Office at 604.877.6000 x 6277 or [email protected] DOSAGE TUMOUR PROTOCOL DRUG APPROVED INDICATIONS CLASS NOTES FORM SITE CODES Therapy for Metastatic Castration-Sensitive Prostate Cancer using abiraterone tablet Genitourinary UGUMCSPABI* R Abiraterone and Prednisone Palliative Therapy for Metastatic Castration Resistant Prostate Cancer abiraterone tablet Genitourinary UGUPABI R Using Abiraterone and prednisone acitretin capsule Lymphoma reversal of early dysplastic and neoplastic stem changes LYNOS I first-line treatment of epidermal -
How to Manage Acute Promyelocytic Leukemia
Leukemia (2012) 26, 1743 -- 1751 & 2012 Macmillan Publishers Limited All rights reserved 0887-6924/12 www.nature.com/leu HOW TO MANAGEy How to manage acute promyelocytic leukemia J-Q Mi, J-M Li, Z-X Shen, S-J Chen and Z Chen Acute promyelocytic leukemia (APL) is a unique subtype of acute myeloid leukemia (AML). The prognosis of APL is changing, from the worst among AML as it used to be, to currently the best. The application of all-trans-retinoic acid (ATRA) to the induction therapy of APL decreases the mortality of newly diagnosed patients, thereby significantly improving the response rate. Therefore, ATRA combined with anthracycline-based chemotherapy has been widely accepted and used as a classic treatment. It has been demonstrated that high doses of cytarabine have a good effect on the prevention of relapse for high-risk patients. However, as the indications of arsenic trioxide (ATO) for APL are being extended from the original relapse treatment to the first-line treatment of de novo APL, we find that the regimen of ATRA, combined with ATO, seems to be a new treatment option because of their targeting mechanisms, milder toxicities and improvements of long-term outcomes; this combination may become a potentially curable treatment modality for APL. We discuss the therapeutic strategies for APL, particularly the novel approaches to newly diagnosed patients and the handling of side effects of treatment and relapse treatment, so as to ensure each newly diagnosed patient of APL the most timely and best treatment. Leukemia (2012) 26, 1743--1751; doi:10.1038/leu.2012.57 Keywords: acute promyelocytic leukemia (APL); all-trans-retinoic acid (ATRA); arsenic trioxide (ATO) INTRODUCTION In this review, we introduce the therapeutic strategies of APL, Acute promyelocytic leukemia (APL) is a distinct subtype of acute including the treatment of newly diagnosed and relapsed myeloid leukemia (AML) characterized by its abnormal promye- patients, as well as the ways to deal with the side effects. -
How I Treat How I Treat Hyperleukocytosis in Acute Myeloid Leukemia
From www.bloodjournal.org by guest on January 2, 2016. For personal use only. How I Treat How I treat hyperleukocytosis in acute myeloid leukemia Christoph R¨olligand Gerhard Ehninger Medizinische Klinik und Poliklinik I, Universit¨atsklinikumder Technischen Universit¨at Dresden, Germany Hyperleukocytosis (HL) per se is a labora- chronic leukemias, and particularly leuko- lactate dehydrogenase as an indicator for tory abnormality, commonly defined by stasis occurs more often in acute myeloid high proliferation are part of prognostic a white blood cell count >100 000/mL, leukemia (AML) for several reasons. Only scores guiding risk-adapted consolidation caused by leukemic cell proliferation. Not a small proportion of AML patients present strategies, HL at initial diagnosis must be the high blood count itself, but complica- with HL, but these patients have a partic- considered a hematologic emergency and tions such as leukostasis, tumor lysis syn- ularly dismal prognosis because of (1) a requires rapid action of the admitting drome, and disseminated intravascular higher risk of early death resulting from physician in order to prevent early death. coagulation put the patient at risk and HL complications; and (2) a higher proba- (Blood. 2015;125(21):3246-3252) require therapeutic intervention. The risk bility of relapse and death in the long run. of complications is higher in acute than in Whereas initial high blood counts and high Incidence and pathophysiology In untreated acute myeloid leukemia (AML), ;5% to 20% of patients factor VII.18 TLS may occur as a result of spontaneous or treatment- present with hyperleukocytosis (HL).1-10 In a patient with HL, under- induced cell death. -
Methotrexate Cross-Resistance in a Mitoxantrone-Selected Multidrug-Resistant MCF7 Breast Cancer Cell Line Is Attributable to Enhanced Energy-Dependent Drug Efflux1
[CANCER RESEARCH 60, 3514–3521, July 1, 2000] Methotrexate Cross-Resistance in a Mitoxantrone-selected Multidrug-resistant MCF7 Breast Cancer Cell Line Is Attributable to Enhanced Energy-dependent Drug Efflux1 Erin L. Volk, Kristin Rohde, Myung Rhee, John J. McGuire, L. Austin Doyle, Douglas D. Ross, and Erasmus Schneider2 Wadsworth Center, New York State Department of Health, Albany, New York 12201 [E. L. V., K. R., M. R., E. S.]; Department of Biomedical Sciences, School of Public Health, University at Albany, Albany, New York 12201 [E. L. V., E. S.]; Grace Cancer Drug Center, Roswell Park Cancer Institute, Buffalo, New York 14263 [J. J. M.]; Greenbaum Cancer Center of the University of Maryland, Baltimore, Maryland 21201 [L. A. D., D. D. R.]; Department of Medicine, Division of Hematology/Oncology, University of Maryland School of Medicine, Baltimore, Maryland 21201 [L. A. D., D. D. R.]; and Baltimore Veterans Medical Center, Department of Veterans Affairs, Baltimore, Maryland 21201 [D. D. R.] ABSTRACT resistance has been shown to be caused by decreased uptake attribut- able to the absence (2) of or defects (5, 6) in RFC1, reduced poly- Cellular resistance to the antifolate methotrexate (MTX) is often caused glutamylation either through decreased FPGS activity and/or expres- by target amplification, uptake defects, or alterations in polyglutamyla- sion (7), or enhanced ␥-GH activity and/or expression (8), and DHFR tion. Here we have examined MTX cross-resistance in a human breast carcinoma cell line (MCF7/MX) selected in the presence of mitoxantrone, overexpression (9) or mutation (10–12). an anticancer agent associated with the multidrug resistance (MDR) In contrast, a putative role for drug efflux in MTX resistance, phenotype. -
Cellular Pharmacology of Mitoxantrone in P
Leukemia (1997) 11, 2066–2074 1997 Stockton Press All rights reserved 0887-6924/97 $12.00 Cellular pharmacology of mitoxantrone in p-glycoprotein-positive and -negative human myeloid leukemic cell lines U Consoli, NT Van, N Neamati, R Mahadevia, M Beran, S Zhao and M Andreeff Department of Hematology, Section of Experimental Hematology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA Previous reports suggest that resistance to mitoxantrone in dif- protein is particularly important because it confers cross-resist- ferent tumor cell lines is unrelated to the overexpression of p- ance to several structurally unrelated drugs.9 The mechanisms glycoprotein. In order to determine the role of p-glycoprotein in the cellular pharmacology of mitoxantrone flow cytometry of action of mitoxantrone resistance are not well known. and confocal microscopy were used to study two human Although mitoxantrone seems to select for a unique drug- myeloid leukemia cell lines selected for resistance to mitoxan- resistance phenotype, some cross-resistance with anthracy- trone (HL-60MX2) and doxorubicin (HL-60DOX). To optimize the clines has been shown in vitro.10,11 Human colon carci- detection of intracellular mitoxantrone, we determined the noma,12 leukemia13 and gastric carcinoma14 cell lines selec- maximum excitation (607 nm) and emission (684 nm) wave- length by fluorescence spectroscopy. The modified flow cyto- ted by continuous exposure to increasing concentrations of metric conditions using 568.2 nm laser emission for excitation mitoxantrone had no p-glycoprotein overexpression. Clinical and a 620 nm long pass filter for fluorescence collection cross-over studies have not demonstrated complete cross- resulted in a 1-log increase in sensitivity, compared with stan- resistance between mitoxantrone and doxorubicin,15,16 pro- dard 488-nm laser excitation. -
Single-Agent Arsenic Trioxide in the Treatment of Newly Diagnosed Acute Promyelocytic Leukemia: Durable Remissions with Minimal Toxicity
CLINICAL TRIALS AND OBSERVATIONS Single-agent arsenic trioxide in the treatment of newly diagnosed acute promyelocytic leukemia: durable remissions with minimal toxicity Vikram Mathews, Biju George, Kavitha M. Lakshmi, Auro Viswabandya, Ashish Bajel, Poonkuzhali Balasubramanian, Ramachandran Velayudhan Shaji, Vivi M. Srivastava, Alok Srivastava, and Mammen Chandy Arsenic trioxide, as a single agent, has of 25 months (range: 8-92 months), the men was administered on an outpatient proven efficacy in inducing molecular remis- 3-year Kaplan-Meier estimate of EFS, DFS, basis. Single-agent As2O3, as used in this -sion in patients with acute promyelocytic and OS was 74.87% ؎ 5.6%, 87.21% ؎ series, in the management of newly diag leukemia (APL). There is limited long- 4.93%, and 86.11% ؎ 4.08%, respectively. nosed cases of APL, is associated with term outcome data with single-agent Patients presenting with a white blood responses comparable with conventional As O in the management of newly diag- cell (WBC) count lower than 5 ؋ 109/L and chemotherapy regimens. Additionally, this 2 3 nosed cases of APL. Between January a platelet count higher than 20 ؋ 109/L at regimen has minimal toxicity and can be have an excel- administered on an outpatient basis after ([%30.6] 22 ؍ to December 2004, 72 newly diag- diagnosis (n 1998 nosed cases of APL were treated with a lent prognosis with this regimen (EFS, remission induction. (Blood. 2006;107: regimen of single-agent As2O3 at our cen- OS, and DFS of 100%). The toxicity pro- 2627-2632) ter. Complete hematologic remission was file, in the majority, was mild and revers- achieved in 86.1%. -
Acute Lymphoblastic Leukemia (ALL) (Part 1 Of
LEUKEMIA TREATMENT REGIMENS: Acute Lymphoblastic Leukemia (ALL) (Part 1 of 12) Note: The National Comprehensive Cancer Network (NCCN) Guidelines® for Acute Lymphoblastic Leukemia (ALL) should be consulted for the management of patients with lymphoblastic lymphoma. Clinical Trials: The NCCN 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 healthcare 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 only provided to supplement the latest treatment strategies. The NCCN Guidelines are a work in progress that may be refined as often as new significant data becomes available. They 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