August 2019: Additions and Deletions to the Drug Product List
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Induction with Mitomycin C, Doxorubicin, Cisplatin And
British Journal of Cancer (1999) 80(12), 1962–1967 © 1999 Cancer Research Campaign Article no. bjoc.1999.0627 Induction with mitomycin C, doxorubicin, cisplatin and maintenance with weekly 5-fluorouracil, leucovorin for treatment of metastatic nasopharyngeal carcinoma: a phase II study RL Hong1, TS Sheen2, JY Ko2, MM Hsu2, CC Wang1 and LL Ting3 Departments of 1Oncology, 2Otolaryngology and 3Radiation Therapy, National Taiwan University Hospital, National Taiwan University, No. 7, Chung-Shan South Road, Taipei 10016, Taiwan Summary The combination of cisplatin and 5-fluorouracil (5-FU) (PF) is the most popular regimen for treating metastatic nasopharyngeal carcinoma (NPC) but it is limited by severe stomatitis and chronic cisplatin-related toxicity. A novel approach including induction with mitomycin C, doxorubicin and cisplatin (MAP) and subsequent maintenance with weekly 5-FU and leucovorin (FL) were designed with an aim to reduce acute and chronic toxicity of PF. Thirty-two patients of NPC with measurable metastatic lesions in the liver or lung were entered into this phase II trial. Mitomycin C 8 mg m–2, doxorubicin 40 mg m–2 and cisplatin 60 mg m–2 were given on day 1 every 3 weeks as initial induction. After either four courses or remission was achieved, patients received weekly dose of 5-FU 450 mg m–2 and leucovorin 30 mg m–2 for maintenance until disease progression. With 105 courses of MAP given, 5% were accompanied by grade 3 and 0% were accompanied by grade 4 stomatitis. The dose-limiting toxicity of MAP was myelosuppression. Forty per cent of courses had grade 3 and 13% of courses had grade 4 leukopenia. -
Arsenic Trioxide Is Highly Cytotoxic to Small Cell Lung Carcinoma Cells
160 Arsenic trioxide is highly cytotoxic to small cell lung carcinoma cells 1 1 Helen M. Pettersson, Alexander Pietras, effect of As2O3 on SCLC growth, as suggested by an Matilda Munksgaard Persson,1 Jenny Karlsson,1 increase in neuroendocrine markers in cultured cells. [Mol Leif Johansson,2 Maria C. Shoshan,3 Cancer Ther 2009;8(1):160–70] and Sven Pa˚hlman1 1Center for Molecular Pathology, CREATE Health and 2Division of Introduction Pathology, Department of Laboratory Medicine, Lund University, 3 Lung cancer is the most frequent cause of cancer deaths University Hospital MAS, Malmo¨, Sweden; and Department of f Oncology-Pathology, Cancer Center Karolinska, Karolinska worldwide and results in 1 million deaths each year (1). Institute and Hospital, Stockholm, Sweden Despite novel treatment strategies, the 5-year survival rate of lung cancer patients is only f15%. Small cell lung carcinoma (SCLC) accounts for 15% to 20% of all lung Abstract cancers diagnosed and is a very aggressive malignancy Small cell lung carcinoma (SCLC) is an extremely with early metastatic spread (2). Despite an initially high aggressive form of cancer and current treatment protocols rate of response to chemotherapy, which currently com- are insufficient. SCLC have neuroendocrine characteristics bines a platinum-based drug with another cytotoxic drug and show phenotypical similarities to the childhood tumor (3, 4), relapses occur in the absolute majority of SCLC neuroblastoma. As multidrug-resistant neuroblastoma patients. At relapse, the efficacy of further chemotherapy is cells are highly sensitive to arsenic trioxide (As2O3) poor and the need for alternative treatments is obvious. in vitro and in vivo, we here studied the cytotoxic effects Arsenic-containing compounds have been used in tradi- of As2O3 on SCLC cells. -
5-Fluorouracil + Adriamycin + Cyclophosphamide) Combination in Differentiated H9c2 Cells
Article Doxorubicin Is Key for the Cardiotoxicity of FAC (5-Fluorouracil + Adriamycin + Cyclophosphamide) Combination in Differentiated H9c2 Cells Maria Pereira-Oliveira, Ana Reis-Mendes, Félix Carvalho, Fernando Remião, Maria de Lourdes Bastos and Vera Marisa Costa * UCIBIO, REQUIMTE, Laboratory of Toxicology, Faculty of Pharmacy, University of Porto, Rua de Jorge Viterbo Ferreira, 228, 4050-313 Porto, Portugal; [email protected] (M.P.-O.); [email protected] (A.R.-M.); [email protected] (F.C.); [email protected] (F.R.); [email protected] (M.L.B.) * Correspondence: [email protected] Received: 4 October 2018; Accepted: 3 January 2019; Published: 10 January 2019 Abstract: Currently, a common therapeutic approach in cancer treatment encompasses a drug combination to attain an overall better efficacy. Unfortunately, it leads to a higher incidence of severe side effects, namely cardiotoxicity. This work aimed to assess the cytotoxicity of doxorubicin (DOX, also known as Adriamycin), 5-fluorouracil (5-FU), cyclophosphamide (CYA), and their combination (5-Fluorouracil + Adriamycin + Cyclophosphamide, FAC) in H9c2 cardiac cells, for a better understanding of the contribution of each drug to FAC-induced cardiotoxicity. Differentiated H9c2 cells were exposed to pharmacological relevant concentrations of DOX (0.13–5 μM), 5-FU (0.13–5 μM), CYA (0.13–5 μM) for 24 or 48 h. Cells were also exposed to FAC mixtures (0.2, 1 or 5 μM of each drug and 50 μM 5-FU + 1 μM DOX + 50 μM CYA). DOX was the most cytotoxic drug, followed by 5-FU and lastly CYA in both cytotoxicity assays (reduction of 3-(4,5-dimethylthiazol-2- yl)-2,5-diphenyl tetrazolium bromide (MTT) and neutral red (NR) uptake). -
Characteristics of Doxorubicin‑Selected Multidrug‑Resistant Human Leukemia HL‑60 Cells with Tolerance to Arsenic Trioxide and Contribution of Leukemia Stem Cells
ONCOLOGY LETTERS 15: 1255-1262, 2018 Characteristics of doxorubicin‑selected multidrug‑resistant human leukemia HL‑60 cells with tolerance to arsenic trioxide and contribution of leukemia stem cells JING CHEN, HULAI WEI, JIE CHENG, BEI XIE, BEI WANG, JUAN YI, BAOYING TIAN, ZHUAN LIU, FEIFEI WANG and ZHEWEN ZHANG Key Laboratory of Preclinical Study for New Drugs of Gansu Province, School of Basic Medical Sciences, Lanzhou University, Lanzhou, Gansu 730000, P.R. China Received December 29, 2015; Accepted June 9, 2017 DOI: 10.3892/ol.2017.7353 Abstract. The present study selected and characterized resistance (MDR) frequently induces therapy failure or tumor a multidrug-resistant HL-60 human acute promyelocytic recurrence (1-3). MDR involves various mechanisms including, leukemia cell line, HL-60/RS, by exposure to stepwise adenosine triphosphate-binding cassette (ABC) transporters, incremental doses of doxorubicin. The drug-resistant P-glycoprotein (P-gp), multidrug-resistance-related protein HL-60/RS cells exhibited 85.68-fold resistance to doxoru- (MRP) and breast-cancer-resistance protein (BCRP) overex- bicin and were cross-resistant to other chemotherapeutics, pression, which function to efflux certain molecules out of including cisplatin, daunorubicin, cytarabine, vincristine the cells (4-8). In addition, mechanisms of acquired MDR and etoposide. The cells over-expressed the transporters in leukemia also include abnormal drug metabolism and the P-glycoprotein, multidrug-resistance-related protein 1 presence of leukemia stem cells (LSC). LSCs are particu- and breast-cancer-resistance protein, encoded by the larly of interest and considered to serve an important role adenosine triphosphate-binding cassette (ABC)B1, ABCC1 in leukemia resistance and relapse (4). -
Cyclophosphamide-Doxorubicin Ver
Chemotherapy Protocol BREAST CANCER CYCLOPHOSPHAMIDE-DOXORUBICIN Regimen Breast Cancer – Cyclophosphamide-Doxorubicin Indication Primary systemic (neoadjuvant) therapy of breast cancer Adjuvant therapy of high risk (greater than 5%) node negative breast cancer WHO Performance status 0, 1, 2 Toxicity Drug Adverse Effect Cyclophosphamide Dysuria, haemorrhagic cystitis, taste disturbances Doxorubicin Cardio toxicity, urinary discolourisation (red) The adverse effects listed are not exhaustive. Please refer to the relevant Summary of Product Characteristics for full details. Monitoring Regimen FBC, U&E’s and LFT’s prior to each cycle. Ensure adequate cardiac function before starting treatment with doxorubicin. Baseline LVEF should be measured, particularly in patients with a history of cardiac problems or in the elderly. Dose Modifications The dose modifications listed are for haematological, liver and renal function only. Dose adjustments may be necessary for other toxicities as well. In principle all dose reductions due to adverse drug reactions should not be re- escalated in subsequent cycles without consultant approval. It is also a general rule for chemotherapy that if a third dose reduction is necessary treatment should be stopped. Version 1.1 (Aug 2014) Page 1 of 6 Breast – Cyclophosphamide-Doxorubicin Please discuss all dose reductions / delays with the relevant consultant before prescribing if appropriate. The approach may be different depending on the clinical circumstances. The following is a general guide only. Haematological Prior to prescribing the following treatment criteria must be met on day 1 of treatment. Criteria Eligible Level Neutrophil equal to or more than 1x109/L Platelets equal to or more than 100x109/L Consider blood transfusion if patient symptomatic of anaemia or has a haemoglobin of less than 8g/dL If counts on day one are below these criteria for neutrophil and/or platelets then delay treatment for seven days. -
Combination Chemotherapy with Estramustine Phosphate, Ifosfamide and Cisplatin for Hormone-Refractory Prostate Cancer
Acta Med. Okayama, 2006 Vol. 60, No. 1, pp. 43ﾝ49 CopyrightⒸ 2006 by Okayama University Medical School. Original Article http ://www.lib.okayama-u.ac.jp/www/acta/ Combination Chemotherapy with Estramustine Phosphate, Ifosfamide and Cisplatin for Hormone-refractory Prostate Cancer Haruki Kakua, Takashi Saikaa＊, Tomoyasu Tsushimab, Atsushi Nagaia, Teruhiko Yokoyamaa, Fernando Abarzuaa, Shin Ebaraa, Daisuke Manabea, Yasutomo Nasua, and Hiromi Kumona aDepartment of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 700ﾝ8558, Japan, and bDepartment of Urology, Medival center of Okayama, Okayama 701-1192, Japan We evaluated the effi ciency and toxicity of estramustine phosphate (ECT), ifosfamide (IFM) and cis- platin (CDDP) combination chemotherapy in twenty-one patients with hormone-refractory prostate cancer (HRPC), for which there is currently no eff ective treatment. Patients received a daily dose of 560 mg ECT in combination with 1.2 g/m2 IFM on days 1 to 5 and 70 mg/m2 CDDP on day 1. This combination therapy was given every 3 to 4 weeks. An objective response of more than 50ｵ reduc- tion in prostate-specifi c antigen was observed in 9 of 18 patients (50ｵ), and a more than 50ｵ reduc- tion in bi-dimensionally measurable soft-tissue lesions was observed in 2 of 7 patients (29ｵ). The median duration of response among the cases showing partial response was 40 weeks, while the median duration of response of overall partial-response plus stable cases was 30 weeks. The median survival duration of all cases was 47 weeks. Toxicity was modest and acceptable. In conclusion, the ECT, IFM and CDDP combination chemotherapy regimen is a viable treatment option for HRPC. -
Chemotherapy Protocol
Chemotherapy Protocol BREAST CANCER CYCLOPHOSPHAMIDE-DOCETAXEL-DOXORUBICIN (TAC) Regimen Breast Cancer – Cyclophosphamide-Docetaxel-Doxorubicin (TAC) Indication Adjuvant therapy for node positive early breast cancer WHO Performance status 0, 1, 2 Toxicity Drug Adverse Effect Cyclophosphamide Dysuria, haemorrhagic cystitis, taste disturbances Hypersensitivity, fluid retention, neuropathy, joint pains, nail Docetaxel changes, fatigue Doxorubicin Cardio toxicity, urinary discolourisation (red) The adverse effects listed are not exhaustive. Please refer to the relevant Summary of Product Characteristics for full details. Monitoring Regimen FBC, U&E’s and LFT’s prior to each cycle. Ensure adequate cardiac function before starting treatment. Baseline LVEF should be measured, particularly in patients with a history of cardiac problems or in the elderly. Dose Modifications The dose modifications listed are for haematological, liver and renal function only. Dose adjustments may be necessary for other toxicities as well. In principle all dose reductions due to adverse drug reactions should not be re- escalated in subsequent cycles without consultant approval. It is also a general rule for chemotherapy that if a third dose reduction is necessary treatment should be stopped. Version 1.1 (Aug 2014) Page 1 of 8 Breast – Cyclophosphamide-Docetaxel-Doxorubicin (TAC) Please discuss all dose reductions / delays with the relevant consultant before prescribing if appropriate. The approach may be different depending on the clinical circumstances. The following is a general guide only. Haematological Prior to prescribing the following treatment criteria must be met on day one of treatment. Criteria Eligible Level Neutrophil equal to or more than 1x109/L Platelets equal to or more than 100x109/L Consider blood transfusion if patient symptomatic of anaemia or has a haemoglobin of less than 8g/dL If counts on day one are below these criteria for neutrophils and/or platelets then delay treatment for seven days. -
SAVACM Protocol
BC Cancer Protocol Summary for the Treatment of Sarcomas with Pelvic Primaries or Chemotherapy-Induced Hematuria using vinCRIStine, DOXOrubicin, Cyclophosphamide and Mesna Protocol Code SAVACM Tumour Group Sarcoma Contact Physician Dr. Christine Simmons ELIGIBILITY: . Ewing’s sarcoma/peripheral neuroectodermal tumour or rhabdomyosarcoma in pelvic sites or pediatric type small round blue cell tumours in patients for whom alternating protocol is not appropriate where treatment includes pelvic radiotherapy . Patients with hematuria due to ifosfamide or cyclophosphamide . Good performance status . Adequate bone marrow, liver and kidney function TESTS: . Baseline and before each treatment: CBC and diff, platelets, creatinine, bilirubin, ALT, alkaline phosphatase, GGT, LDH . Urine dipstick for blood before each treatment and every 8 hours during treatment – if positive at any time, notify doctor and send urine sample for urinalysis and verification and accurate determination - refer to supportive care protocol SCMESNA (follow SCMESNA (SAVACM) preprinted order) . If clinically indicated: ECG PREMEDICATIONS: . Antiemetic protocol for highly emetogenic chemotherapy protocols (see SCNAUSEA) . LORazepam 1 mg SL every 4 to 6 hours as needed . prochlorperazine 10 mg PO every 4 to 6 hours as needed . nabilone 1 mg PO every 6 to 8 hours as needed TREATMENT: . Repeat every 3 weeks. SAVACM is not given during radiotherapy; omit DOXOrubicin and continue with vinCRIStine, cyclophosphamide and mesna. BC Cancer Protocol Summary SAVACM Page 1 of 3 Activated: N/A Revised: 1 Apr 2021 (prochlorperazine route) Warning: The information contained in these documents are a statement of consensus of BC Cancer professionals regarding their views of currently accepted approaches to treatment. Any clinician seeking to apply or consult these documents is expected to use independent medical judgement in the context of individual clinical circumstances to determine any patient's care or treatment. -
Protocol Code: BRAJACTW Tumour Group: Breast Contact Physician: Dr
BC Cancer Protocol Summary for Neoadjuvant or Adjuvant Therapy for Early Breast Cancer Using DOXOrubicin and Cyclophosphamide followed by Weekly PACLitaxel Protocol Code: BRAJACTW Tumour Group: Breast Contact Physician: Dr. Caroline Lohrisch ELIGIBILITY: A number of studies suggest that the schedule of delivery of PACLitaxel is important in maximizing efficacy. The preferred delivery method of PACLitaxel after AC chemotherapy is either every two weeks with G-CSF (see protocol BRAJACTG) or weekly for 12 weeks, as described in this protocol. Neoadjuvant or adjuvant treatment for 1 or more axillary lymph node metastasis(es), or node negative but with high risk of recurrence EXCLUSIONS: . Pregnancy . Severe cardiovascular disease with LVEF less than 55% . AST and/or ALT greater than 10 times the Upper Limit of Normal (ULN) . total bilirubin greater than 128 micromol/L TESTS: . Baseline and Prior to Cycle #5: CBC & diff, platelets, bilirubin, ALT . Baseline if clinically indicated: alk phos, LDH, GGT . Before each treatment: CBC & diff, platelets . If clinically indicated: bilirubin, ALT, creatinine PREMEDICATIONS: . For the 4 cycles of DOXOrubicin and cyclophosphamide: Antiemetic protocol for highly emetogenic chemotherapy (see protocol SCNAUSEA) . For the 4 cycles (=12 weeks) of PACLitaxel: PACLitaxel must not be started unless the following drugs have been given: 45 minutes prior to PACLitaxel: . dexamethasone 10 mg IV in 50 mL NS over 15 minutes 30 minutes prior to PACLitaxel: . diphenhydrAMINE 25 mg IV in NS 50 mL over 15 minutes and famotidine 20 mg IV in NS 100 mL over 15 minutes (Y-site compatible) . If no PACLitaxel infusion reactions occur, no premedications may be needed for subsequent PACLitaxel doses and may be omitted at physician’s discretion. -
Multiple Myeloma
MULTIPLE MYELOMA ARSENIC TRIOXIDE Arsenic trioxide 0.25 mg/kg/day IV* Monday - Friday of Weeks 1 and 2** *Administer over 1 hour; **Administer Monday - Friday (5 days per week) during the first 2 weeks of each 4 week cycle. Repeat cycles every 28 days. NOTE: Ensure that serum electrolytes are assessed and corrected, particularly potassium and magnesium, prior to start of treatment, and maintain these values throughout the cycle. Avoid medication known to prolong the QTc interval. Obtain a 12-lead ECG prior to the first dose and ensure that the QTc interval is not greater than 460 msec. Reference: Hussein MA, et al. Br J Haematol 2004;125:470 - 6. BORTEZOMIB Bortezomib 1.3 mg/m2 IVB Days 1, 4, 8 and 11 Repeat cycle every 21 days to a maximum of 8 cycles. NOTE: Patients with progressive disease after 2 cycles or stable diseases after 4 cycles were able to receive dexamethasone 20 mg on the day of and the day after bortezomib. Reference: Richardson PG, et al. N Engl J Med 2003;348:2609 – 17. BORTEZOMIB – DOXORUBICIN - DEXAMETHASONE Bortezomib 1.3 mg/m2 IVB Days 1, 4, 8 and 11 Dexamethasone 40 mg /day PO See below (cycle dependent) Doxorubicin 9 mg/m2/day IV Days 1 - 4 Repeat cycle every 21 days for 4 cycles. NOTE: Dexamethasone dosing: 40 mg PO/day was administered on days 1 – 4, 8 – 11, and 15 – 18 of cycle 1 and on days 1 – 4 of cycles 2 – 4. Concurrent bisphosphonate therapy, gastric protection, erythropoietin and Pneumocystis carinii prophylaxis were given. -
Doxorubicin Liposome (Doxil®) Pronounced: “Doks-Oh-ROO-Bi-Sin Lye-Po-Soam”
Doxorubicin Liposome Chemotherapy: Doxorubicin Liposome (Doxil®) Pronounced: “doks-oh-ROO-bi-sin lye-po-soam” How drug is given: By vein (IV) Purpose: To stop the growth of cancer cells in many different types of cancer. This drug is a special form of the cancer drug doxorubicin, mixed in a special solution of liposomes (“fat bodies”). Things that may occur during or within hours of treatment • An allergic reaction may occur. Tell your cancer care team right away if you have fever, chills, chest pain, trouble breathing, itching, rash, or dizziness. This can be life threatening. • You may be given drugs before you start doxorubicin liposome that will try to keep this from happening. You may be asked to take dexamethasone (a steroid) at home before you start treatment. • Your blood pressure may drop, or your heart rate may slow down while you are getting this drug. You might feel lightheaded or dizzy. This usually goes back to normal on its own. It is important to ask for assistance and take your time when you stand up during or after your treatment. • If you feel any burning or tingling near your IV, please tell your nurse right away. If you develop any swelling or redness after you go home, call your cancer care team right away. Things that may occur a few days to weeks later • Mild to moderate nausea, vomiting, and loss of appetite may occur. You may be given drugs to help with this. • Some of your hair may thin and fall out with treatment. • Tingling and peeling of the skin may occur. -
Antitumor Antibiotics
ANTITUMOR ANTIBIOTICS ANTHRACYCLINES ANTHRACENEDIONES DOXORUBICIN MITOXANTRONE ® ® ® ® (ADRIAMYCIN PFS , RUBEX , ADRIAMYCIN RDF )(NOVANTRONE ) DAUNORUBICIN PIXANTRONE* ® (CERUBIDINE ) (*NOT AVAIL; FDA FAST TRACK 7/04) IDARUBICIN ® ® (IDAMYCIN , IDAMYCIN PDF ) EPIRUBICIN ® (ELLENCE ) DOXORUBICIN/DAUNORUBICIN/IDARUBICIN/EPIRUBICIN I. MECHANISM OF ACTION A) These four drugs diffuse freely across cell membranes and into the cell nucleus. B) Once inside, they intercalate with DNA, which means they physically enter the double helix and interfere with uncoiling. C) More importantly, the drugs interfere with topoisomerase II, an enzyme that promotes strand breakage and resealing. Topoisomerase II is one of the enzymes that repair DNA. Apparently, intercalation alters the shape of DNA such that topoisomerase II cannot repair damaged DNA. D) When topoisomerase II, DNA and an anthracycline are bound together, DNA strand breaks appear. E) In addition, doxorubicin, daunorubicin and epirubicin cause formation of free radicals, chemicals with one too many electrons, which chemically damage cell structures. Free radical formation involves water or iron. Free radical formation most certainly contributes to the cardiotoxicity of these drugs and possibly to their antineoplastic activity. The heart lacks a good defense system against free radicals along with rapid production of hydrogen peroxide, both of which make the heart very sensitive to the anthracyclines. F) Resistance is due to P-glycoprotein, alteration of topoisomerase function or decreased topoisomerase concentration. II. PHARMACOKINETICS A) Idarubicin has an oral bioavailability of 30%. More of the active metabolite, idarubicinol, is formed by the oral route than the IV route. Idarubicinol is an active metabolite and is equi- or more potent than the parent compound. B) Distribution- Enters cells rapidly.