DOCSLIB.ORG

Emetogenic Potential of Antineoplastic Agents

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Emetogenic Potential of Antineoplastic Agents EMETOGENIC POTENTIAL OF ANTINEOPLASTIC AGENTS (Part 1 of 2) INTRAVENOUS/INJECTABLE AGENTS HIGH RISK (>90% frequency)† AC combination: any regimen containing anthracycline + Dacarbazine cyclophosphamide Doxorubicin ≥60mg/m² Carboplatin AUC ≥4 Epirubicin (Ellence) >90mg/m² Carmustine (BiCNU) >250mg/m² Ifosfamide (Ifex) ≥2g/m² per dose Cisplatin Mechlorethamine Cyclophosphamide >1,500mg/m² Streptozocin (Zanosar) MODERATE RISK (>30–90% frequency)† Aldesleukin (Proleukin) >12−15 million IU/m² Dual-drug liposomal cytarabine + daunorubicin (Vyxeos) Amifostine (Ethyol) >300mg/m² Dinutuximab (Unituxin) Arsenic trioxide (Trisenox) Doxorubicin <60mg/m²* Azacitidine (Vidaza) Epirubicin (Ellence) ≤90mg/m²* Bendamustine (Treanda) Idarubicin (Idamycin PFS) Busulfan (Busulfex) Ifosfamide (Ifex) <2g/m² per dose* Carboplatin AUC <4* Interferon alfa (Intron A) ≥10 million IU/m² Carmustine (BiCNU) ≤250mg/m²* Irinotecan (Camptosar)* Clofarabine (Clolar) Melphalan (Alkeran, Evomela) Cyclophosphamide ≤1,500mg/m² Methotrexate ≥250 mg/m²* Cytarabine >200mg/m² Oxaliplatin (Eloxatin)* Dactinomycin (Cosmegen)* Temozolomide (Temodar) Daunorubicin (Cerubidine)* Trabectedin (Yondelis)* LOW RISK (10–30% frequency)† Ado-trastuzumab emtansine (Kadcyla) Interferon alfa (Intron A) >5−<10 million IU/m² Aldesleukin (Proleukin) ≤12 million IU/m² Ixabepilone (Ixempra) Amifostine (Ethyol) ≤300mg/m² Methotrexate >50mg/m²−<250mg/m² Axicabtagene ciloleucel (Yescarta) Mitomycin Belinostat (Beleodaq) Mitoxantrone Brentuximab vedotin (Adcetris) Necitumumab (Portrazza) Cabazitaxel (Jevtana) Olaratumab (Lartruvo) Carfilzomib (Kyprolis) Omacetaxine (Synribo) Copanlisib (Aliqopa) Paclitaxel (Taxol) Cytarabine (low dose) 100−200mg/m² Paclitaxel-albumin (Abraxane) Docetaxel (Taxotere) Pemetrexed (Alimta) Doxorubicin liposomal (Doxil) Pentostatin Eribulin (Halaven) Pralatrexate (Folotyn) Etoposide (Etopophos) Romidepsin (Istodax) Floxuridine Talimogene laherparepvec (Imlygic) Fluorouracil (5-FU) Thiotepa (Tepadina) Gemcitabine (Gemzar) Tisagenlecleucel (Kymriah) Gemtuzumab ozogamicin Topotecan (Hycamtin) Inotuzumab ozogamicin (Besponsa) Ziv-aflibercept (Zaltrap) MINIMAL RISK (<10% frequency)† Alemtuzumab (Campath) Nelarabine (Arranon) Atezolizumab (Tecentriq) Nivolumab (Opdivo) Avelumab (Bavencio) Obinutuzumab (Gazyva) Asparaginase (Erwinaze) Ofatumumab (Arzerra) Bevacizumab (Avastin) Panitumumab (Vectibix) Bleomycin Pegasparagase (Oncaspar) Blinatumomab (Blincyto) Peginterferon (Sylatron) Bortezomib (Velcade) Pembrolizumab (Keytruda) Cetuximab (Erbitux) Pertuzumab (Perjeta) Cladribine Ramucirumab (Cyramza) Cytarabine <100mg/m² Rituximab (Rituxan) Daratumumab (Darzalex) Rituximab + hyaluronidase (Rituxan Hycela) Decitabine (Dacogen) Siltuximab (Sylvant) Denileukin diftitox (Ontak) Temsirolimus (Torisel) Dexrazoxane (Totect, Zinecard) Trastuzumab (Herceptin) Durvalumab (Imfinzi) Valrubicin (Valstar) Elotuzumab (Empliciti) Vinblastine Fludarabine Vincristine Interferon alfa (Intron A) ≤5 million IU/m² Vincristine liposomal (Marqibo) Ipilimumab (Yervoy) Vinorelbine (Navelbine) Methotrexate ≤50mg/m² (continued) EMETOGENIC POTENTIAL OF ANTINEOPLASTIC AGENTS (Part 2 of 2) ORAL AGENTS MODERATE TO HIGH RISK (≥30% frequency)† Altretamine (Hexalen) Lomustine single day (Gleostine) Busulfan (Myleran) ≥4mg/day Midostaurin (Rydapt) Ceritinib (Zykadia) Mitotane (Lysodren) Crizotinib (Xalkori) Niraparib (Zejula) Cyclophosphamide ≥100mg/m²/day Olaparib (Lynparza) Dabrafenib (Tafinlar) Procarbazine (Matulane) Enasidenib (Idhifa) Rucaparib (Rubraca) Estramustine (Emcyt) Temozolomide (Temodar) >75mg/m²/day Etoposide Trifluridine/tipiracil (Lonsurf) Lenvatinib (Lenvima) MINIMAL TO LOW RISK (<30% frequency)† Abemaciclib (Verzenio) Larotrectinib (Vitrakvi) Acalabrutinib (Calquence) Lenalidomide (Revlimid) Afatinib (Gilotrif) Lorlatinib (Lorbrena) Alectinib (Alecensa) Melphalan (Alkeran) Axitinib (Inlyta) Mercaptopurine Bexarotene (Targretin) Methotrexate Binimetinib (Mektovi) Neratinib (Nerlynx) Brigatinib (Alunbrig) Nilotinib (Tasigna) Bosutinib (Bosulif) Osimertinib (Tagrisso) Busulfan (Myleran) <4mg/day Palbociclib (Ibrance) Cabozantinib (Cabometyx, Cometriq) Panobinostat (Farydak) Capecitabine (Xeloda) Pazopanib (Votrient) Chlorambucil (Leukeran) Pomalidomide (Pomalyst) Cobimetinib (Cotellic) Ponatinib (Iclusig) Cyclophosphamide <100mg/m²/day Regorafenib (Stivarga) Dacomitinib (Vizimpro) Ribociclib (Kisqali) Dasatinib (Sprycel) Ruxolitinib (Jakafi) Duvelisib (Copiktra) Sonidegib (Odomzo) Encorafenib (Braftovi) Sorafenib (Nexavar) Erlotinib (Tarceva) Sunitinib (Sutent) Everolimus (Afinitor) Talazoparib tosylate (Talzenna) Fludarabine Temozolomide (Temodar) ≤75mg/m²/day Gefitinib (Iressa) Thalidomide (Thalomid) Gilteritinib (Xospata) Thioguanine Glasdegib (Daurismo) Topotecan (Hycamtin) Hydroxyurea (Hydrea) Trametinib (Mekinist) Ibrutinib (Imbruvica) Tretinoin Idelalisib (Zydelig) Vandetanib (Caprelsa) Imatinib (Gleevec) Vemurafenib (Zelboraf) Ivosidenib (Tibsovo) Venetoclax (Venclexta) Ixazomib (Ninlaro) Vismodegib (Erivedge) Lapatinib (Tykerb) Vorinostat (Zolinza) NOTES † Frequency of emesis in the absence of effective antiemetic prophylaxis. * May be highly emetogenic in certain patients. REFERENCES National Comprehensive Cancer Network. NCCN Clinical Practice Guidelines in Oncology: Antiemesis. Version 1.2019 – February 28, 2019. https://www.nccn.org/professionals/physician_gls/pdf/antiemesis.pdf. Accessed January 23, 2020. (Rev. 2/2020).
Load more

Recommended publications
  • Identification of Recurrent Mutational Events in Anorectal Melanoma
    Modern Pathology (2017) 30, 286–296 286 © 2017 USCAP, Inc All rights reserved 0893-3952/17 $32.00 Identification of recurrent mutational events in anorectal melanoma Hui Min Yang1,2,6, Susan J Hsiao1,6, David F Schaeffer2, Chi Lai3, Helen E Remotti1, David Horst4, Mahesh M Mansukhani1 and Basil A Horst1,5 1Department of Pathology & Cell Biology, Columbia University Medical Center, New York, NY, USA; 2Department of Pathology & Laboratory Medicine, University of British Columbia, Vancouver, BC, Canada; 3Department of Pathology and Laboratory Medicine, University of Ottawa, Ottawa, ON, Canada; 4Pathologisches Institut, Ludwig-Maximilians-Universitaet, Muenchen, Germany and 5Department of Dermatology, Columbia University Medical Center, New York, NY, USA Anorectal melanoma is a rare disease that carries a poor prognosis. To date, limited genetic analyses confirmed KIT mutations as a recurrent genetic event similar to other mucosal melanomas, occurring in up to 30% of anorectal melanomas. Importantly, a subset of tumors harboring activating KIT mutations have been found to respond to c-Kit inhibitor-based therapy, with improved patient survival at advanced tumor stages. We performed comprehensive targeted exon sequencing analysis of 467 cancer-related genes in a larger series of 15 anorectal melanomas, focusing on potentially actionable variants based on gain- and loss-of-function mutations. We report the identification of oncogenic driver events in the majority (93%) of anorectal melanomas. These included variants in canonical MAPK pathway effectors rarely observed in cutaneous melanomas (including an HRAS mutation, as well as a BRAF mutation resulting in duplication of threonine 599), and recurrent mutations in the tumor suppressor NF1 in 20% of cases, which represented the second-most frequently mutated gene after KIT in our series.
    [Show full text]
  • The TP53 Apoptotic Network Is a Primary Mediator of Resistance to BCL2 Inhibition in AML Cells
    Published OnlineFirst May 2, 2019; DOI: 10.1158/2159-8290.CD-19-0125 RESEARCH ARTICLE The TP53 Apoptotic Network Is a Primary Mediator of Resistance to BCL2 Inhibition in AML Cells Tamilla Nechiporuk1,2, Stephen E. Kurtz1,2, Olga Nikolova2,3, Tingting Liu1,2, Courtney L. Jones4, Angelo D’Alessandro5, Rachel Culp-Hill5, Amanda d’Almeida1,2, Sunil K. Joshi1,2, Mara Rosenberg1,2, Cristina E. Tognon1,2,6, Alexey V. Danilov1,2, Brian J. Druker1,2,6, Bill H. Chang2,7, Shannon K. McWeeney2,8, and Jeffrey W. Tyner1,2,9 ABSTRACT To study mechanisms underlying resistance to the BCL2 inhibitor venetoclax in acute myeloid leukemia (AML), we used a genome-wide CRISPR/Cas9 screen to identify gene knockouts resulting in drug resistance. We validated TP53, BAX, and PMAIP1 as genes whose inactivation results in venetoclax resistance in AML cell lines. Resistance to venetoclax resulted from an inability to execute apoptosis driven by BAX loss, decreased expression of BCL2, and/or reliance on alternative BCL2 family members such as BCL2L1. The resistance was accompanied by changes in mitochondrial homeostasis and cellular metabolism. Evaluation of TP53 knockout cells for sensitivities to a panel of small-molecule inhibitors revealed a gain of sensitivity to TRK inhibitors. We relate these observations to patient drug responses and gene expression in the Beat AML dataset. Our results implicate TP53, the apoptotic network, and mitochondrial functionality as drivers of venetoclax response in AML and suggest strategies to overcome resistance. SIGNIFICANCE: AML is challenging to treat due to its heterogeneity, and single-agent therapies have universally failed, prompting a need for innovative drug combinations.
    [Show full text]
  • Duvelisib Eliminates CLL B Cells, Impairs CLL- Supporting Cells, and Overcomes Ibrutinib Resistance in Preclinical Models
    Duvelisib Eliminates CLL B Cells, Impairs CLL- Supporting Cells, and Overcomes Ibrutinib Resistance in Preclinical Models Shih-Shih Chen ( [email protected] ) Karches Center for Oncology Research, the Feinstein Institutes for Medical Research Jacqueline Barrientos Karches Center for Oncology Research, the Feinstein Institutes for Medical Research Gerardo Ferrer Josep Carreras Leukaemia Research Institute (IJC) https://orcid.org/0000-0002-4084-6815 Priyadarshini Ravichandran Karches Center for Oncology Research, the Feinstein Institutes for Medical Research Michael Ibrahim Karches Center for Oncology Research, the Feinstein Institutes for Medical Research Yasmine Kieso Karches Center for Oncology Research, the Feinstein Institutes for Medical Research Jeff Kutok Innity Pharmaceuticals Marisa Peluso Innity Pharmaceuticals, Inc Sujata Sharma Innity Pharmaceuticals, Inc David Weaver Institute of Health Sciences, Anhui University Jonathan Pachter Verastem Inc. Kanti Rai The Karches Center for Oncology Research. The Feinstein Institutes for Medical Research. Nicholas Chiorazzi Karches Center for Oncology Research, the Feinstein Institutes for Medical Research Article Keywords: chronic lymphocytic leukemia, cancer therapy, Bruton’s Tyrosine Kinase (BTKi), phosphoinositide 3-kinase (PI3Ki) Page 1/23 Posted Date: July 21st, 2021 DOI: https://doi.org/10.21203/rs.3.rs-701669/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Page 2/23 Abstract Inhibitors of Bruton’s Tyrosine Kinase (BTKi) and phosphoinositide 3-kinase (PI3Ki) have signicantly improved therapy of chronic lymphocytic leukemia (CLL). However, the emergence of resistance to BTKi has introduced an unmet therapeutic need. Here we demonstrate in vitro and in vivo the essential roles of PI3K-δ for CLL B-cell survival and migration and of PI3K-γ in T-cell migration and macrophage polarization; and more ecacious inhibition in CLL-cell burden by dual inhibition of PI3K-δ,γ.
    [Show full text]
  • PI3K Inhibitors in Cancer: Clinical Implications and Adverse Effects
    International Journal of Molecular Sciences Review PI3K Inhibitors in Cancer: Clinical Implications and Adverse Effects Rosalin Mishra , Hima Patel, Samar Alanazi , Mary Kate Kilroy and Joan T. Garrett * Department of Pharmaceutical Sciences, College of Pharmacy, University of Cincinnati, Cincinnati, OH 45267-0514, USA; [email protected] (R.M.); [email protected] (H.P.); [email protected] (S.A.); [email protected] (M.K.K.) * Correspondence: [email protected]; Tel.: +1-513-558-0741; Fax: +1-513-558-4372 Abstract: The phospatidylinositol-3 kinase (PI3K) pathway is a crucial intracellular signaling pathway which is mutated or amplified in a wide variety of cancers including breast, gastric, ovarian, colorectal, prostate, glioblastoma and endometrial cancers. PI3K signaling plays an important role in cancer cell survival, angiogenesis and metastasis, making it a promising therapeutic target. There are several ongoing and completed clinical trials involving PI3K inhibitors (pan, isoform-specific and dual PI3K/mTOR) with the goal to find efficient PI3K inhibitors that could overcome resistance to current therapies. This review focuses on the current landscape of various PI3K inhibitors either as monotherapy or in combination therapies and the treatment outcomes involved in various phases of clinical trials in different cancer types. There is a discussion of the drug-related toxicities, challenges associated with these PI3K inhibitors and the adverse events leading to treatment failure. In addition, novel PI3K drugs that have potential to be translated in the clinic are highlighted. Keywords: cancer; PIK3CA; resistance; PI3K inhibitors Citation: Mishra, R.; Patel, H.; Alanazi, S.; Kilroy, M.K.; Garrett, J.T.
    [Show full text]
  • = 'NH., Diseases, Central Nerrous System M)Ury and Different Foims of Mflannnation
    (12) INTERNATIONAL APPLICATION Pl;BLISHED 1. NDER THE PATENT COOPERATION TREATY (PCT) (19) World intellectual Property Organraation llIlllIlllIlIllllllllIlllllIIllIllIlllIlllllllllllIlllIllIlIlllIllIlIllIllIlIIIIIIIIIIIIIIIIIII International Bureau (10) International Publication Number (43) International Publication Date WO 2020/114892 Al 11 June 2020 (11.06.2020) W 4 P Gl I P 0 T (51) International Patent Classification: C07D 401/06 (200G 0 I) AGJK31/454 (200G 0l) C07D dt)J//4 (2006 01) A61P35/ttd (200G 0l) (21) International Application Number: PCT/EP2019/l)8 3014 (22) International Filing Date: 29 Nosember 2019 (29.11.2019) (25) Filing Language: Enghsh (26) Publication Language Enghsh (30) Priority Data: 1820972/i 1 03 December 20)8 (03 12 2018) EP (71) Applicant: MERCK PATENT GMBH IDE/DE]. Frm&(s- furter Strasse 230. 64293 DARMSTADT (DE) (72) Inventors: BUCHSTALLER, Hans-Peter. Ncc)sa&strasse G. G4347 GRIESHELVI (DE). ROHDICH, Feliru Saalbaus- tmssc 23. 64283 DARMSTADT (DE). (81) Designated States /unless i&themmse n&d&ct&md, /or e&ery hind of national protect«&n menial&le/ AF, AG, AL, AVI AO, AT. AU. AZ, BA, BB, BG, BH. B N. BR, BW, BY. BZ. CA. CH, CL, CN. CO, CR. C U, CZ. DE, DJ, DK. DM DO. DZ, EC. EE, EG. ES. FI, GB. GD. GE. GH, GM. GT. HN. HR. HU, ID, IL. IN, IR, IS. JO, JP, KE. KG, KH. KN, KP. KR. KW, KZ, LA. L C, LK. LR, LS, LU. LY. MA. MD, ME. WIG. MK. MN, MW, MX. MY. MZ. NA. NG. NI, NO. NZ. OM, PA. PE, PG. PH, PL. PT. QA, RO, RS.
    [Show full text]
  • Tumour-Agnostic Therapy for Pancreatic Cancer and Biliary Tract Cancer
    diagnostics Review Tumour-Agnostic Therapy for Pancreatic Cancer and Biliary Tract Cancer Shunsuke Kato Department of Clinical Oncology, Juntendo University Graduate School of Medicine, 2-1-1, Hongo, Bunkyo-ku, Tokyo 113-8421, Japan; [email protected]; Tel.: +81-3-5802-1543 Abstract: The prognosis of patients with solid tumours has remarkably improved with the develop- ment of molecular-targeted drugs and immune checkpoint inhibitors. However, the improvements in the prognosis of pancreatic cancer and biliary tract cancer is delayed compared to other carcinomas, and the 5-year survival rates of distal-stage disease are approximately 10 and 20%, respectively. How- ever, a comprehensive analysis of tumour cells using The Cancer Genome Atlas (TCGA) project has led to the identification of various driver mutations. Evidently, few mutations exist across organs, and basket trials targeting driver mutations regardless of the primary organ are being actively conducted. Such basket trials not only focus on the gate keeper-type oncogene mutations, such as HER2 and BRAF, but also focus on the caretaker-type tumour suppressor genes, such as BRCA1/2, mismatch repair-related genes, which cause hereditary cancer syndrome. As oncogene panel testing is a vital approach in routine practice, clinicians should devise a strategy for improved understanding of the cancer genome. Here, the gene mutation profiles of pancreatic cancer and biliary tract cancer have been outlined and the current status of tumour-agnostic therapy in these cancers has been reported. Keywords: pancreatic cancer; biliary tract cancer; targeted therapy; solid tumours; driver mutations; agonist therapy Citation: Kato, S. Tumour-Agnostic Therapy for Pancreatic Cancer and 1.
    [Show full text]
  • Minutes of the CHMP Meeting 14-17 September 2020
    13 January 2021 EMA/CHMP/625456/2020 Corr.1 Human Medicines Division Committee for medicinal products for human use (CHMP) Minutes for the meeting on 14-17 September 2020 Chair: Harald Enzmann – Vice-Chair: Bruno Sepodes Disclaimers Some of the information contained in these minutes is considered commercially confidential or sensitive and therefore not disclosed. With regard to intended therapeutic indications or procedure scopes listed against products, it must be noted that these may not reflect the full wording proposed by applicants and may also vary during the course of the review. Additional details on some of these procedures will be published in the CHMP meeting highlights once the procedures are finalised and start of referrals will also be available. Of note, these minutes are a working document primarily designed for CHMP members and the work the Committee undertakes. Note on access to documents Some documents mentioned in the minutes cannot be released at present following a request for access to documents within the framework of Regulation (EC) No 1049/2001 as they are subject to on- going procedures for which a final decision has not yet been adopted. They will become public when adopted or considered public according to the principles stated in the Agency policy on access to documents (EMA/127362/2006). 1 Addition of the list of participants Official address Domenico Scarlattilaan 6 ● 1083 HS Amsterdam ● The Netherlands Address for visits and deliveries Refer to www.ema.europa.eu/how-to-find-us Send us a question Go to www.ema.europa.eu/contact Telephone +31 (0)88 781 6000 An agency of the European Union © European Medicines Agency, 2020.
    [Show full text]
  • PRIOR AUTHORIZATION CRITERIA for APPROVAL Initial Evaluation Target Agent(S) Will Be Approved When ONE of the Following Is Met: 1
    Self-Administered Oncology Agents Through Preferred Prior Authorization Program Summary FDA APPROVED INDICATIONS3-104 Please reference individual agent product labeling. CLINICAL RATIONALE For the purposes of the Self -Administered Oncology Agents criteria, indications deemed appropriate are those approved in FDA labeling and/or supported by NCCN Drugs & Biologics compendia with a category 1 or 2A recommendation, AHFS, or DrugDex with level of evidence of 1 or 2A. SAFETY3-104 Agent(s) Contraindication(s) Afinitor/Afinitor Disperz Hypersensitivity to everolimus, to other rapamycin (everolimus) derivatives None Alecensa (alectinib) Alunbrig (brigatinib) None Ayvakit (avapritinib) None Balversa (erdafitinib) None Hypersensitivity to bosutinib Bosulif (bosutinib) Braftovi (encorafenib) None Brukinsa (zanubrutinib) None Cabometyx None (cabozantinib) Calquence None (acalabrutinib) Caprelsa Congenital long QT syndrome (vandetanib) Cometriq None (cabozantinib) Copiktra (duvelisib) None Cotellic (cobimetinib) None Daurismo (glasdegib) None None Erivedge (vismodegib) Erleada (apalutamide) Pregnancy None Farydak (panobinostat) Fotivda (tivozanib) None Gavreto (pralsetinib) None None Gilotrif (afatinib) Gleevec None (imatinib) Hycamtin Severe hypersensitivity to topotecan (topotecan) None Ibrance (palbociclib) KS_PS_SA_Oncology_PA_ProgSum_AR1020_r0821v2 Page 1 of 19 © Copyright Prime Therapeutics LLC. 08/2021 All Rights Reserved Effective: 10/01/2021 Agent(s) Contraindication(s) None Iclusig (ponatinib) Idhifa (enasidenib) None Imbruvica (ibrutinib)
    [Show full text]
  • DRUGS REQUIRING PRIOR AUTHORIZATION in the MEDICAL BENEFIT Page 1
    Effective Date: 08/01/2021 DRUGS REQUIRING PRIOR AUTHORIZATION IN THE MEDICAL BENEFIT Page 1 Therapeutic Category Drug Class Trade Name Generic Name HCPCS Procedure Code HCPCS Procedure Code Description Anti-infectives Antiretrovirals, HIV CABENUVA cabotegravir-rilpivirine C9077 Injection, cabotegravir and rilpivirine, 2mg/3mg Antithrombotic Agents von Willebrand Factor-Directed Antibody CABLIVI caplacizumab-yhdp C9047 Injection, caplacizumab-yhdp, 1 mg Cardiology Antilipemic EVKEEZA evinacumab-dgnb C9079 Injection, evinacumab-dgnb, 5 mg Cardiology Hemostatic Agent BERINERT c1 esterase J0597 Injection, C1 esterase inhibitor (human), Berinert, 10 units Cardiology Hemostatic Agent CINRYZE c1 esterase J0598 Injection, C1 esterase inhibitor (human), Cinryze, 10 units Cardiology Hemostatic Agent FIRAZYR icatibant J1744 Injection, icatibant, 1 mg Cardiology Hemostatic Agent HAEGARDA c1 esterase J0599 Injection, C1 esterase inhibitor (human), (Haegarda), 10 units Cardiology Hemostatic Agent ICATIBANT (generic) icatibant J1744 Injection, icatibant, 1 mg Cardiology Hemostatic Agent KALBITOR ecallantide J1290 Injection, ecallantide, 1 mg Cardiology Hemostatic Agent RUCONEST c1 esterase J0596 Injection, C1 esterase inhibitor (recombinant), Ruconest, 10 units Injection, lanadelumab-flyo, 1 mg (code may be used for Medicare when drug administered under Cardiology Hemostatic Agent TAKHZYRO lanadelumab-flyo J0593 direct supervision of a physician, not for use when drug is self-administered) Cardiology Pulmonary Arterial Hypertension EPOPROSTENOL (generic)
    [Show full text]
  • Mutant Cancers 2 3 Heinz Hammerlindl1*, Dinoop Ravindran Menon1*, Sabrina Hammerlindl1, Abdullah Al
    Author Manuscript Published OnlineFirst on December 1, 2017; DOI: 10.1158/1078-0432.CCR-16-2118 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Hammerlindl et. al 1 Acetylsalicylic Acid Governs the Effect of Sorafenib in RAS Mutant Cancers 2 3 Heinz Hammerlindl1*, Dinoop Ravindran Menon1*, Sabrina Hammerlindl1, Abdullah Al 4 Emran1, Joachim Torrano1, Katrin Sproesser3, Divya Thakkar1, Min Xiao3, Victoria G. 5 Atkinson5, Brian Gabrielli4, Nikolas K. Haass2, Meenhard Herlyn3, Clemens Krepler3, Helmut 6 Schaider1,2† 7 8 1Dermatology Research Centre, The University of Queensland, The University of 9 Queensland Diamantina Institute, Translational Research Institute, Brisbane, Australia; 10 2The University of Queensland, The University of Queensland Diamantina Institute, 11 Translational Research Institute, Brisbane, Australia; 12 3The Wistar Institute, Philadelphia, PA, U.S.A.; 13 4Mater Medical Research Institute, The University of Queensland, Translational Research 14 Institute, Brisbane, Australia; 15 5Division of Cancer Services, Princess Alexandra Hospital, Brisbane, Australia; 16 *These authors contributed equally to the study 17 18 Running title: 19 Combined aspirin and sorafenib for RAS-mutant cancer therapy 20 21 Key words: 22 Melanoma, Lung Cancer, NRAS, Sorafenib, Aspirin, RAS, ERK, AMPK 23 24 25 26 27 28 1 Downloaded from clincancerres.aacrjournals.org on September 24, 2021. © 2017 American Association for Cancer Research. Author Manuscript Published OnlineFirst on December 1, 2017; DOI: 10.1158/1078-0432.CCR-16-2118 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Hammerlindl et. al 1 2 Grant Support 3 This work was funded by the Epiderm Foundation (H.S.), the Princess Alexandra Hospital 4 Research Foundation (PARSS2016_NearMiss) (H.S.), NIH grants PO1 CA114046, P50 5 CA174523, and the Dr.
    [Show full text]
  • Re-Visiting Hypersensitivity Reactions to Taxanes: a Comprehensive Review
    Clinic Rev Allerg Immunol DOI 10.1007/s12016-014-8416-0 Re-visiting Hypersensitivity Reactions to Taxanes: A Comprehensive Review Matthieu Picard & Mariana C. Castells # Springer Science+Business Media New York 2014 Abstract Taxanes (a class of chemotherapeutic agents) Keywords Taxane . Paclitaxel . Taxol . Docetaxel . are an important cause of hypersensitivity reactions Taxotere . Nab-paclitaxel . Abraxane . Cabazitaxel . (HSRs) in cancer patients. During the last decade, the Chemotherapy . Hypersensitivity . Allergy . Skin test . development of rapid drug desensitization has been key Desensitization . Challenge . Diagnosis . Review . IgE . to allow patients with HSRs to taxanes to be safely re- Complement . Mechanism treated although the mechanisms of these HSRs are not fully understood. Earlier studies suggested that solvents, such as Cremophor EL used to solubilize paclitaxel, Introduction were responsible for HSRs through complement activa- tion, but recent findings have raised the possibility that Hypersensitivity reactions (HSRs) to chemotherapy are in- some of these HSRs are IgE-mediated. Taxane skin creasingly common and represent an important impediment testing, which identifies patients with an IgE-mediated to the care of cancer patients as they may entail serious sensitivity, appears as a promising diagnostic and risk consequences and prevent patients from being treated with stratification tool in the management of patients with the most efficacious agent against their cancer [1]. During the HSRs to taxanes. The management of patients following last decade, different groups have developed rapid drug de- a HSR involves risk stratification and re-exposure could sensitization (RDD) protocols that allow the safe re- be performed either through rapid drug desensitization introduction of a chemotherapeutic agent to which a patient or graded challenge based on the severity of the initial is allergic, and their use have recently been endorsed by the HSR and the skin test result.
    [Show full text]
  • Jevtana® (Cabazitaxel)
    AUSTRALIAN PRODUCT INFORMATION – JEVTANA® (CABAZITAXEL) 1 NAME OF THE MEDICINE Cabazitaxel 2 QUALITATIVE AND QUANTITATIVE COMPOSITION The concentrated solution for injection contains 60 mg cabazitaxel in 1.5 mL polysorbate 80. Diluent contains 13% w/w ethanol in 4.5 mL water for injections. Excipients of known effect: Diluent contains 13% w/w ethanol. For the full list of excipients, see Section 6.1 List of excipients. 3 PHARMACEUTICAL FORM The concentrated solution for injection is a clear oily yellow to brownish yellow solution. The diluent is a clear, colourless solution. 4 CLINICAL PARTICULARS 4.1 THERAPEUTIC INDICATIONS Jevtana in combination with prednisone or prednisolone is indicated for the treatment of patients with metastatic castration resistant prostate cancer previously treated with a docetaxel containing regimen. 4.2 DOSE AND METHOD OF ADMINISTRATION The use of Jevtana should be confined to units specialised in the administration of cytotoxics and it should only be administered under the supervision of a physician experienced in the use of anticancer chemotherapy. Premedication Premedicate at least 30 minutes prior to each administration of Jevtana with the following intravenous medications to reduce the risk and severity of a hypersensitivity reaction: jevtana-ccdsv10-piv11-10nov20 Page 1 of 26 antihistamine (equivalent to dexchlorpheniramine 5 mg or diphenhydramine 25 mg or equivalent), corticosteroid (dexamethasone 8 mg or equivalent) and with H2 antagonist (ranitidine or equivalent). Antiemetic prophylaxis is recommended and can be given orally or intravenously as needed (see Section 4.4 Special warnings and precautions for use). Recommended Dosage The recommended dose of Jevtana is 20 mg/m2 administered as a 1-hour intravenous infusion every 3 weeks in combination with oral prednisone (or prednisolone) 10 mg administered daily throughout Jevtana treatment.
    [Show full text]