Cancer Drugs Flashcards
Cyclophosphamide MOA
Alkylating agent: alkylates DNA on N7 and O6 of guanine, adds an alophatic chain
Major side effect of alkylating agents
Leukogenic: partial or total chromosomal deletions may cause a 2nd cancer
Cancers treated wih cyclophosphamide
Burkitts, CLL, non hodgkins, breast cancer surgery, organ transplant
Bleomycin MOA
Creates free radicals through Fe2+ and O2 interactions which causes DNA strand breaks
Cancers treated with bleomycin
Leukemia, testicular and ovarian cancer
Cisplatin, carboplatin, and oxaliplati MOA
Adds platin to N7 and O6 of guanine which causes intrachain crosslinking
Major side effect of cisplatin, oxaliplatin, and carboplatin
Hearing loss
Anthracyclines (doxorubicin/daunorubicin) MOA
Intercalates between DNA bases which inhibits topoisomerase II causing DNA strand breaks
Etoposide MOA
Inhibits topoisomerase II causing strand breaks
Methotrexate MOA
Folate antagonistand competitive inhibitor of dihydrofolate reductase which inhibits thymidylate and purine sythesis
Cancers treated with methotrexate
Lung, colon, and ALL
Leucoverin rescue
Selective rescue of normal cells which allows or higher dosing of methotrexate
Asparginase MOA
Converts L-aspargine to aspartic acid which depletes aspargine required or DNA synthesis
Cancer treated with asparginase
Lymphocytic leukemia
Hydroxyurea MOA
Inhibits ribonucleotide diphosphate reductase which is the rate limiting step in dNTP synthesis
Vinea alkaloid MOA
Inhibits microtubule formation (M phase specific)
Vinblastine MOA
M phase specific
Cancer treated with vinblastine
Hodgkins and childhood leukemias
Treatment options for Hogkins
ABVD: Adriamycin Bleomycin Vinblastine Dicarbazine
Paclitaxel MOA
Promotes microtubule formation but prevents disassembly (M phase specific)
How glucocorticoids treat cancer
Decrease lymphocytes, antiinflammatiory
Cancer treated with glucocorticoids
All leukemias
Induction therapy for ALL
Glucocorticoid, vincristine, asparaginase
Imatinib mesylate (Gleevec) MOA
Signal transduction inhibitor
Cancer treated with Gleevec
CML
Drug alternative to treat CML with Gleevec resistance
Desatinib: it has a sloppier fit to ATP binding pocket so it is more difficult for tumor cells to have mutations that make them resistant
Bevacizumab (Avastin) MOA
Monoclonal Ab against VEGF
Thalidomide MOA
Immune stimmulant –> T cell and NK activation
Antiangiogenic
Induces apoptosis
Decreases adhesion of myeloma cells to bone marrow stromal cells
Bortezomib MOA
Proteosome inhibitor
Inhibits proteolysis
Arsenic (ATO) MOA
Induces apoptosis by increasing free radicals –> mitochondrial damage –> caspase activation
Decreases VEGF
Stimulates apoptosis in supporting endothelial cells as well
