Exam 5 Flashcards
mechlorethamine, melphalan, ifosfamide, cyclophosphamide, chlorambucil - class
nitrogen mustards - DNA damaging agents
carmustine, streptozoxin - class
nitrosoureas - DNA damaging agents
oxaliplatin, carboplatin, cisplatin - class
platinum coordination complexes - DNA damaging agents
mechlorethamine, melphalan, ifosfamide, cyclophosphamide, chlorambucil, carmustine, streptozoxin, oxaliplatin, carboplatin, cisplatin - Target
causes intra/interstrand cross links
mechlorethamine, melphalan, ifosfamide, cyclophosphamide, chlorambucil, carmustine, streptozoxin, oxaliplatin, carboplatin, cisplatin - biochemical/physiological responses
inability of cell to separate DNA, initiation of DNA repair mechanisms
cell can’t replicate DNA or make proteins - cell undergoes apoptosis if can’t repair in time
mechlorethamine, melphalan, ifosfamide, cyclophosphamide, chlorambucil, carmustine, streptozoxin, oxaliplatin, carboplatin, cisplatin - adverse effects
hematological (myelosuppression), hepatotoxicity, nephrotoxicity, neurotoxicity, nausea, dehydration, malnutrition
mechlorethamine, melphalan, ifosfamide, cyclophosphamide, chlorambucil, carmustine, streptozoxin, oxaliplatin, carboplatin, cisplatin - interactions
TNF blockers, clozapine, deferiprone, leflunomide, zidovudine, thalidomide, nephrotoxic agents
temozolomide, decarbazine - class
triazenes- DNA damaging agents
temozolomide, decarbazine - target
addition of methyl group to DNA bases (guanine)
temozolomide, decarbazine - biochemical/physiological
incorrect DNA base matching during replication
loss of DNA fidelity - leads to mutation and loss of protein function
temozolomide, decarbazine - adverse effects
hematological (myelosuppression), immunosuppression, hepatotoxicity, nausea, dehydration, malnutrition
temozolomide, decarbazine - interactions
TNF blockers, clozapine, deferiprone, leflunomide, zidovudine, thalidomide, nephrotoxic agents
daunorubicin, doxorubicin, idarubicin - class
anthracycline antibiotics - DNA damaging agents
daunorubicin, doxorubicin, idarubicin - target
intercalates into DNA and inhibits topoisomerase 2
daunorubicin, doxorubicin, idarubicin - biochemical/physiological
inability to replicate DNA or make proteins, initiates DNA repair mechanisms
halt of DNA cell cycle progression, loss of cellular function - cell undergoes apoptosis if can’t repair DNA in time
daunorubicin, doxorubicin, idarubicin - adverse effects
hematological, cardiovascular, nausea, dehydration, malnutrition
daunorubicin, doxorubicin, idarubicin - interactions
clozapine, deferiprone, TNF blockers, leflunomide, thalidomide, prolongs QT interval
bleomycin, mitomycin - class
anthracenedione antibiotics - DNA damaging agents
bleomycin, mitomycin - target
intercalates into DNA causing DNA crosslinks and double/single strand breaks
bleomycin, mitomycin - biochemical, physiological
inability to replicate DNA or make proteins, initiates DNA repair mechanisms
halt of DNA cell cycle progression, loss of cellular function - cell undergoes apoptosis if can’t repair in time
bleomycin, mitomycin - adverse effects
hematological, nausea, dehydration, malnutrition, nephrotoxicity, lung fibrosis
bleomycin, mitomycin - interactions
clozapine, deferiprone, TNF blockers, leflunomide, thalidomide
methotrexate - class
DNA replication - antimetabolite
methotrexate - target
competitive inhibitor of dihydrofolate reductase
methotrexate - biochemical/physiological
inability to convert DHF into active THF, can’t convert dUMP to dTMP
no new strands of DNA (loss of monomers), loss of proliferation
methotrexate - adverse effects
hematological (myelosuppression), nephrotoxicity, hepatotoxicity
methotrexate - interactions
other nephrotoxic agents, trimethoprim, clozapine, deferiprone, TNF blockers
capecitabine, floxuridine - class
DNA replication - antimetabolites
capecitabine, floxuridine - target
inhibition of thymidylate synthase
capecitabine, floxuridine - biochemical, physiological
inability of cell to synthesize dTMP from dUMP
cell can’t create new strands of DNA (loss of proliferation)
capecitabine, floxuridine - adverse effects
hematological, nausea, dehydration, malnutrition
capecitabine, floxuridine - interactions
clozapine, deferiprone, TNF blockers, leflunomide, thalidomide
cytarabine - class
DNA replication - antimetabolite
cytarabine - target
inhibits DNA polymerase
cytarabine - biochemical/physiological
cells can’t synthesize new DNA
cells can’t replicate DNA
cytarabine - adverse effects
hematological, pancreatitis, nausea, dehydration, malnutrition, neurotoxicity
cytarabine - interactions
clozapine, deferiprone, TNF blockers, leflunomide, thalidomide
mercaptopurine, thioguanine - class
DNA replication - antimetabolites
mercaptopurine, thioguanine - target
inhibits DNA polymerase, inhibits de novo purine synthesis
mercaptopurine, thioguanine - biochemical/physiological
cells can’t synthesize new DNA/proteins
cells can’t replicate DNA
mercaptopurine, thioguanine - adverse effects
hematological, hyperuricemia due to nephrotoxicity, hepatotoxicity
mercaptopurine, thioguanine - interactions
clozapine, deferiprone, ribavirin, TNF blockers, leflunomide, thalidomide, azathioprine
cladribine - class
DNA replication - antimetabolite
cladribine - target
causes inhibition of DNA polymerase and strand breaks
cladribine - biochemical/physiological
cells can’t synthesize DNA/proteins, initiates DNA repair mechanisms
cells can’t replicate DNA or make proteins - cell undergoes apoptosis if can’t repair in time
cladribine - adverse effects
hematological
cladribine - interactions
TNF blockers, leflunomide
gemcitabine, fludarabine - class
DNA replication - antimetabolites
gemcitabine, fludarabine - target
inhibits RR and DNA polymerase
gemcitabine, fludarabine - biochemical/physiological
inability of cells to create deoxyribonucleosides (RR inhibition), inability of cells to create DNA (DNA polymerase inhibition)
cells can’t replicate DNA
gemcitabine, fludarabine - adverse effects
hematological, pulmonary distress, hepatotoxicity, neurotoxicity
gemcitabine, fludarabine - interactions
clozapine, deferiprone, TNF blockers, leflunomide, thalidomide
hydroxyurea - class
DNA replication - antimetabolite
hydroxyurea - target
inhibits RR
hydroxyurea - biochemical/physiological
cells can’t synthesize deoxyribonucleosides
cell can’t synthesize new DNA
hydroxyurea - adverse effects
neurotoxicity, hematological, hepatotoxicity, nausea, dehydration, malnutrition
hydroxyurea - interactions
clozapine, deferiprone, TNF blockers, leflunomide, thalidomide
pentostatin - class
DNA replication - antimetabolite
pentostatin - target
inhibits adenosine deaminase - disruption of nucleic acid metabolism resulting in inhibition of RR
pentostatin - biochemical/physiological
cells can’t make deoxyribonucleosides
cells can’t make new DNA
pentostatin - adverse effects
hematological, nausea, dehydration, malnutrition
pentostatin - interactions
clozapine, deferiprone, TNF blockers, thalidomide
bortezomib - class
DNA replication - antimetabolite
bortezomib - target
inhibits 26S proteasome
bortezomib - biochemical/physiological
cell can’t degrade proteins - particularly those with rapid turnover/pro-apoptotic proteins
induction of apoptosis due to presence of apoptotic proteins
bortezomib - adverse effects
peripheral neuropathy, cardiovascular, hematological
bortezomib - interactions
deferiprone
irinotecan, topotecan - class
DNA replication - topoisomerase inhibitors
irinotecan, topotecan - target
inhibits topoisomerase 1
irinotecan, topotecan - biochemical/physiological
cells can’t unwind DNA
cells can’t replicate DNA or make proteins
irinotecan, topotecan - adverse effects
hematological, hepatotoxicity, nephropathy, nausea, dehydration, malnutrition
irinotecan, topotecan - interactions
clozapine, deferiprone, TNF blockers, leflunomide, thalidomide, CYP3A4 substrate
etoposide, teniposide - class
DNA replication - topoisomerase inhibitors
etoposide, teniposide - target
inhibits topoisomerase 2
etoposide, teniposide - biochemical/physiological
cells can’t unwind DNA
cells can’t replicate DNA or make proteins
etoposide, teniposide - adverse effects
hematological, cardiovascular, nausea, dehydration, malnutrition
etoposide, teniposide - interactions
clozapine, deferiprone, TNF blockers, leflunomide, thalidomide
vinblastine, vincristine - class
mitotic inhibitors
vinblastine, vincristine - target
inhibits polymerization of tubulin into microtubules
vinblastine, vincristine - biochemical/physiological
inability of cells to form microtubules and separate cell components equally
parent cell cannot divide into 2 daughter cells
vinblastine, vincristine - adverse effects
hematological, neuropathy, nausea, dehydration, malnutrition
vinblastine, vincristine - interactions
clozapine, deferiprone, TNF blockers, leflunomide, thalidomide, CYP3A4 substrate
paclitaxel, docetaxel - class
mitotic inhibitors
paclitaxel, docetaxel - target
inhibits depolymerization of microtubules into tubulin
paclitaxel, docetaxel - biochemical/physiological
cells can’t pull components of cell apart during mitosis
parent cell cannot divide into 2 daughter cells
paclitaxel, docetaxel - adverse effects
hematological, peripheral neuropathy
paclitaxel, docetaxel - interactions
clozapine, deferiprone, TNF blockers, leflunomide, thalidomide, CYP3A4 substrate
tamoxifen, toremifene - class
hormone receptor antagonists
tamoxifen, toremifene - target
estrogen receptor antagonist
tamoxifen, toremifene - biochemical/physiological
inability of cells to transcribe genes under control of estrogen receptor
cells can’t proliferate or evade immune system
tamoxifen, toremifene - adverse effects
menopause-like symptoms (hot flashes, sweating, nausea, vaginal discharge, dizziness, vomiting), hematological, cardiovascular
tamoxifen, toremifene - interactions
prolongs QT interval, toremifene (substrate of CYP3A4), tamoxifen (substrate of CYP2D6)
anastrozole, exemestane, letrozole - class
hormone receptor antagonists
anastrozole, exemestane, letrozole - target
inhibits enzyme aromatase
anastrozole, exemestane, letrozole - biochemical/physiological
cells can’t produce estrogen from precursors
cells can’t activate estrogen receptor - results in ability to proliferate and evade immune system
anastrozole, exemestane, letrozole - adverse effects
menopause-like symptoms (hot flashes, sweating, vaginal discharge, dizziness, vomiting), hematological, hepatotoxicity, cardiovascular
anastrozole, exemestane, letrozole - interactions
thalidomide, letrozole CYP2C19 inhibitor
nilutamide, flutamide - class
hormone receptor antagonists
nilutamide, flutamide - target
androgen receptor antagonists
nilutamide, flutamide - biochemical/physiological
cells can’t transcribe genes under control of androgen receptor
cells can’t proliferate and evade immune system
nilutamide, flutamide - adverse effects
hepatotoxicity, nausea, dehydration, malnutrition
nilutamide, flutamide - interactions
none severe
gefitinib, erlotinib - class
protein tyrosine kinase inhibitors
gefitinib, erlotinib - target
inhibition of EPIDERMAL growth factor receptor
gefitinib, erlotinib - biochemical/physiological
cells can’t initiate growth factor cascade
cells can’t proliferate or metastasize - increase in cellular apoptosis
gefitinib, erlotinib - adverse effects
hematological, pulmonary toxicity, nausea, dehydration, malnutrition
gefitinib, erlotinib - interactions
clozapine, deferiprone, TNF blockers, leflunomide
imatinib - class
protein tyrosine kinase inhibitor
imatinib - target
inhibits bcr-abl chimeric tyrosine kinase
imatinib - biochemical/physiological
cells can’t initiate growth factor signal cascade
cells can’t proliferate or metastasize - increase in cellular apoptosis
imatinib - adverse effects
hematological, cardiovascular
imatinib - interactions
clozapine, deferiprone, TNF blockers, leflunomide, CYP 3A4, 2D6, 2C9 inhibitor
trastuzumab - receptor
HER2/ErbB-2 EPIDERMAL growth factor receptor
bevacizumab - receptor
VEGFR1/2 (vascular-ENDOTHELIAL growth factor)
cetuximab - receptor
EPITHELIAL growth factor receptor
trastuzumab, bevacizumab, cetuximab - target
inhibits over-expressed antigens on cell surface
trastuzumab, bevacizumab, cetuximab - biochemical/physiological
cells can’t initiate growth factor signal cascade
cells can’t proliferate or metastasize - increase in cellular apoptosis
rituximab - receptor
CD20
alemtuzumab - receptor
CD52
nivolumab - receptor
PD1
durvalumab - receptor
PD-L1
rituximab, alemtuzumab, nivolumab, durvalumab - target
binding to overexpressed antigen - directs immune system to initiate a response
rituximab, alemtuzumab, nivolumab, durvalumab - biochemical/physiological
immune system mediated initiation of apoptosis signal cascade
immune system directed cell lysis or apoptosis of neoplastic cell
ibritumomab - receptor
CD20
brentuximab - receptor
CD30
ibritumomab, brentuximab - target
binding to overexpressed antigen - release of conjugated radioactive particle/chemotherapeutic (DNA damaging agent)
ibritumomab, brentuximab - biochemical/physiological
inability to replicate DNA or make proteins, initiates DNA repair mechanisms
halt of DNA cell cycle progression, loss of cellular function - cell undergoes apoptosis if can’t repair in time
all immune system modulators - adverse effects, interactions
hematological, cardiovascular
clozapine, TNF blockers, leflunomide, thalidomide