Drugs for Testicular Cancer Flashcards
Bleomycin moa
binds DNA in presence of iron with ferrous oxide-mediated DNA strand breakage
cisplatin moa
binds to N7 site on purines and causes oxidative stress, elicited apoptosis via BAK and BAX as well as the VDAC1 channel, and activates p53
carboplatin MOA
causes nuclear and mitochondrial DNA damage (but slower and less potent than cisplatin)
etoposide moa
stabilizes DNA and topoisomerase II complexes resulting in strand breakage
ifosfamide moa
metabolically-activated alkylating agent producing intra- and inter strand DNA cross-links
paclitaxel moa
promotes microtubule assembly and stabilizes their formation by inhibiting depolymerization
vinblastine moa
binds to low-affinity sites on tubulin, resulting in splitting of the microtubules into spiral aggregates or protofilaments; this leads to the disintegration of the microtubule
mesna moa
forms acrolein-mesna thither complexes which are inactive and eliminated in the urine without causing hemorrhagic cystitis
bleomycin toxicity
pulmonary fibrosis and interstitial pneumonitis (dose-limiting), skin toxicity
cisplatin toxicity
renal toxicity (dose limiting), ototoxicity, neurotoxicity, inhibition of lipid breakdown for energy
carboplatin toxicity
thrombocytopenia (dose-limiting); neurotoxicity, ototoxic, nephrotoxic
etoposide toxicity
leukopenia (dose limiting), N/v, stomatitis and diarrhea; hepatic toxicity at high dose
ifosfamide toxicity
myelosuppression (dose-limiting); neurotoxicity (coma, seizures, ataxia)
paclitaxel toxicity
bone marrow suppression (dose limiting); peripheral neuropathy
vinblastine toxicity
neuropathy (dose-limiting)