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oncology
drugs
| Question | Answer |
|---|---|
| which drug is a reversible inhibitor of EGFR? | Gefitinib |
| interstitial lung disease is seen with what drugs? | Gefitinib and osemertinib, pralsetinib , amivantamab-vmjw |
| this drug competes with ATP binding to cytoplasmic tyrosine kinase domain and also causes cell cycle arrest at the G0/G1 boundary? | Gefitinib |
| What targets does Lapatinib hit | HER2 EGFR |
| what is a BBW seen with Lapatinib | hepatotoxicity |
| What drugs are the irreversible inhibitors of EGFR | Lapatinib Afatinib Osimertinib |
| what targets does Neratinib and Afatinib hit? | HER2, EGFR, HER4 |
| what is the drug interaction of using neratinib and BTK inhibitors | PPIs |
| Is omeprazole a drug interaction for the use of neratinib? | yes |
| True of false: Tucatinib is highly selective for HER2 | true |
| side effect of tucatinib | diarrhea and hepatotoxicity |
| what is the purpose of using tucatinib and trastuzumab together? | improves outcomes probably due to targeting intracellular and extracellular domains of HER2. Together have increased anti-tumor activity compared to either drug alone |
| This drug is an irreversible EGFR antagonist for mutant/variant forms of EGFR. Including T790M, L858R, and exon 19 deletion | osimertinib |
| this drug has lung, GI, and dermatologic toxicity? | osimertinib |
| what do you need to evaluate for before using Cetuximab? | KRAS mutation |
| osimertinib targets what | EGFR |
| tucatinib targets HER2 or EGFR | HER2 |
| BBW of cetuximab | infusion reactions and cardiopulmonary arrest |
| This drug targets EGFR and what BBW does it have | dermatologic reactions |
| this drug is a human IgG2 kappa monoclonal antibody | panitumumab |
| BBW of trastuzumab | cardiomyopathy |
| what drug has a DI with warfarin, therefore they monitor prothrombin time ratio or INR | trastuzumab |
| what drug can you not substitute for trastuzumab | ado-trastuazumab emtansine |
| what drug is cardiotoxic and decreases LVEF | ado-trastuzumab emtansine |
| what drug is used with trastuzumab as they target different regions on HER2 receptor | pertuzumab |
| what drug has left ventricular dysfunction and embryo-fetal toxicity as a BBW | pertuzumab |
| what are the targets that crizotinib hits | ALK, ROS1, MET |
| what is the common side effect seen with crizotinib | vision disturbances |
| which drugs are the second-generation ALK inhibitors that have better BBB penetration | Brigatinib, Ensartinib, Alectinib |
| with what drug do you see the side effect of hyperlipidemia? | ensartinib |
| when using brigatinib, what do you have to do to decrease risk of pulmonary toxicites? | dose escalation |
| this drug is a third generation ALK inhibitor and ROS1 inhibitor | lorlatinib |
| what drug is used in combo with cytotoxic chemotherapy for the treatmetns of FLT3-positive AML | midostaurin |
| this drug has an active metabolite AC886? | quizartinib |
| what are the 2 variants that midostaurin inhibits | ITD & TKD |
| is midostaurin or quizartinib more potent for the ITD varian | quizartinib |
| what are the CI when using quizartinib | severe hypokalemia, severe hypomagnesemia, long QT syndrome |
| what is a serious side effect of using larotrectinib | neurotoxicity & hepatotoxicity |
| larotrectinib inhibits what? | TRKA, TRKB, TRKC |
| which drug is the second generation inhibitor of TRKA, TRKB, and TRKC kinases and ROS1 | repotrectinib |
| what are the serious side effects of using repotrectinib | neurotoxicity, hepatotoxicity, pneumonia |
| this drug inhibits TRKA, TRKB, TRKC, ROS1, AND ALK kinases, what is it | entrectinib |
| this receptor is involved in the development of different organ systems including hematopoiesis, CNS, AND GIT | RET |
| this drug requires close monitoring ever 2 weeks and has an adverse effect of impaired wound healing? | selpercatinib |
| what does selpercatinib inhibit | wild-type and mutated RET isoforms, VEGFR & FGFRs |
| are the RET inhibitors metabolized by CYP3A4 | yes |
| this RET inhibitor can cause severe interstitial lung disease/pneumonitis & hypertension | pralsetinib |
| this is a tyrosine kinase receptor that's ligand is hepatocyte growth factor | MET |
| What drugs are RET inhibitors | selpercatinib & praslsetinib |
| what drugs are MET inhibitors | Capmatinib, tepotinib, amivatamab-vmjw |
| this drug has an AE of tumor lysis syndrome | selpercatinib |
| this is a SELECTIVE MET kinase inhibitor | capmatinib |
| these drugs can cause peripheral edema | MET inhibitors Capmatinib & Tepotinib |
| what are the AE of tepotinib | peripheral edema, fatigue, dyspepsia, and musculo-skeletal pain |
| capmatinib and tepotinib are what | met INHIBITORS |
| what drug is new and targets both MET & EGFR at the same time | amivantamab-vmjw |
| this drug has affinity for EGFR exon 19 deletions, exon 21 L858R substitutions, and exam 20 insertions? | amivantamab- vmjw |
| with what drug do you have to be aware of DVT, clots, pulmonary embolism | amivantamab-vmjw |
| what drugs are the BTK inhibitors | acalabrutinib and Zanubrutinib |
| Acalabrutinib and Zanubrutinib are what | second generation BTK inhibitors: more selective |
| are the BTK inhibitors reversible or irreversible | irreversible |
| what are the DI of using BTK inhibitors | PPIs, antacids, cyp3A4 inhibitor |
| serious effect of using acalabrutinib or zanubrutinib | hemorrhaging |
| which drug may have a better AE profile. acalabrutinib or zanubrutinib | acalabrutinib |
| which is the fusion protein created by the abnormal philadelphia chromosome, which characterizes chronic myeloid leukemia | BCR-ABL |
| activation of this growth hormone may contribute to cancer pathology by causing angiogenesis & metastasis | PDGFR |
| muatations to this gene are associated with various leukemias and GI stromal tumors | KIT |
| what are the 3 different pathways that EGFR goes through | RAS-MAP , PI3K - AKT, JAK-STAT |
| Which signal transduction antagonists hits all 3 signals pathways | Imatinib |
| MOA of imatinib | Targets ABL'S ATP binding site when activation loop is closed; stabilizes BCR-ABL in inactive conformation and hold that kinase in an inactive form until drug falls off receptor. it is reversible |
| what is the clinical toxicity seen with the use of imatinib | neutropenia & thrombocytopenia |
| Imatinib targts what | BCR-ABL, PDGFR, KIT |
| with what drug do you see elevated liver enzymes | imatinib |
| out of Dasatinib and Nilotinib, which one has the highest affinity for wild type BCR-ABL | nilotinib |
| MOA of Bosutinib | will inhibit most imatinib-resistance BCR-ABL genetic variant except T315I mutant |
| what is the difference between Bosutinib and ponatinib | Bosutinib inhibits most imatinib-resistance BCR- ABL genetics variant except T315I but pontinib inhibits T315I |
| MOA of asciminib | asciminib bind to the myristate pocket and that ABL can't be active, preventing BCR-ABL kinase activity; a STAMP drug |
| what drugs are the BRAF inhibitors | Dabrafenib and encorafenib |
| what are the most common mutations seen in the activation loop of BRAF | must mutations at codon 600 V600E and V699K |
| what are the AE seen with both BRAF inhibitors | QT prolongation, severe dermatologic reactions, and photosensitivity |
| what drugs are the MEK inhibitors | Tremetinib and Binimetinib |
| MOA of both tremetinib and binimetinib | inhibits MEK1 & 2 as well as BRAF V600E |
| secondary resistance is seen with the MEK inhibitors, but why | -activation of alternative signaling pathways -mutations in the allosteric binding socket and activation loop of MEK1 -occurs with 6-7 months of first use |
| what drugs are the CDK inhibitors | palbociclib ribociclib abemaciclib |
| MOA of the CDK inhibitors | selectively inhibits CDK4/6 |
| what is a good counseling point of using a CDK inhibitor | take with food |
| with what CDK inhibitor do you avoid the use of other QT interval elongating drugs | ribociclib |