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Oncology > Pathway Targeted Therapies > Flashcards

Pathway Targeted Therapies Flashcards

1
Q

EGFR Tyrosine Kinase Inhibitors (TKIs)

A

Erlotinib, Gefitinib, Afatinib, Osimertinib

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2
Q

Antibody inhibitors of EGFRs

A

Cetuximab, Panitumumab, Necitumumab

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3
Q

Antibody inhibitors of HER2/Neu

A

Trastuzumab and Pertuzumab

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4
Q

HER2/Neu TKIs

A

Lapatinib and Neratinib

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5
Q

Inhibitors of mutated RAF kinase

A

Vemurafenib and Dabrafenib

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6
Q

Inhibitors of MEK

A

Trametinib and Cobimetinib

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7
Q

Cyclin Dependent Kinase (CDK 4/6 inhibitors)

A

Palbociclib, Abemaciclib, and Ribociclib

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8
Q

Inhibitors of Histone Deacetylase?

A

Panobinostat and Romidepsin

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9
Q

Anti-CTLA4

A

Ipilimumab

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10
Q

Anti-PD1

A

Nivolumab and Pembrolizumab

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11
Q

AntiPDL1

A

Atezolimumab

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12
Q

Inhibitors of BCR-ABL Kinase

A

EGFR TKIs (Imatinib, Dasatinib, Nilotinib)

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13
Q

Drugs targeting Angiogenesis

A

Bevacizumab, Afilbercept, Ramucirumab, TKIs (pazopanib, sorafenib, sunitinib)

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14
Q

What is targeted cancer therapies?

A

drugs that block the growth and spread of cancer by interfering with specific molecules that drive malignant progression of human cancers

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15
Q

Targeted cancer therapy vs. standard chemo

A

acts on specific molecular targets
deliberately chosen to interact with target
cytostatic (block tumor cell proliferation)
Antibody drugs–combine biologic and cytotoxic mechanisms

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16
Q

Targeted Cancer Therapies

A

Growth factors and receptors in cancer
Intracellular Kinases
Tumor host interactions aberrant tumor angiogenesis
restoring immune recognition
targets that control cancer cell behavior

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17
Q

EGFR binding MOA

A

Phosphorylation of downstream adapter proteins (MAPK, PI3K/Akt, and STAT)—>stimulates signaling pathways–>cell growth and proliferation

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18
Q

Epithelial cancers?

A

overexpression of EGFR and mutational activation of EGFR—>dependence of EGFR signaling

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19
Q

Drugs that target the EGFR Pathway?

A

TKIs or monoclonal antibodies

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20
Q

Erlotinib MOA?

A

reversible inhibitor of EGFR TK–>competively inhibits ATP binding as the active site of the kinase

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21
Q

Erlotinib and PPIs?

A

PPIs decrease Elotinib bioavailabilty by 50%

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22
Q

Erlotinib and Warfarin?

A

Poor extrinsic coagulation (elevated INR)

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23
Q

Erlotinib Usage?

A

Advanced or metastatic NSCLC after failure of Platnium based treatment
Approved for patients with EGFR mutations ONLY

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24
Q

Gefitinib absorption?

A

reduced by drugs that cause elevations in gastric pH

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25
Q

Afatinib MOA

A

Irreversible inhibitor of EGFR and HER2 receptor kinases

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26
Q

Afatinib is a substrate of

A

Pgp

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27
Q

what is first line treatment for metastatic NSCLC with EGFR mutations?

A

Afatinib

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28
Q

EGFR gatekeeper residue T790M

A

prevents binding of TKIs
It is an acquired second EGFR mutation

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29
Q

Osimertinib (3rd gen) is for?

A

T790M mutant EGFR treatment-use if resistant to TKI

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30
Q

Osimertinib MOA?

A

irreversible inhibitor of T790M-mutant EGFR

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31
Q

C797S is?

A

A third mutation; resistance to Osimertinib

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32
Q

Cetuximab MOA?

A

Antibody that binds to extracellular domain III EGFR–>prevents ligand dependent signaling and receptor dimerization –blocks cell growth/survival

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33
Q

Cetuximab use?

A

Metastatic colon cancers (KRAS wild type)
Head and neck squamous cell carcinoma

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34
Q

Cetuximab AE?

A

infusion reactions
fetal harm

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35
Q

Cetuximab mediates?

A

antibody dependent cellular cytoxicity

36
Q

Overexpression of wild-type HER2?

A

activates the intracellular tyrosine kinase and oncogenic signaling in the absence of activating mutations, coreceptors, or ligands

37
Q

Overexpression of HER2 causes gene amplification of ______ and is in __________

A

chromosome 17 (aggressive and low response)
Human breast cancer

38
Q

Trastuzumab use?

A

HER2 overexpressing breast and gastric cancer
combines with taxanes

39
Q

Trastuzumab AE?

A

Heart Failure
Cardiotoxicity by interruption of HER 2//4 heterodimer signaling

40
Q

Trastuzumab cardiac toxicity can be reduced with _______

41
Q

Trastuzumab MOA?

A

binds to extracellular domain IV of HER2 and inhibits hetero and homodimerization
long T1/2=6 days

42
Q

Pertuzumab MOA?

A

antibody against extracellular receptor dimerization domain II of HER2
T1/2=18 days

43
Q

Pertuzumab Use?

A

HER2 positive metastatic and inflammatory early stage breast cancer
give with trastuzumab and docetaxel

44
Q

Pertuzumab AE?

A

Cardiotoxicity: pertuzumab + trastuzumab does NOT cause increase
Cause fetal harm with taxanes

45
Q

Lapatinib MOA?

A

inhibitor of EGFR and HER2 Tyrosine Kinases

46
Q

Lapatinib Use?

A

Metastatic HER2 + and trastuzumab refractory breast cancer -give with Capecitabine
postmenopausal women with hormone receptor + breast cancer =give with letrozole

47
Q

Lapatinib AE

A

Cardiotoxicity less pronounced

48
Q

Neratinib MOA?

A

irreversible inhibitor of HER2 and EGFR protein tyrosine kinase

49
Q

BRAF mutation?

A

in melanoma and substitution of valine to glutamic acid (V600E) or to lysine (V600K)=protein kinase activation

50
Q

BRAF Inhibitors?

A

Vemurafenib and Dabrafenib
-for mutant BRAF melanoma

51
Q

Activated mutant BRAF is an _____________

A

oncogenic driver

52
Q

Vemurafenib MOA?

A

inhibitor for mutated BRAF V600E and effective against V600K mutation

53
Q

Vemurafenib USe?

A

metastatic melanoma with activating BRAF mutations
NOT melanoma of wildtype BRAF

54
Q

Vemurafenib AE?

A

squamous cell carcinoma and keratocanthomas

55
Q

To prevent drug resistance of Vemurafenib?

A

combo treat with MEK inhibitor (trametinib or Cobimetanib) that acts downstream of BRAF can delay development of resistance

56
Q

Dabrafenib MOA?

A

inhibits wild-type BRAF and cRAF

57
Q

Dabrafenib Use?

A

for BRAF V600 E mutation + advanced melanoma
Dabrafenib +Trametinib=delays the development of resistance

58
Q

Dabrafenib AE?

A

cutaneous squamous cell carcinoma
Cardiomyopathy

59
Q

Trametinib MOA?

A

Reversible, allosteric inhibitor of ATP binding to MEK1/2 kinases

60
Q

Trametinib Use?

A

monotherapy for patients with mutant BRAF V600E/K melanoma

61
Q

For mutant V600E/K metastatic melanoma and mutant V600 E metastatic NSCLC use?

A

Trametinib + Dabrafenib

62
Q

Trametinib AE?

A

Does NOT cause cutaneous sarcoma carcinoma
Fetal Harm

63
Q

Activation of PI3K/Akt, mTOR, STAT3 can cause?

A

Trametinib drug resistance by bypassing MEK inhibition

64
Q

Cobimetinib + Vemurafenib

A

for BRAF V600 E/K mutation

65
Q

CDK 4/6 ?

A

enhances phosphorylation of Rb–>inactivating Rb–allowing transcription of G1 into S phase

66
Q

Palbociclib MOA?

A

inhibitor of CDK4 and CDK6

67
Q

Abemaciclib use?

A

HER2 negative breast cancer

68
Q

Ribocriclib use?

A

HER2 negative advanced breast cancer

69
Q

Philadelphia chromosome translocation

A

mutated fusion protein of BCR-ABL an active protein kinase

70
Q

Treatment for Imatinib-resistant ABL mutations?

A

Dasatinib and nilotinib

71
Q

Inhibitors of BCR-ABL Kinase?

A

Imatinib =1st gen
Dasatinib and Nilotinib=2nd gen

72
Q

Inhibitors of BCR-ABL kinase for? AE?

A

chronic phase CML
Myelosuppression

73
Q

Bevacizumab

A

antibody targeting VEGF

74
Q

Afilbercept

A

protein binding VEGF

75
Q

Antibody targeting VEGFR (receptor)?

A

ramucirumab

76
Q

Small drug inhibitors of VEGFR?

A

pazopanib, sorafenib, suntinib

77
Q

PARP Inhibitors?

A

multiple strand breaks in cancer cells BRCA mutations

78
Q

PARP inhibitors?

A

Olaparib, Rucaparib, Niraparib, Talazoparib
-Combine with radiotherapy

79
Q

Olaparib use?

A

monotherapy for germline BRCA 1/2 mutated advanced ovarian cancer and HER2 negative metastatic breast cancer

80
Q

Rucaparib use?

A

BRCA mutant ovarian cancer

81
Q

Olaparib + Rucaparib

A

treat prostate cancer with BRCA 1/2 mutations

82
Q

Gemtuzumab Ozogamicin MOA?

A

monoclonal antibody CD33, derivative of calicheamicin
present on hematopoietic cells of AMLs and myeloid cells with myelodysplastic syndrome

83
Q

Gemtuzumab Ozogamicin Use?

A

greater than 60 years old with AML first relapse

84
Q

Brentuximab Vedotin Use?

A

For anti CD30, is a antimitotic drug
For Hodgkin Lymphoma and large cell lymphoma

85
Q

Brentuximab Vedotin works on which phase?

86
Q

Panobinostat

A

nonselective pan HDAC inhibitor
for multiple myeloma

Oncology (10 decks)

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