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iho-week 4 > Drugs Targeting Protein Function > Flashcards

Drugs Targeting Protein Function Flashcards

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1
Q

What drugs inhibit EGFR?

A

Cetuximab, Erlotinib, Gefitinib, Panitumumab

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2
Q

What drugs inhibit HER2?

A

Pertuzumab, Trastuzumab

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3
Q

What do tyrosine kinases do?

A

regulators of intracellular signal transduction pathways

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4
Q

What role do Tyrosine kinases play in cancer?

A

TK receptors are often mutated or overexpressed in cancers

-signal transduction inhibitors and abs made to target these

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5
Q

What is overexpressed in many epithelial-derived cancers?

A

EGFR

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6
Q

What is the MOA for Cetuximab and Panitumumab?

A

Mabs against EGFR to prevent actions of EGFR + identify cells that express the receptor for degradation

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7
Q

What are the unique toxicities associated with Cetuximab and Panitumumab?

A

skin (rash, photosensitivity, necrotizing fasciitis), lung (interstitial lung disease)

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8
Q

What is the MOA for Trastuzumab?

A

interferes with Her2 signaling + identifies Her2-overexpressing cells for degradation

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9
Q

What is the MOA for pertuzumab?

A

dimerization inhibitor - prevents Her2 from dimerizing with other HER receptors

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10
Q

What is the MOA for Ado-Trastuzumab Emtansine?

A

internalized and degraded in lysosomes to form Trastuzumab + DM1 (inhibits microtubules by binding tubulin)

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11
Q

What resistance forms to Trastuzumab/pertuzumab?

A

altering Her2 so ab cannot recognize it

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12
Q

What are the toxicities of Trastuzumab?

A

infusion/hypersensitivity rxns, infections, birth defects/fetal loss

unique: ventricular dysfunction and CHF

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13
Q

What is the major difference between drugs that target mutated/overexpressed proteins and drugs that target altered intracellular processes?

A

the later tends to be less specific for cancer - more AE

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14
Q

What is the mechanism that L-asparaginase uses to deplete asparagine?

A

asparagine is converted to aspartate so that cancer cells cannot directly transport asparagine into the cell –> die due to lack of asparagine

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15
Q

How does L-asparaginase have selective toxicity?

A

ALL cancer cells lack asparagine synthase, so they cannot transport aspartate; normal cells can transport aspartate

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16
Q

Why is L-asparaginase often given with Mtx?

A

Mtx given FIRST, L-asparaginase given SECOND has synergistic cytotoxicity (more total cells killed than using either alone; timing matters)

17
Q

What drugs inhibit proteosomes?

A

Bortezomib, Carfilzomib

18
Q

What is the MOA for Bortezomib/ Carfilzomib?

A

inhibit the 26S proteosome –> triggers apoptosis

19
Q

What are the toxicities associated with Bortezomib/ Carfilzomib?

A

thrombocytopenia, neutropenia, anemia, peripheral neuropathy

20
Q

What drugs inhibit HDACs?

A

Romidepsin, Vorinostat

21
Q

What is the MOA for Romidepsin, Vorinostat?

A

inhibit HDAC –> increase transcription –> cell cycle arrest and apoptosis result

22
Q

What do HDACs do in cancer?

A

work with HAT to regulate gene expression - cancer cells can overexpress/recruit HDACs –> prevent transcription –> silence tumor suppressor genes

23
Q

What are toxicities associated with Romidepsin/ Vorinostat?

A

Hemato: PE, DVT

Drug-Drug interactions: valproic acid, Warfarin (causes warfarin to increase - bleeding)

24
Q

What are the drugs that induce differentiation?

A

Tretinoin (Atra, Retin-A), Arsenic Trioxide (ATO), Bexarotene

25
Q

MOA for differentiating agents

A

induce tumor cell differentiation to ultimately lead to apoptosis

26
Q

What differentiation block occurs in APL?

A

fusion protein PML-RAR-alpha has retinoic receptor and promyelocytic leukemia protein, t(15;17)

27
Q

What is the MOA for tretinoin?

A

activates differentiation and promotes degradation of PML-RAR fusion protein; used to treat APL

28
Q

Why is arsenic trioxide or anthracycline abx given with tretinoin?

A

tretinoin doesn’t kill cells - other drugs cause cell death

29
Q

What are the toxicities for Tretinoin?

A
  • CNS toxicity
  • Differentiation syndrome (fever, dyspnea, wt gain, pulmonary infiltrates) w/ or w/o pleural and pericardial effusions and leukocytosis
  • birth defects
30
Q

What is the MOA for Arsenic Trioxide?

A

heavy metal toxin that promotes cell death thru apoptosis and necrosis; causes death of granulocytes when given with Tretinoin

31
Q

What are the toxicities associated with Arsenic Trioxide?

A

arrhythmia, leukocyte maturation syndrome

32
Q

What is the MOA for Bexarotene?

A

rexinoid - activates retinoid X receptors involved in differentiation

33
Q

Tx uses for Bexarotene

A

Cutaneous T-cell lymphoma

34
Q

How is Bexarotene metabolized?

A

CYP34A

35
Q

What are the toxicities associated bexarotene?

A

lipid abnormalities and pancreatitis, teratogenic

iho-week 4 (6 decks)

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