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Year 2 Pharmacology > Antineoplastic agents II > Flashcards

Antineoplastic agents II Flashcards

1
Q

what class of antimetabolite are 6-TG and 6-MP? what is the mechanism of action?

A
  1. purine analog
  2. inhibit purine synthesis - reduces RNA and DNA precursors
  3. incorporate into DNA
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2
Q

which enzyme activates 6-TG and 6-MP? what are the activation products?

A
  1. hypoxanthine guanine phosphoribyl transferase (HGPRT)

2. thio-IMP and thio-GMP

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3
Q

what is the mechanism of resistance for 6-TG and 6-MP?

A

decreased activity of HGPRT

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4
Q

which enzyme inactivates 6-TG and 6-MP?

A

thiopurine methyltransferase (TPMT)

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5
Q

what class of antimetabolite is fludarabine? what is the mechanism of action?

A
  1. purine analog
  2. incorporated into DNA and RNA
  3. inhibits DNA polymerase and ribonucleotide reductase
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6
Q

which enzyme is necessary to activate fludarabine?

A

deoxycytidine kinase

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7
Q

what class of antimetabolite is cladribine? what is the mechanism of action?

A
  1. purine analog
  2. incorporated into DNA
  3. causes strand breaks
  4. inhibits ribonucleotide reductase (lowers precursor pool)
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8
Q

which type of cancer is cladribine commonly used for?

A

hairy cell leukemia

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9
Q

which enzyme is necessary to activate cladribine?

A

deoxycytidine kinase

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10
Q

what is the most nucleophilic group in the DNA backbone?

A

7-nitrogen group on guanine

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11
Q

what class of drug is cyclophosphamide? what is the MOA?

A
  1. classical alkylating agent

2. causes DNA cross linking and strand breakage

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12
Q

what is an important side effect of cyclophosphamide? why?

A
  1. hemorrhagic cystitis

2. active form can convert to acrolein (toxic to bladder cells)

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13
Q

coadministration of which drug can inactivate acrolein and mitigate the side effects of cyclophosphamide?

A

mesna

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14
Q

why is carmustine a good agent for brain tumors?

A

very lipophilic - can cross BBB

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15
Q

what class of drug is carmustine? what is the MOA?

A
  1. classical alkylating agent

2. causes DNA cross linking and strand breakage

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16
Q

what are the general adverse effects of alkylating agents?

A
  1. mutagenic
  2. teratogenic
  3. myelosuppressive
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17
Q

what are the mechanisms of resistance for alkylating agents?

A
  1. inactivation by glutathione
  2. reduced uptake
  3. accelerated DNA repair
  4. increased expression of MGMT (removes alkyl groups from guanine before cross links occur)
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18
Q

what are the non-classical alkylating agents?

A
  1. cisplatin
  2. carboplatin
  3. oxaliplatin
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19
Q

what is the MOA of the non-classical alkylating agents?

A

target nucleophilic center (guanine N7)

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20
Q

what are the differences in side effects between cisplatin and carboplatin?

A
  1. carboplatin - less nausea (dose limiting toxicity is myelosuppression)
  2. cisplatin - peripheral neuropathy and neurotoxicity
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21
Q

what class of drug are vinblastine and vincristine? what is the MOA?

A
  1. antimicrotubule

2. inhibit polymerization of tubulin (microtubules) - improper segregation of chromosomes in mitosis

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22
Q

what are the adverse effects of vincristine?

A

mostly neurological - numbness, tingling in extremities, motor weakness

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23
Q

what are the adverse effects of vinblastine?

A

mostly myelosuppression

24
Q

what class of drug is paclitaxel? what is the MOA?

A
  1. antimicrotubule

2. prevents depolymerization of microtubules - arrests cells in mitosis

25
Q

what are the main adverse effects of paclitaxel?

A
  1. peripheral neuropathy

2. hypersensitivity

26
Q

paclitaxel is used with which drug to reduce myelosuppression?

A

filgrastim (GCSF)

27
Q

what are the topoisomerase I inhibitors?

A
  1. irinotecan

2. topotecan

28
Q

what is the topoisomerase II inhibitor?

A

etoposide

29
Q

what class of drug is doxorubicin? what is the MOA?

A
  1. antracycyline antibiotic
  2. intercalates with DNA, inhibits DNA polymerase
  3. inhibits topoisomerase II
  4. binds iron and generates free radicals - kills by DNA and protein damage
30
Q

what is the important adverse effect of doxorubicin? why?

A
  1. irreversible cardiomyopathy

2. iron-generated free radical damage

31
Q

coadministration of which drug mitigates the toxicity of doxorubicin?

A

dexrazoxane (iron chelator)

32
Q

what is the MOA of bleomycin?

A

binds to DNA - causes single and double strand breaks

33
Q

what is an advantage of bleomycin?

A

minimally myelosuppressive and immunosuppressive

34
Q

what is the dose limiting toxicity of bleomycin?

A

pulmonary toxicity

35
Q

bleomycin causes cells to arrest in which phase?

A

G2

36
Q

the majority of cytotoxic agents induce what major adverse effect?

A

myelosuppression

37
Q

what is the MOA of tamoxifen?

A
  1. competitively binds estrogen receptor

2. reduces growth of estrogen dependent breast cancers

38
Q

what class of drug is anastrazole? what is the MOA?

A
  1. aromatase inhibitor (inhibits conversion of testosterone to estrogen)
  2. lowers estrogen levels in post-menopausal women
39
Q

what class of drug is flutamide? what is the MOA?

A
  1. androgen receptor antagonist

2. prevent dihydrotestosterone from binding to androgen receptors - for prostate cancer

40
Q

what class of drug is leuprolide? what is the MOA?

A
  1. GnRH agonist

2. desensitizes gonadotropin receptors over the long run, decreases LH and FSH levels and thus testosterone levels

41
Q

what class of drug is trastuzamab (herceptin)? what is the MOA?

A
  1. inhibitor of kinase signal transduction

2. monoclonal Ab that binds HER-2 receptor - prevents it from signaling

42
Q

what class of drug is cetuximab? what is the MOA?

A
  1. inhibitor of kinase signal transduction

2. monoclonal Ab that binds EGFR receptor - prevents it from signaling

43
Q

what is the drug of choice for breast cancers with amplified HER-2?

A

trastuximab (herceptin)

44
Q

what is the main toxicity for trastuximab (herceptin)?

A

cardiotoxic

45
Q

cetuximab is used for what types of tumors?

A

colorectal

46
Q

activation of what protein precludes the use of cetuximab?

A

Ras

47
Q

bevacizumab is a monoclonal antibody directed against what growth factor?

A

VEGF

48
Q

what is the MOA of lapatinib?

A

inhibits both EGFR and HER-2 kinase activity

49
Q

what drug can be used to treat breast cancers that are HER-2 amplified but resistant to trastuzamab?

A

lapatinib

50
Q

what is the MOA of erlotinib?

A
  1. EGFR inhibitor

2. ATP competitive inhibitor

51
Q

what type of cancer is imatinib used for? what is the MOA?

A
  1. CML

2. inhibits BCR-ABL fusion protein from Philadelphia chromosome - inhibits tyrosine kinase activity

52
Q

what type of cancer is asparaginase used for? what is the MOA?

A
  1. ALL
  2. causes degradation of L-asparagine to L-aspartate
  3. selective starvation of asparagine
  4. occurs in serum
53
Q

what is a unique adverse effect specific to asparaginase?

A

hypersensitivity

54
Q

bortezomib is what class of drug? what is the MOA?

A
  1. proteasome inhibitor

2. elevates p53 levels

55
Q

what is the unique adverse effect of bortezomib?

A

peripheral neuropathy

56
Q

temsirolimus is used to treat what type of cancer? what is the MOA?

A
  1. renal cell carcinoma

2. inhibits mTOR - reduces protein translation, inhibits cell cycle, promotes apoptosis

Year 2 Pharmacology (70 decks)

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