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PHRM 864 Therapeutics > Antimetabolites Dykhuizen > Flashcards

Antimetabolites Dykhuizen Flashcards

1
Q

which of the following drugs target Her2? (review)

a. sirolimus
b. alectinib
c. vemurafinib
d. tucatinib

A

d. tucatinib

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2
Q

Which of the following drugs targets a kinase that is produced by formation of the Philadelphia chromosome? (review)

a. Alectinib
b. Gefitinib
c. Imatinib
d. binimetinib

A

c. Imatinib

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3
Q

Which compound below is NOT a covalent kinase inhibitor? (review)

A. Gefitinib
B. Osimertinib
C. Afatinib
D. Acalabrutinib

A

A. Gefitinib

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4
Q

Which type of kinase inhibitor can bind in the ATP binding site and stabilize the inactive confirmation of a kinase? (review)

	A. Type I
	B. Type II 
	C. Type III
	D. Type IV
A

B. Type II

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5
Q

A CML patient initially tested positive for the Philadelphia chromosome and has enjoyed a 5-year response to imatinib. Unfortunately, the disease has recurred and now tests positive for a T315I mutation.

-Describe how T315l prevents the efficacy of imatinib.
-What might the next course of BCR-Abl targeted therapy might include? (review)

A

-The T315l mutation prevents the binding of imatinib to BCR-abl
-Ponatinib is indicated upon identification of the T315l mutation

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6
Q

T or F: anti-metabolites block the production of nucleotide building blocks for DNA replication and transcription

A

T

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7
Q

what is myelosuppression?

A

common SE of chemotherapy; it is when bone marrow activity is decreased, resulting in fewer RBCs, WBCs, and platelets

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8
Q

which bases are paired together in DNA?

A. Adenine with Cytosine, Thymine with Guanine
B. Cytosine with Guanine, Adenine with Thymine
C. Adenine with Guanine, Thymine with Cytosine

A

B. Cytosine with Guanine, Adenine with Thymine

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9
Q

Which two are the purines?

A. Adenine and Cytosine
B. Cytosine and Guanine
C. Adenine and Guanine
D. Thymine and Guanine
E. Thymine and Uracil

A

C. Adenine and Guanine

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10
Q

5-FU interferes with __________ synthesis

a. purine
b. pyrimidine

A

b. pyrimidine

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11
Q

________ analogs primarily inhibit thymidine synthesis from uracil

A

uridine

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12
Q

in the presence of folates, _______ _______ synthesizes thymidine monophosphate (TMP) from deoxy uridine monophosphate (dUMP)

a. thymine synthase
b. thymidine phosphorylase
c. dihydropyrimidine dehydrogenase (DPD)
d. thymidylate synthase

A

d. thymidylate synthase

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13
Q

what percent of the population has gene polymorphisms that result in a deficiency of the enzyme DPD which breaks down 5-FU, as well as naturally occurring pyrimidines?

A

~5%

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14
Q

drug rescue agent used for 5-FU overdose

A

thymidine

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15
Q

drug synergy agent used with 5-FU

A

leucovorate

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16
Q

cytarabine is converted to ________ intracellularly

A

Ara-CTP

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17
Q

Ara-CTP is a competitive inhibitor of which enzyme? (slide 28)

A

DNA polymerase alpha

18
Q

which enzyme converts cytarabine to non-toxic uracil arabinoside?

a. cytosine deaminase
b. cytidine deaminase
c. DNA polymerase alpha
d. thymidine phosphorylase

A

b. cytidine deaminase

19
Q

________ levels of cytidine deaminase in the CNS makes Ara-C highly toxic in meningeal leukemia and lymphoma

a. increased
b. decreased

A

b. decreased

20
Q

drug synergy agent with cytarabine

a. leucovorate
b. tetrahydrouridine
c. thymidine

A

b. tetrahydrouridine

21
Q

tetrahydrouridine is an inhibitor of what enzyme?

A

cytidine deaminase (CDA)

22
Q

Which drug is a NUCLEOSIDE analog

A. 5-FU
B. Cytarabine

A

B. Cytarabine

23
Q

6-mercaptopurine is a thiol analog of

a. adenine
b. guanine
c. cytosine
d. thymine

A

a. adenine

24
Q

function of 6-mercaptopurine

A

blocks synthesis of purine nucleotides

25
Q

6-MP is converted to its active metabolite by what enzyme?

A

HGPRT

26
Q

when does 6-MP resistance occur?

A

with the loss of HGPRT, the activating enzyme

27
Q

6-MP is inactivated by which enzyme?

a. xanthine oxidase
b. thiopurine methyl transferase (TPMT)
c. dihydrofolate reductase (DHFR)
d. HGPRT

A

b. thiopurine methyl transferase (TPMT)

28
Q

TPMT polymorphisms occur in ~____% of children in the US

A

~10%

29
Q

what drug does 6-MP have a major drug interaction with?

A

allopurinol

30
Q

Which drug primarily interferes with purine biosynthesis?

a. 5-Fluorouracil

b. Capecitabine

c. 6-Mercaptopurine

d. Cytosine arabinoside

A

c. 6-Mercaptopurine

31
Q

______ inhibition reduces FH4 pools, folate pools accumulate as inactive dihydrofolate

a. CDA
b. DHFR
c. thymidylate synthase
d. thymidine phosphorylase

A

b. DHFR (dihydrofolate reductase)

32
Q

folic acid enters the folate pool as _________; reduction to tetrahydrofolate is done by _______ _______ (enzyme)

A

dihydrofolate; dihydrofolate reductase

33
Q

major effect of DHFR inhibition

A

inhibition of thymidine monophosphate (TMP) synthesis (also inhibits synthesis of RNA, protein, purine and pyrimidine bases)

34
Q

methotrexate is an inhibitor of which enzyme?

A

DHFR (dihydrofolate reductase)

35
Q

compounds that bind to and inhibit DHFR are _____ mimics

A

folate

36
Q

how does polyglutamation relate to methotrexate (MTX) resistance?

A

decreased polyglutamation results in dec intracellular MTX accumulation and resistance; polyglutamation of intracellular MTX helps keep it inside the cell

37
Q

drug for methotrexate toxicity

A

leucovorin

38
Q

how does leucovorin “rescue” normal tissues from methotrexate toxicity? (3 things)

A

-stable folate cofactor that is converted to tetrahydrofolate intracellularly
-increases intracellular pools of tetrahydrofolate and reverses toxic effects of DHFR inhibition
-competes with methotrexate for transporters

39
Q

Anti-folates all share the following characteristics except:

a. They inhibit DHFR

b. They cause myelosuppression

c. They induce a G2/M cell cycle block

d. The toxic effects are “rescued” by Leucovorin

A

c. They induce a G2/M cell cycle block

(they cause an S phase block)

40
Q
A

PHRM 864 Therapeutics (22 decks)

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