Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PT3 Oncology > med chem > Flashcards

med chem Flashcards

1
Q

two main ways anti metabolites fight cancer

A
  • inhibit nucleotide metabolism

- get incorporated into DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

5-FU resembles which bases

A

uracil

thymine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

antimetabolites are all what

A

prodrugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

potential resistance mechanism of all antimetabolites

A

down regulation of metabolic enzymes which are needed to activate the drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

thymidylate synthase does what

A

converts dUMP to TMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

5-FU mechanism

A

is a substrate of thymidylate synthase and gets incorporated into DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

enzyme that degrades 5-FU

A

dihydropyrimidine dehydrogenase (DPD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

5-FU ADME

A

low oral bioavailability

short half life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how to increase 5-FU bioavailability

A

make a prodrug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

5-FU prodrug

A

capecitabine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how is cisplatin activated

A

exchange the chloride with water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

most reactive position in DNA

A

guanine N-7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

intercalator drugs

A

mitoxantrone

doxorubicin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how do intercalator drugs work

A

they stack in between bases of DNA using the quinone group, inhibiting topoisomerase II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what makes intercalator drugs have cardio toxicity

A

quinone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

where do taxanes bind

A

inner surface of microtubules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how to taxanes work

A
  • stabilize microtubules
  • inhibit mitosis
  • cause cell death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

vinca alkaloids do what at high concentrations

A

bind alpha,beta-tubulin dimers and destabilize microtubules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

vinca alkaloids do what at low concentrations

A

interfere with microtubule dynamics

20
Q

amino acids that get phosphorylated by kinases and are commonly used by growth factors

A

tyr
ser
thr

21
Q

protein kinase inhibitors mostly target what

A

tyrosine kinases

22
Q

active site of tyrosine kinases are… (structural feature)

A

highly rigid

23
Q

ion needed for activation of phosphates for hydrolysis

A

magnesium

24
Q

features of the inactive conformation of kinases

A

-a-loop partially occupies ATP binding pocket and substrate binding is blocked

25
Q

features of the active conformation of kinases

A
  • a-loop folded onto ATP binding site
  • DFG flipped inwards
  • p-loop binds phosphates
26
Q

type 1 kinase inhibitor MoA

A

binds ATP pocket in active conformation

27
Q

type 2 kinase inhibitor MoA

A

binds ATP pocket in inactive conformation

28
Q

type 3 kinase inhibitor MoA

A

binds allosteric site

29
Q

type 4 kinase inhibitor MoA

A

binds to distant site

30
Q

what makes selective inhibition difficult

A

active site is largely conserved among kinases

31
Q

one benefit of having a nonselective kinase inhibitor

A

single mutations are not as effective as a resistance mechanism
*sunitinib

32
Q

bcr-abl is responsible for what

A

chronic myeloid leukemia

33
Q

part of the kinase that is responsible for selectivity

A

gatekeeper

34
Q

4 design principles of kinase inhibitors

A
  • interaction with hinge region
  • gatekeeper controls selectivity
  • target hydrophobic pocket
  • bind allosteric pocket near ATP binding site
35
Q

common sites of mutation resistance to imatinib

A

a-loop
p-loop
hinge

36
Q

nilotinib features

A
  • more potent that imatinib

- hydrophobic, so less sensitive to H-bonding mutations

37
Q

what type of kinase inhibitor is dasatinib

A

type 1

38
Q

what type of kinase inhibitor is imatinib

A

type 2

39
Q

what interaction is critical for activity of imatinib

A

hydrogen bonding to thr315

40
Q

only bcr-abl inhibitor effective for T315 mutants

A

ponatinib

41
Q

reaction that covalent inhibitors use

A

michael addition

42
Q

types of inhibitors that have increased selectivity

A

allosteric and covalent

43
Q

bispecific antibodies

A

chimeras of two Abs

  • one targets cancer marker
  • other recruits immune cells
44
Q

toxicity of Ab drugs compared to other anticancers

A

Abs carry most toxic compounds

45
Q

3 regions of Ab drugs

A

Ab
linker
drug

46
Q

types of linkers

A

hydrazone
disulfide
non-cleavable

47
Q

major issue with Ab drugs

A

penetration of Abs through the whole tumor

PT3 Oncology (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions