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Chemotherapy > Chemo Drugs > Flashcards

Chemo Drugs Flashcards

1
Q

Alkylating Agents Classes

A

Nitrogen mustards
Nitrosureas
Platinum Drugs
Miscellanous

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2
Q

Nitrogen Mustards

A

Melphalan, Cyclophosphamide, Ifosfamide, Chlorambucil and Estramustine

Men Can Inject Cocaine Everday

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3
Q

Nitrosureas

A

Carmustine, Lomustine, Nimustine and Streptozocin (Streptozotocin

“Ustines” and streptozocin

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4
Q

Platinum Drugs

A

Carboplatin, Cisplatin, and Oxaliplatin

“Platins”

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5
Q

Miscellanous Alkylating Drugs

A

Busulfan, Procarbazine

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6
Q

Nitrogen Mustards MOA

A
  • Link two Guanine molecules together causing DNA damage

(Azridium intm. –> Chloro)

N-7 Alkylation

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7
Q

Nitrosurea Alkylating Agents MOA

A
  • Have a chloroethyl group that attaches to oxygen on Guanine
  • 06 alkylation
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8
Q

Streptozcin MOA

A
  • Has a methyl group
  • Get an O6 methylation to Guanine
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9
Q

Platinum Alkylating Agents MOA

A
  • Alkylate and cross link (inter or intra) two Guanine molecules
  • DNA damage –> N7 alkylation
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10
Q

Bulsulfan MOA

A

Remove mesylate (CH3SO3-) to form R–CH2+

Cause intra- and inter-crosslink of DNA molecules

N7 alkylation

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11
Q

Procarbazine MOA

A

Form methyldiazonium ion (CH3-N+≡N) and methyl cation (CH3+)

Nonspecific alkylating agent which methylates guanine at O6

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12
Q

Antimetabolite Examples And…..

A

5-Fluorouracil (5-FU), capecitabine, gemcitabine, cytarabine and azacitidine

“ines”

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13
Q

Antimetabolite MOA

A

Incoporate into the double strand of the DNA molecule  Cause breaks  Destroy the DNA molecules

Miscoding due to incorporation into DNA/RNA (incorporation into DNA molecule)

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14
Q

Antimitotics Examples

A

Taxanes

Paclitaxel
Docetaxel

“axes”

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15
Q

Antimitotic MOA

A

Bind to free tubulin (mitotic spindle) –> Stable bonding
Produce stable microtubules
Inhibit microtubule disassembly (spindles stick)

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16
Q

Vinca Alkyloids Examples

A

Vinblastine, vincristine, vindesine and vinorelbine

“Vin”

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17
Q

MOA Vinca Alkyloids

A

Prevent microtube polymerization

  • Do not allow microtubule to form spindle

Inhibit formation of mitotic spindle

18
Q

Antitumour Antibiotics Examples

A
  • Antracyclines
  • DNA intercelating agents

Daunorubicin, doxorubicin, epirubicin, idarubicin and mitoxantrone

“ubicins”

19
Q

Anthracyclines MOA

A

Intercalate with DNA perpendicular to its longitudinal axis
Cause single and double stranded DNA cleavage

20
Q

PARP Inhibitors MOA

What does PARP Stand for?

A

Involved in DNA repair (inhibit DNA repair)

PARP: Poly (ADP-ribose) polymerase

21
Q

PARP Inhibitor Examples

A

Olaparib, rucaparib, niraparib, iniparib and talazoparib

“paribs” suffix

22
Q

PARP Inhibitors MOA

A

Block DNA repair in cancer cells and cause cancer cell death

23
Q

Targeted Tx Agents

A
  • Tyrosine Kinase Inhibitors

Monoclonal Antibodies

Apoptosis Inducing Agents

Angiogenesis Inhibitors

24
Q

Tyrosine Kinase Inhibitor Examples

A

Imatinib, Gefitinib, Ibrutinib

“inibs”

25
Q

Monoclonal ANtibodies Examples

A

Prastuzumab, Pertuzumab, T-DM1, Bevacizumab, Rituximab

“umabs”

26
Q

Apoptosis Inducing Examples

A

Bortezomib, Oblimersen (nucleotide drug),

THINK O’s

27
Q

Angiogenesis Inhibitors

A

Bevacizumab, Sunitinib

28
Q

Tyrosine Kinase Inhibitor MOA

A

Tyrosine kinase (TK) domain is present in growth factor receptors, such as epidermal growth factor receptor (EGFR) and vascular endothelial growth factor receptor (VEGFR), and signaling protein kinases such as Ras and Raf

  • Inhibit angiogensis
29
Q

Immatinib MOA

A

Tyrosine-Kinase Inhibitor

Inhibit BCR-ABL tyrosine kinase
Inhibit proliferation and induce apoptosis in BCR-ABL positive cells

30
Q

Gefitnib MOA

A

Inhibitor of epidermal growth factor receptor (EGFR)

Signaling via EGF-EGFR promotes DNA synthesis, proliferation, migration and survival

31
Q

Monoclonal Antibodies MOA

A

Bind to subdomain IV of Her2 protein

32
Q

Pertuzumab MOA

A

Monoclonal antibody binds to subdomain II of Her2 protein
Block homodimerization of Her2 and heterodimerization of Her2-Her3
-
Inhibit Her2-signaling pathway and decrease cell growth

THINK ER

33
Q

Bortezomib MOA

A

Proteasome inhibitor and apoptosis-inducing agent

Bind to 26S proteasome, prevent proteosome-mediated degradation of pro-apoptotic factors and induce apoptosis

34
Q

Bevacizumab MOA

A
  • Starve Cancer cells
  • Anti-angiogenesis monoclonal antibody blocking vascular endothelial growth factor (VEGF)
  • VEGF and its receptors (VEGFR) can induce and promote angiogenesis (take out either one)
35
Q

Sunlitib MOA

A

Multiple-targeted tyrosine kinase inhibitor
Inhibit VEGFR, platelet-derived growth factor receptor (PDGFR), colony stimulating factor receptor (CSFR) and tyrosine-protein kinase KIT (CD117)
Angiogenesis inhibitor

Sun –> Star –> Millions

36
Q

PD-1 Mechanism

A

programmed cell death protein 1 (CD279)
Surface protein on T-cells
Prevent T-cells from killing other cells upon binding PD-L1
Check immune responses

37
Q

PD- L1 Mechanism

A

programmed cell death ligand 1 (CD274 or B7-H1)
Transmembrane protein
Prevent T-cells from killing PD-L1-containging cells

38
Q

PD-1 and PD-L1 Cancer Mechanism. Prevent cancer?

A

PD-L1 binds to PD-1 and inhibits T-cell killing of tumour cell

Blocking PD-L1 allows T cell killing of tumour cell

39
Q

Pd-1 Inhibitors

A

Pembrolizumab
Nivolumab
Cemiplimab

40
Q

PD-L1 Inhibitors

A

Atezolizumab
Avelumab
Durvalumab

41
Q

Tamoxifen MOA and What is it?

A
  • Block ER and inhibit breast cancer cell growth
    May slightly increase the chance of getting uterine cancer (ER in breast to block function, if goes to uterus activates ER)
  • Hormonal Tx

Think TAMMY

42
Q

How do hormones promote cancer?

A

Hormones can bind estrogen receptor (ER) and progesterone receptor (PR) to promote cancer cell growth

Chemotherapy (1 decks)

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