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Pharm II > Anti-Cancer Drugs > Flashcards

Anti-Cancer Drugs Flashcards

1
Q

Alkylating agents

A

cyclophosphamide

Cisplatin

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2
Q

Alkylating agents: mode of action

A

Alkylating agents: mode of action
inhibit DNA synthesis
*works in ANY phase of the cell cycle

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3
Q

Alkylating agents: mechanism of action

A

physically binding to DNA to stop cell growth

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4
Q

Anti-metabolites

A

Methotrexate
5-FU
Capecitabine

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5
Q

Anti-metabolites: mode of action

A

block DNA synth in S phase

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6
Q

Anti-metabolites: mechanism of action

A

remove critical proteins in DNA replication (methotrexate)

become false substrates for DNA synthetic enzymes (5-fluorouracil & capecitabine)

ie blocking folic acid, purine, pyrimidine

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7
Q

What are the 2 plant alkaloids?

A

Vincas & Taxenes

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8
Q

Plant metabolites - VINCAS

A 
Vincristine
Vinblastine
Vinorelbine
Vindestine
(Vin-)
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9
Q

VINCAS: mode of action

A

arrest of cell division

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10
Q

VINCAS: mechanism of action

A

prevent formation of mitotic spindle during the M phase

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11
Q

Plant metabolites - TAXENES

A

Paclitaxel
Docetaxel
(-taxel)

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12
Q

TAXENES: mode of action

A

stabilize microtubule assembly to prevent cell division

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13
Q

TAXENES: mechanism of action

A

spindle forms but cannot come apart during the M phase

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14
Q

Antitumor antibiotics

A

doxorubicin & epirubicin

-rubicin

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15
Q

Antitumor Antibiotics: Mode of action

A

Causing DNA strand breaks

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16
Q

Antitumor Antibiotics: Mechanism of Action

A

Inhibits topoisomerase II (enzyme that unwinds/reseals for synthesis)

*fit in between the strands of DNA - called intercalation

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17
Q

ANTI-ANDROGENS:

A

bicalutamide, flutamide, nilutamide

-utamide

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18
Q

ANTI-ANDROGENS: MOA

A

inhibit and/or degrade the androgen receptor

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19
Q

ANTI-ANDORGENS: Use

A

androgen dependent prostate cancer

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20
Q

KINASE INHIBITORS

A

erlotinib - EGFR1
lapatinib - EGFR1&2
sutinib - VEGFR/PDGFR
sorafenib - VEGFR/PDGFR

(-nib)

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21
Q

KINASE INHIBITORS EGCR1/2 MOA

on tumor cells

A

blocks growth factor signaling leads to decreased TUMOR growth and survival

22
Q

KINASE INHIBITORS-VEGFR & PDGFR MOA

A

VEGFR - on endothelial cells of blood vessels
PDGFR - on smooth muscle cells of blood vessel

Cane lead to decreased tumor BLOOD VESSEL growth (angiogenesis)

23
Q

Immune checkpoint inhibitor drugs

A

CTLA-4 inhibitors:
Ipilumumab
PD-1/OD-1L inhibitors:
1) PD-1 inhibitors: pembrolizumab, nivolumab
2) PD-1L inhibitors: atezolizumab, avelumab

*(-mab)

24
Q

CTLA-4 inhibitors MOA

A

blocking CTLA-4 sustains the cytotoxic T cell kill of cancer cells

  • enhances the immune system to kill tumors
  • acts within the lymph system
25
Q

PD-1/PD-1L inhibitors MOA:

A

act at the level of the tumor cells/periphery

- trigger the immune system to kill tumor cells

26
Q

PD-1 Inhibitors MOA

A

antibody inhibitors of PD-1

- programmed cell death receptor-1

27
Q

PD-1L inhibitors MOA

A

antibody inhibitors of PD-1L

- ligand for PD-1

28
Q

Oncolytic Virus drugs

A

talimogene laherparepvec T-VEC

29
Q

Oncolytic Virus drugs MOA

A

triggers tumor lysis

  • Triggers release of the cytokine GM-CSF within tumor which triggers tumor lysis
  • This in turn triggers an immune antitumor response (i.e., kills more tumor cells)
  • **Currently - only approved for injection directly into tum
30
Q

Gene therapy drugs

A

Tisagenlecleucel & Axicabtagene ciloleucel

-leucel

31
Q

Gene therapy drugs MOA

A
  • Actually adoptive T cell transfer with cells containing new gene
  • Gene (called CAR-T) encodes a receptor that targets leukemia cells and triggers the T cells to kill them
32
Q

What is gene therapy drugs used for?

A

acute lymphoblastic leukemia

33
Q

Antibody conjugate drug

A

Inotuzumab ozogamicin

-mab

34
Q

What are the 2 parts of the Antibody conjugate drug?

A

Antibody (missile)

Toxin (Payload)

35
Q

Antibody conjugate drug MOA

A

1) Antibody (missile): TARGETS the toxic drug or toxin protein to the cancer cells
ex: the antibody inotuzumab is against CD22 antibody - expressed on tumors
2) Toxin (payload): small molecule or bacterial toxin that is tethered to the antibody
ex: ozogamicin (a toxic small molecule) is tethered to the antibody

36
Q

What is the most common dose-limiting toxicity of chemotherapeutic agents?

A

myelosuppression

- dose and agent related

37
Q

Why is myelosuppression a problem?

A

1) decreased RBCs –> decrease oxygen to tissues –> FATIGUE
2) decrease platelets –> decrease clotting
3) Kill off WBCs –> decrease immunity –> increase chance of infection

38
Q

Treatments for myelosuppression

A

1) Neutropenia
- colony stimulating factors similar to G-CSF (filgrastim, pegfilgrastim). Growth factors to raise blood count
- antibiotics to prevent infection
2) Thrombocytopenia
- blood infusion
3) Anemia
- Epoetin-alpha - erythropoetin- RBC growth factor or blood infusion

39
Q

What are the dermatologic toxicities?

A

1) Alopecia
2) Extravasation necrosis
3) hand-foot syndrome
4) mucositis
5) rash

40
Q

What is extravasation necrosis and its tx?

A

dermatologic toxicity - localized damage to tissue if drug is accidentally administered outside blood vessel

Tx/prevention: heat or cold at the site (agent dependent) and hyaluronidase

41
Q

What is hand-foot syndrome and its tx?

A

dermatologic toxicity - erythema of palms and soles of feet

Tx/prevention: avoiding heat and friction to those surfaces; applying lotions and cold compresses/packs

42
Q

What is the mucositis and its Tx?

A

dermatologic toxicity - inflamed/damage mucous membranes

Tx: oral anesthetics, palifermin (drug that stimulates mucosal cell health and growth)

43
Q

What can a rash be a sign of?

A

hypersensitivity - derm toxicity

44
Q

What are some GI toxicities?

A

1) nausea and vomiting
- most upsetting to a patient
- can lead to dehydration, electrolyte disturbances, etc. is unchecked

45
Q

What are the MOA of GI toxicities?

A
  • direct irritation of GI membranes
  • death of protective GI mucosal cells
  • Stimulation of part of the brain called the CHEMORECEPTOR TRIGGER ZONE
  • NEW: autoimmune attacking of GI mucosa with new PD-1 inhibitors
  • Strong psychological component
46
Q

What are the Tx for GI toxicities?

A

1) 5-HT3 antagonists- ondansetron, granisetron
- 5-HT = serotonin
- antagonize aspects of what is called the chemoreceptor trigger zone (vomit reflex)
2) corticosteroids - prednisone, dexamethasone
- stimulate appetite, reduce inflammation
3) Neurokinin-1 antagonist - aprepitant
- like 5-HT3 antagonists, antagonize aspects of what is called the chemoreceptor trigger zone

47
Q

What is peripheral neuropathy & Tx?

A

misc toxicities - pain, tingling, numbness in hands and feet

Tx: pain modulating agents like the anti-epileptic drug pregabalin

48
Q

What is cardiotoxicity & Tx?

A

misc toxicity - with anticyclines (doxorubicin, etc.)
Mechanism: iron mediated free radical damage
Tx: dexrazoxane - chelates iron in heart to make it less reactive

49
Q

What is secondary tumor?

A

misc toxicity - many (especially older) agents are carcinogenic

50
Q

What is teratogenesis?

A

misc toxicity - because of there inherent cytotoxicity, most agents are teratogenic

51
Q

What is autoimmune reactions?

A

misc. toxicity - especially with immune checkpoint inhibitors
- GI, thyroid, lung, and renal

Pharm II (4 decks)

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