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Pharm II > Anti-Cancer Drugs > Flashcards

Anti-Cancer Drugs Flashcards

(51 cards)

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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

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A

blocks growth factor signaling leads to decreased TUMOR growth and survival

22
Q

KINASE INHIBITORS-VEGFR & PDGFR MOA

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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

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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

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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
PD-1/PD-1L inhibitors MOA:
act at the level of the tumor cells/periphery | - trigger the immune system to kill tumor cells
26
PD-1 Inhibitors MOA
antibody inhibitors of PD-1 | - programmed cell death receptor-1
27
PD-1L inhibitors MOA
antibody inhibitors of PD-1L | - ligand for PD-1
28
Oncolytic Virus drugs
talimogene laherparepvec T-VEC
29
Oncolytic Virus drugs MOA
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
Gene therapy drugs
Tisagenlecleucel & Axicabtagene ciloleucel | -leucel
31
Gene therapy drugs MOA
- 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
What is gene therapy drugs used for?
acute lymphoblastic leukemia
33
Antibody conjugate drug
Inotuzumab ozogamicin -mab
34
What are the 2 parts of the Antibody conjugate drug?
Antibody (missile) | Toxin (Payload)
35
Antibody conjugate drug MOA
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
What is the most common dose-limiting toxicity of chemotherapeutic agents?
myelosuppression | - dose and agent related
37
Why is myelosuppression a problem?
1) decreased RBCs --> decrease oxygen to tissues --> FATIGUE 2) decrease platelets --> decrease clotting 3) Kill off WBCs --> decrease immunity --> increase chance of infection
38
Treatments for myelosuppression
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
What are the dermatologic toxicities?
1) Alopecia 2) Extravasation necrosis 3) hand-foot syndrome 4) mucositis 5) rash
40
What is extravasation necrosis and its tx?
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
What is hand-foot syndrome and its tx?
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
What is the mucositis and its Tx?
dermatologic toxicity - inflamed/damage mucous membranes Tx: oral anesthetics, palifermin (drug that stimulates mucosal cell health and growth)
43
What can a rash be a sign of?
hypersensitivity - derm toxicity
44
What are some GI toxicities?
1) nausea and vomiting - most upsetting to a patient - can lead to dehydration, electrolyte disturbances, etc. is unchecked
45
What are the MOA of GI toxicities?
- 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
What are the Tx for GI toxicities?
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
What is peripheral neuropathy & Tx?
misc toxicities - pain, tingling, numbness in hands and feet Tx: pain modulating agents like the anti-epileptic drug pregabalin
48
What is cardiotoxicity & Tx?
misc toxicity - with anticyclines (doxorubicin, etc.) Mechanism: iron mediated free radical damage Tx: dexrazoxane - chelates iron in heart to make it less reactive
49
What is secondary tumor?
misc toxicity - many (especially older) agents are carcinogenic
50
What is teratogenesis?
misc toxicity - because of there inherent cytotoxicity, most agents are teratogenic
51
What is autoimmune reactions?
misc. toxicity - especially with immune checkpoint inhibitors - GI, thyroid, lung, and renal

Pharm II (4 decks)

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