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ANTICANCER DRUGS Flashcards

1
Q

Name at least 2 alkylating agents

A
  1. chorambucil
  2. cyclophosphamide
  3. carmustine (-mustines)
  4. dacarbazine (-carbazines)
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2
Q

MOA of alkylating agents

A

alkyl group forms covalent bond with DNA -> cross linkage/ strand breakage -> inhibit DNA replication -> apoptosis

majory site of alkylation is N7 position of guanine

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3
Q

Adverse effects of alkylating agents

A
  1. nausea, vomiting
  2. myelosuppresion
  3. alopecia
  4. pulmonary fibrosis
  5. increased 2ndary malignancies
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4
Q

Possible resistance mechanisms for alkylating agents

A
  1. decreased drug transportation into cell
  2. increased capacity to repair DNA lesions
  3. increased expression of glutathione associated proteins (help with DNA repair)
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5
Q

What are cell cycle non-specific drugs?

A

drugs that kill throughout cell cycle
1. alkylating agents
2. platinum analogues
3. cytotoxic antibiotics
4. topoisomerase inhibitors

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6
Q

What are cell cycle specific drugs?

A

drugs that kill specific parts of cell cycle during replication
1. anti-metabolites (S phase)
2. microtubules inhibitors

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7
Q

Name 3 platinum analogues?

A
  1. cisplatin
  2. carboplatin
  3. oxaliplatin
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8
Q

MOA of platinum analogues

A

act like alkylating agents, increase cross-linking of DNA preventing DNA replication= apoptosis

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9
Q

Adverse effects of platinum analogues

A
  1. myelosuppression
  2. nephrotoxicity
  3. peripheral sensory neuropathy
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10
Q

How are platinum analogues cleared?

A

R.E unchanged

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11
Q

When is cisplatin contradicted?

A

creatine clearance < 60ml/min

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12
Q

Can carboplatin be used in mild renal impairment?

A

yes, use with dose adjusment

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13
Q

Anti cancer drugs that are antimetabolites?

A
  1. methotrexate
  2. 5-fluorouracil

HIGHLY CELL SPECIFIC: S PHASE

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14
Q

MOA for methotrexate

A

inhibit dihydrofolate reductase needed for recyling of folate, i inhibit synthesis of thymidine monophosphate

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15
Q

methotrexate clinical indication?

A

tumours eg breast cancer and lymphoma

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16
Q

MOA of 5-fluorouracil

A

inhibit thymidylate synthase, misincoporation into RNA and DNA => damage

inactivtaed by being converted to dihydrofluoracil by dihydropyrimidine dehydrogenase

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17
Q

5-fluorouracil clinical indication?

A

colorectal cancer

18
Q

Adverse effects for anti-metabolites?

A
  1. nausea and vomiting (GI)
  2. myelosuppresion
  3. nephrotoxicity
  4. pulmonary fibrosis
19
Q

Anti cancer drugs that are cytotoxic antibiotics?

A
  1. anthracyclines: doxorubicin (most common cancer drug) , daunorubicin
  2. mitomycin C, bleomycin
20
Q

MOA of cytotoxic antibiotics?

A
  1. inhibit dna/rna synthesis via intercalation (insertion of molecules) between base pairs, prevent DNA replication
  2. inhibit topoisomerase 2
  3. create Fe-mediated O2 free radicals that damages DNA
  4. alter membrane fluidity and ion transport
21
Q

adverse effects of cytotoxic antibiotics

A
  1. myelosuppression
  2. local toxicity
  3. cardiotoxicity
  4. nausea and vomiting (GI)
22
Q

Anti cancer drugs that are microtuble ihibitors?

A
  1. vinca alkaloids
    - vinblastine
  2. taxanes
    - paclitaxel (-taxels)

CELL CYCLE SPECIFIC

23
Q

MOA of microtubule inhibitors?

A

bind to beta subunit of tubulin, disrupt microtuble functions

viniblastine: bind to polymerising end to prevemt elongation of microtubules
paclitaxel: stabilise microtubule to prevent shortening

24
Q

Adverse effects of microtubule inhibitors?

A
  1. myelosuppression
  2. myaglia
  3. peripheral neuropathy
  4. bradycardia
  5. hypersensitivity
25
Anti cancer drugs that are topoisomerase inhibitors?
topoisomerase 1 inhibitor: irinotecan, topotecan topoisomerase 2 inhibitor: amsacrine, etoposide, teniposide CELL CYCLE NON SPECIFIC
26
MOA of topoisomerase inhibitors
inhibit topoisomerase, interfere with DNA transcription and replication
27
Adverse effects of topoisomerase inhibitors?
1. myelosuppresion 2. nausea and vomitting (GI) 3. alopecia
28
Reasons for resistance to topoisomerase inhibitors?
1. site of tumour, drug does not cross bbb 2. size of tumour 3. bypass pathways due to mutations of tumours
29
tyrosine kinase inhibitor: imatinib
competes with ATP for BCR-ABL, preventing signalling for growth used in Philadelphia Chromosone Positive Chronic Myelogenous Leukemia
30
Immunotherapy: antibodies MOA
1. opsonisation and phagocytosis (IgG) 2. neutralisation (IgG and IgA) 3. ADCC (IgG) 4. Complement activation (IgM and IgG) 5. Histamine release (IgE) 6. Agglutination (IgM and IgG) 7. antibody drug conjugates
31
Avastin (neutralising antibody)
binds to VEGF, prevents angiogenesis, tumour cell no oxygen and nutrients, cell death
32
Brentuximab (antibody-drug conjugate MOA)
Ab brings cancer drug to site of cancer cells, antibody-drug conjugate internalised into cancer cell, conjugate linkage cleaved inside cancer cell, drug takes effect - brentuximab recognises CD30 on tumour cells linked with a mitotic inhibitor, once conjugate linkage cleaved in the cell, brentuximab takes effect
33
molecular-targeted radiotherapy (antibody-drug conjugate MOA)
- antibody conjugated with radiotherapy drug - conjugate does not get internalised, but attach to cancer cell membrane - radiotherapy can affect adjacent non-cancer cells
34
CAR T cells immunotherapy
- chimeric antigen receptor - synthesis T cell receptors specific to tumour antigen CD19 on APC
35
structure of CAR T cells
extracellular: receptor that recognises cd19 (tumour specific antigen) intracellular: costimulatory signals (CD28) - newer gen of CAR T cell has more than one costimulatory signal - has a transmembrane domain: CD3ζ -> signalling for T cell proliferation - stronger activation for T cells
36
process to make CAR T cell
1. extract T cells from patient 2. insert gene encoding for CAR into T cell 3. proliferate T cells in vitro 4. precondition patient by lowering WBC to accept incoming T cells 5. insert modified T cell into patient
37
ipilimumab ( yervoy, immune checkpoint inhibitor for CTLA-4)
bind to CTLA-4, preventing it from binding to B7, allowing CD28 to continue to bind to B7, costimulatory signals, activate T cells to fight cancer cells moa:neutralising antibody
38
Nivolumab and Pembrolizumab ( immune checkpoint inhibitor for PD-L1)
bind to PD-L1 on cancer cell, preventing it from binding to PD-1 on T cell
39
chemotherapy
target highly proliferating cells
40
Adverse effects of chemo
1. nausea vomiting 2. myelosuppresion 3. alopecia 4. peripheral neuropathy LONGTERM 1. cardiotoxicity 2. pulmonary toxicity 3, nephrotoxicity 4. neurotoxicity 5. secondary malignancy due to dna damage and genomic instability
41
approaches to receptor targeted therapy
1. blocking antibodies 2. soluble receptors 3. inhibitors of receptor kinases or chaperone proteins 4. inhibit downstream signalling pathways 5. epigenetic modulators

MORE General pharm (4 decks)

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