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Chemotherapy Drugs > Chemotherapy Drugs > Flashcards

Chemotherapy Drugs Flashcards

1
Q

Mechlorethamine:

  • Class
  • Mechanism
  • Cell Cycle Profile
  • Therapeutic Uses
  • Special details (about it’s metabolism and administration)
A
  • Alkylating Agent
  • Cross links DNA to block replication and txn
  • CCNS
  • Hodgkin’s Lymphoma (MOPP)
  • This drug is not excreted, and must be given IV
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2
Q

Cyclophosphamide:

  • Class
  • Mechanism
  • what is the exact binding site?
  • Cell Cycle Profile
  • How does this drug become activated?
  • Toxicity
  • What drug is administered to manage toxicity??? How does this drug work?
  • Uses
A
  • Alkylating Agent
  • Cross links DNA to block replication and txn, *binds Guanine N-7
  • CCNS
  • The liver activates Cyclophosphamide and iphosphamide using a cytochrome P450; this oxidative activation cleaves off Acrolein, opening the molecule for DNA binding.
  • Hemorrhagic cystitis, SIADH
  • MESNA, it binds to Acrolein
  • Burkitt’s lymphoma, acute lymphocytic leukemia, autoimmune diseases
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3
Q

Chlorambucil:

  • Class
  • Mechanism
  • Cell Cycle Profile
  • Toxicity
  • Uses
A
  • Alkylating Agent
  • Cross links DNA to block replication and txn, *binds Guanine N-7
  • CCNS
  • Hepatotoxicity
  • chronic lymphocytic leukemia
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4
Q

Estramustine Phosphate:

  • This drug is a mustard + ___ (look at the name).
  • Mechanism
  • what about the mechanism sets this drug apart from others in its class?
  • Cell Cycle Profile
  • Route of administration and activation
  • when is this drug used?
A
  • estradiol
  • binds to beta tubulin
  • works as an anti mitotic rather than alkylating agent
  • CCNS: M
  • given orally, phosphate cleaved during absorption
  • used as palliative treatment in metastatic or progressive prostate cancer
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5
Q

Busulfan:

  • Class (not a nitrogen mustard)
  • Cell Cycle Profile
  • Toxicity
  • Use, what’s the drawback?
A
  • bis-methyl sulfonate
  • CCNS
  • pulmonary fibrosis and hyper pigmentation of the skin
  • CML, only extends life by ~9 months
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6
Q

Carmustine (BCNU), Lomustine (CCNU), Semustine (methyl-CCNU)

  • Class
  • Cell Cycle Profile
  • Toxicity
  • What’s so special about these drugs that makes them first line treatment for brain tumors???
  • what’s released when these drugs are broken down?
A
  • Nitrosoureas
  • CCNS
  • pulmonary fibrosis and nephrotoxicity
  • they’re highly lipophilic
  • breakdown in vivo liberates alkylating and carbamylating species
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7
Q

Procarbazine (Mulatane, MOPP):

  • Class
  • Cell Cycle Profile
  • mechanism
  • Special Details (hint: this is an MAO inhibitor)
A
  • Nitrosourea
  • CCNS
  • react covalently with nucleic acids, decreasing DNA, RNA, protein synthesis, and inhibiting G1 to S transition
  • avoid use with MAOIs and alcohol
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8
Q

Dacarbazine (DTIC), Temozolomide (T):

  • Class
  • Mechanism
  • Cell Cycle Profile
A
  • Nitrosourea
  • methylates DNA and RNA
  • CCNS
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9
Q

Cisplatin:

  • Class
  • Mechanism
  • Cell Cycle Profile
  • Toxicity
  • *What drug can you give to control this toxicity?
  • Which drugs should you never prescribe with a platin?
  • name two drugs of the same class that are less toxic
A
  • Platinum-containing drug
  • Binds to guanine, forming intrastrand crosslinks
  • CCNS
  • nephrotoxicity and ototoxicity, peripheral neuropathy
  • *furosemide, causes forced diuresis and improves renal clearance, also prevent with amifostine and chloride diuresis
  • Aminoglycosides
  • Oxaliplatin, Carboplatin
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10
Q

Doxorubicin:

  • class
  • which enzyme
  • mechanism
  • cell cycle profile
  • toxicity
  • *which drug controls this toxicity
  • uses
  • name one other drug with a similar mechanism, but is less cardiotoxic
A
  • anthracycline
  • topoisomerase ii
  • intercalates DNA, causes single and double stranded breaks, inhibits repair, *histone eviction
  • CCNS
  • cardiotoxicity
  • *controlled with dexrazoxane
  • breast cancer, sarcoma, MOPP-resistant Hodgkin’s (Anthracyline-BVD)
  • Epirubicin
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11
Q

Daunorubicin:

  • class
  • which enzyme
  • mechanism
  • cell cycle profile
  • toxicity
  • name one other drug with a similar mechanism, but is less cardiotoxic
A
  • anthracycline
  • topoisomerase ii
  • intercalates DNA, causes single and double stranded breaks, inhibits repair, *histone eviction
  • CCNS
  • cardiotoxicity
  • Idarubicin
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12
Q

Mitoxantrone:

  • which enzyme
  • mechanism
  • how is this drug’s mechanism different from Doxorubicin
  • cell cycle profile
  • toxicity
A
  • topoisomerase ii
  • intercalates DNA, causes single and double stranded breaks, inhibits repair, histone eviction
  • does NOT form free radicals
  • CCNS
  • cardiotoxicity, lower than doxo or daunorubicin
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13
Q

Epipodophyllotoxins (Etoposide + Tenopside):

  • which enzyme
  • mechanism
  • cell cycle profile
  • therapeutic uses
A
  • topoisomerase ii
  • forms ternary complex, prevents re-ligation of DNA strands
  • CCS: S and G2
  • testicular, small cell lung cancer
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14
Q

Camptothecin, Topotecan, Irinotecan:

  • class
  • which enzyme
  • mechanism
  • cell cycle profile
  • toxicity
A
  • camptothecin analogs
  • topoisomerase i
  • forms ternary complex
  • CCS: S
  • severe diarrhea
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15
Q

Bleomycins:

  • drug class
  • mechanism
  • cell cycle profile
  • toxicity
  • therapeutic uses
A
  • antibiotic
  • bind reduced iron in cells and cause free radical production
  • CCS: G2
  • pulmonary fibrosis, minor myelosuppression, cutaneous reactions, low grade fever
  • advanced testicular carcinoma
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16
Q

Dactinomycin:

  • drug class
  • mechanism
  • cell cycle profile
  • toxicity
  • therapeutic uses
A
  • antibiotic
  • intercalate DNA, prevent transcription, single strand DNA breaks
  • CCNS
  • oral and GI ulceration, stomatitis
  • methotrexate resistant choriocarcinoma, Wilm’s tumor, Rhabdomyosarcoma, Ewing’s sarcoma, gestational trophoblastic malignancy
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17
Q

Streptozocin

  • class
  • primary use
  • toxicity
A
  • nitrosoureas, this one was listed with carmustine and lomustine for some reason
  • pancreatic cancer
  • pulmonary fibrosis and nephrotoxicity
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18
Q

Methotrexate

  • Class
  • Mechanism
  • Cell cycle profile
  • Toxicity
  • what drug is administered with MTX and why?
A
  • folic acid analog
  • inhibits dihydrofolate reductase, blocks synthesis of thymidylate and purines
  • CCS: S
  • mucositis: oral and GI ulceration, hepatotoxicity, pulmonary toxicity
  • Leucovorin, doesn’t need DHF reductase to become active THF, saves the body from myelosuppression
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19
Q

5-Fluorouracil

  • Class
  • Mechanism
  • Cell cycle profile
  • Toxicity
A
  • pyrimidine analog
  • inhibits thymidylate synthase, incorporates into DNA and RNA
  • CCNS; G1, S
  • oral and GI ulceration
20
Q

Cytarabine, Cytosar

  • Class
  • Mechanism
  • Cell cycle profile
  • Toxicity
A
  • pyrimidine analog
  • inhibit DNA pol alpha, incorporate into DNA
  • CCS: S
  • oral ulceration
21
Q

Gemcitabine

  • Class
  • Mechanism
  • Cell cycle profile
A
  • pyrimidine analog
  • inhibits DNA synthesis with many mechanisms
  • CCNS
22
Q

Mercaptopurine

  • Class
  • Mechanism
  • Cell cycle profile
  • Toxicity
  • Which drug inhibits the activity of mercaptopurine?
A
  • purine analog
  • inhibits synthesis of adenine and guanine by blocking conversion of insinuate to purine precursors
  • CCS: S
  • cholestasis, oral and intestinal ulcers
  • allopurinol
23
Q

Cladribine, Fludarabine

  • Class
  • Mechanism
  • Use
A
  • ADA inhibitor
  • blocks conversion of adenosine to inosine, buildup of dATP leads to cellular toxicity, no DNA synthesis
  • hairy cell leukemia
24
Q

Vincristine, Vinblastine, vinorelbine

  • Class
  • Mechanism
  • Cell cycle profile
  • Toxicity
A
  • Vinca Alkaloid
  • binds to soluble tubulin, inhibits assembly of mitotic spindle during metaphase of mitosis
  • CCS: M
  • peripheral neuropathy, alopecia, nephrogenic SIADH secretion, myelosuppression
25
Q

Paclitaxel (taxol), Docetaxel

  • Class
  • Mechanism
  • Cell cycle profile
  • Toxicity
A
  • Yew alkaloid
  • binds to polymerized microtubule and prevents depolymerization
  • CCS: M
  • peripheral neuropathy (dose limiting)
26
Q

IFN-alpha

  • Class (really obvious)
  • Mechanism
  • Cell cycle profile
A
  • cytokine (duh.)
  • inhibits tumor growth via host immune system, has some direct activity
  • CCNS, slows the progression through the cell cycle
27
Q

Prednisone:

  • Class
  • Mechanism
  • Therapeutic uses
A
  • hormone
  • anti-inflammatory, causes apoptosis in leukemic cells
  • Hodgkin’s lymphoma (MOPP), acute leukemias, relapsed hairy cell lymphoma
28
Q

synthetic progesterone and it’s derivatives

  • Class
  • Mechanism
  • uses
A
  • progestin
  • used in hormone responsive cancers expressing progesterone receptor, blocks progesterone from binding and ceases growth
  • post surgical endometrial carcinoma and metastatic renal cancer
29
Q

Tamoxifen, toremifine

  • Class
  • Therapuetic use (hint: they’re hormonal)
  • which is not a steroid?
A
  • anti-estrogens
  • used in estrogen receptor positive breast and lung cancer
  • tamoxifen is not a steroid
30
Q

Casodex, eulixin, nilandron

  • Class
  • Mechanism
  • what do you combine them with for total ablation?
A
  • anti-androgens
  • prevent tes and dihydrotes from binding to the cancer cell
  • leuprolide, which is an LHRH agonist and keeps LH from being released, thereby decrease tes production
31
Q

Bevuczimab (avastin)

  • Class
  • Mechanism
A
  • antibody

- blocks VEGF-R and prevents angiogenesis

32
Q

Denusomab

  • Class
  • Mechanism
A
  • antibody

- blocks RANK/RANKL in bone (think dense-usomab)

33
Q

Trastuzumab

  • Class
  • Mechanism
A
  • antibody

- blocks HER-2 positive breast and gastric cancers

34
Q

Imatinib (Gleevac)

  • Class
  • Mechanism
  • Therapeutic uses
A
  • targeted inhibitor
  • blocks the BCR-ABL kinase protein resulting from the Philadelphia chromosome
  • CML
35
Q

Erlotinib, Gefitinib

  • Class
  • Mechanism
A
  • targeted inhibitor

- blocks EGFR signaling

36
Q

Crizotinib

  • Class
  • Mechanism
  • Therapeutic uses
A
  • targeted inhibitor
  • blocks ALK-1 kinase
  • non small cell lung cancer (10% of pts are positive for ALK-1)
37
Q

Venetoclax

  • Class
  • Mechanism
  • Therapeutic uses
A
  • anti-apoptotic inhibitor
  • binds Bcl-2 and
  • refractory chronic lymphocytic leukemia
38
Q

Vorinostat, Romidepsin

  • Class
  • Mechanism
A
  • epigenetic signaling

- histone deacetylase (HDAC) inhibition (keeps the chromatin in tight conformation)

39
Q

OLAPARIB

  • Class (which process within the cell does it target?)
  • Mechanism
A
  • target DNA repair

- PARP-1 inhibitor

40
Q

Amirubicin

  • Class
  • Advantage
A
  • anthracylin (like doxorubicin)

- reduced cardiotoxicity

41
Q

Fulvestrant

  • Class
  • Advantage
A
  • estrogen receptor blocker

- lacks partial receptor activity, useful for estrogen responsive cancers

42
Q

Abraxane

  • Class
  • Advantage
A
  • IV nanoparticle, paclitaxel bounds to albumin

- cremophor-free (cremephor is a previously used vehicle known to cause anaphylaxis)

43
Q

Picoplatin

  • Class
  • Advantage
A
  • platinum containing

- doesn’t cause platinum resistance

44
Q
  • Why do cancer cells (and cells in general) take up Melphalan? (what is it about this drug’s structure?
  • Also, how does Melphalan cause cell death?
A
  • Melphalan has a phenylalanine side chain

- Attached to the side chain is a nitrogen mustard, which cross-links (alkylates) guanines at the N-7 position.

45
Q

which drug should be avoided with EtOH?

A

Procarbazine (don’t drink and drive the Pro-car)

46
Q

which drug inhibits ribonucleotide reductase?

A

hydroxyurea

Chemotherapy Drugs (2 decks)

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