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Anti-Cancer Drugs 2 Flashcards

1
Q

Where does the production of androgen occur in males?

A

testes

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2
Q

what are our drugs to treat prostate cancer?

A

Leuprolide/Goserelin

Degareliz

Flutamide

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3
Q

Leuprolide/goserelin

MOA

Side effects

A

Leuprolide/goserelin

  1. MOA: GnRH agonists. An initial surge in LH increases testosterone production causing a downregulation of GnRH receptors and a decline in pituitary response (a negative feedback). after 3-4 weeks the decrease in serum LH leads to decreased testosterone production
  2. SE:
    1. bone pain, urinary obstruction
    2. Androgen deprivation effects
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4
Q

degarelix

MOA

Side Effects

A

Degarelix

  1. MOA: suppress testosterone (GnRH antagonist)
  2. SE:
    1. Androgen deprivation effects: decreased libido; ED
    2. gynecomastia
    3. Hot flashes
    4. decreased muscle mass and strength
    5. hyperglycemia

** androgen deprivation effects basically turn you into a golden girl

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5
Q

Flutamide

MOA

Side Effects

A

Flutamide

  1. MOA: antagonist of the androgen receptor
    1. binds to androgen receptor and competitively inhibits the binding of testosterone and DHT
    2. normal testosterone level
  2. SE:
    1. gynecomastia
    2. Hepatic Failure
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6
Q

Targetet Therapy

BRC-ABL inhibitor

A

imatinib

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7
Q

Targeted Therapy

mTOR inhibitors

A

Rapamycin

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8
Q

Targeted Therapy

BRAF inhibitor

A

Vemurafenib

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9
Q

Targeted Therapy

HER2 inhibitor

A

Trastuzumab

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10
Q

Targeted Therapy

EGFR inhibitor

A

Erlotinib

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11
Q

Targeted Therapy

VEGF inhibitor

A

Bevacizumab

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12
Q

Targeted Therapy

multi-kinase inhibitor

A

Crizotinib

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13
Q

Imatinib

MOA

Side Effects

A

Imatinib- CML that have the t(9;22) chromosome

  1. MOA: competitively binds ATP binding site and inhibits tyrosine phosporylation of BCR-ABL kinase
  2. Side effects:
    1. N/V/D
    2. fluid retention/edema
    3. cardiovascular toxicity
    4. myalgias
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14
Q

Rapamycin (sirolimus) and Everolimus

MOA

Clinical Use

A

Rapamycin (sirolimus) and Everolimus

  1. MOA:
    1. mTOR inhibitor
      1. PI3K/AKT pathway is inhibited
  2. CU:
    1. prevention of rejection after transplant
      1. Everolimus is used in renal, breast, and GI cancers
        2.
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15
Q

Rituximab

MOA

CU

SE

A

Rituximab

  1. MOA:
    1. antibody against CD20
  2. CU:
    1. CD20 (+) B cell NHL, CLL
    2. immune diseases- RA, ITP, Wegener’s granulomatosis
  3. SE:
    1. anemia
    2. hypotension
    3. GI disturbances
    4. skin reactions
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16
Q

Bortezomib

MOA

CU

SE

A

Bortezomib

  1. MOA: reversible binding to the proteasome causing inhibition. This inhibits NF-kB signalling pathways
  2. CU: multiple myeloma
  3. SE: BM suppression
17
Q

Vorinostat

MOA

CU

SE

A

Vorinostat

  1. MOA: HDAC inhibitor (HDACs catalyze the removal of acetyl groups on lysine residue histones)
  2. CU: Cutaneous T-Cell lymphoma
    1. NHL lymphoma that affects skin
    2. raised, rash-like, itchy patches of skin, lumps and enlarged lymphnodes
    3. SE none listed
18
Q

Aldesleukin

MOA

CU

SE

A

Aldesleukin

  1. MOA:
    1. aldesleukin is recombinant human IL-2. This is produced by activated T-cells which acts to promote T-cell proliferation and enhances tumor killing by T-cells and NK cells
  2. CU: renal cell cancer
  3. SE: capillary leak syndrome
19
Q

L-Asparaginase

MOA

CU

SE

A

L-Asparaginase

  1. MOA:
    1. L-Asparginase catalyzes L-Asparagine to L-Aspartate and ammonia. Cancer cells require exogenous L-asparagine for growth, so this drug prevents protein synthesis because the cell does not have access to L-asparagine
  2. CU: childhood ALL
  3. hypersenitivity rxn
20
Q

ATRA (all-trans-retinoic acid)

MOA
CU

SE

A

ATRA

  1. MOA: binds to nuclear receptors and regulates gene transcription
    1. decreases proliferation and induces differentiation and maturation of promyelocytes
  2. CU: APL- often combined with an anthracycline (“-rubicin)
  3. SE:
    1. Black Box
      1. cytokine release syndrome- fever, pulmonary opacities, hypoxemia, respiratory distress, hypotension, etc
      2. leukocytosis- WBC increase
    2. teratogen
    3. CV/CNS/Liver toxicity
21
Q

EPO

MOA

CU

SE

A

EPO

erythropoietin is produced by the kidney and stimulates erythroid proliferation and differentiation

  1. CU: anemia
  2. SE: hypertension and thrombotic complications
22
Q

filgrastim

MOA

CU

A

Filgrastim

  1. Recombinant human G-CSF
    1. stimulates neutrophil progenitors
  2. CU: Neutropenia caused by chemotherapy
23
Q

Sargramostim (GM-CSF)

MOA

CU

A

Sargramostim

recombinant human GM-CSF has a broader biological action than G-CSF. It stimulates granulocytic, erythroid, and megakaryocyte progenitors

Clinical Use: Neutropenic caused by chemotherapy, AML

*remember that megakaryocytes produce platelets

24
Q

Oprelvekin

Clinical Use

A

Oprelvekin (IL-11) is a thrombopoietic GF that stimulates megakaryocyte progenitors and increases platelets

25
Q

Romiplostim and eltrombopag

MOA

CU

A

Romiplostim and eltrombopag

TPO receptor agonists that increase platelets

used in chronic immune thrombocytopenia

GU (5 decks)

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