Anti-Cancer Drugs 2

Question 1

Where does the production of androgen occur in males?

Answer 1

testes

Question 2

what are our drugs to treat prostate cancer?

Answer 2

Leuprolide/Goserelin

Degareliz

Flutamide

Question 3

Leuprolide/goserelin

MOA

Side effects

Answer 3

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

Question 4

degarelix

MOA

Side Effects

Answer 4

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

Question 5

Flutamide

MOA

Side Effects

Answer 5

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

Question 6

Targetet Therapy

BRC-ABL inhibitor

Answer 6

imatinib

Question 7

Targeted Therapy

mTOR inhibitors

Answer 7

Rapamycin

Question 8

Targeted Therapy

BRAF inhibitor

Answer 8

Vemurafenib

Question 9

Targeted Therapy

HER2 inhibitor

Answer 9

Trastuzumab

Question 10

Targeted Therapy

EGFR inhibitor

Answer 10

Erlotinib

Question 11

Targeted Therapy

VEGF inhibitor

Answer 11

Bevacizumab

Question 12

Targeted Therapy

multi-kinase inhibitor

Answer 12

Crizotinib

Question 13

Imatinib

MOA

Side Effects

Answer 13

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

Question 14

Rapamycin (sirolimus) and Everolimus

MOA

Clinical Use

Answer 14

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.

Question 15

Rituximab

MOA

CU

SE

Answer 15

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

Question 16

Bortezomib

MOA

CU

SE

Answer 16

Bortezomib

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

Question 17

Vorinostat

MOA

CU

SE

Answer 17

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

Question 18

Aldesleukin

MOA

CU

SE

Answer 18

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

Question 19

L-Asparaginase

MOA

CU

SE

Answer 19

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

Question 20

ATRA (all-trans-retinoic acid)

MOA
CU

SE

Answer 20

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

Question 21

EPO

MOA

CU

SE

Answer 21

EPO

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

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

Question 22

filgrastim

MOA

CU

Answer 22

Filgrastim

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

Question 23

Sargramostim (GM-CSF)

MOA

CU

Answer 23

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

Question 24

Oprelvekin

Clinical Use

Answer 24

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

Question 25

Romiplostim and eltrombopag MOA CU

Answer 25

Romiplostim and eltrombopag TPO receptor agonists that increase platelets used in chronic immune thrombocytopenia