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Pharm 2015 > Antineoplastic Agents > Flashcards

Antineoplastic Agents Flashcards

1
Q

Antimetabolites

A

= *Structural Analogs of Nucleosides of their Precursors
(Except Hydroxyurea)

  • Function Either By:
    (1) Inhibiting Enzymes that MAKE Nucleosides

(2) Incorporation INTO Nucleic Acids
(Inhibition of DNA and RNA Synthesis;
Disruption of RNA Synthesis/ Processing/ Function)

*Cell-Cycle Specific:
=> *Primarily Function @ G1 and/or S Phase of Cell Cycle

(G1 = preparing building blocks for DNA synthesis)

Resistance:
*Are NOT Substrates for the MDR Mechanism generally

Major Classes:

1) Folate Analogs:
_*Methotrexate (MTX)

2) Pyrimidine Analogs:
_5-Fluorouracil
_Cytosine Arabinoside

3) Purine Analogs:
_6-Mercaptopurine
_6Thioguanine

4) “Other”: *Hydroxyurea
_Inhibits Ribonucleotide Reductase
_Generally only used in Combination or as a Radiation Sensitizer.

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2
Q

*Methotrexate (MTX)

A

Folate Antimetabolites

1) *Mechanism of Action:
= *Inhibits Dihydrofolate Reductase

2) *Inhibiting Purine, Pyrimidine, and Amino Acid Synthesis
3) *Polyglutamylated form is the *More Active Metabolite.

4) *Selectivity:
=> Formation and *Retention of Polyglutamate Derivatives in Tumor Cells

5) Uses:
(i) *Acute Leukemias (extremely effective)
(ii) *Choriocarcinomas
(Both of these are very rapidly dividing cancer, hence why the drug is very effective.)

6) Toxicity:
(i) *Myelosuppression
=> *Can be Reduced with *Leucovorin (Folinic Acid) “Rescue”

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3
Q

*5-Fluorouracil (5-FU)

A

Pyrimidine Antimetabolite

Mechanism:
(1) *Inhibits Thymidylate Synthetase (TS)
(when converted to 5-FdUMP)

(2) *Incorporates into DNA and RNA
(when converted to FdUTP and FUTP)

*Leucovorin Enhances Activity by promoting binding.

Uses:

(1) *Solid Tumors: *GI, *Mainly *Colon; Breast
(2) *Topical: *Skin Warts and *Skin Lesions

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4
Q

Cytosine Arabinoside (Ara-C)

A

Pyrimidine Antimetabolite

Mechanism:
1) *Incorporates into DNA via *Competition with *dCTP
(Deoxycytidine)

2) *Inhibits DNA Synthesis

Use: *Potent Anti-Leukemic
(e.g. AML: Acute Myeloblastic Leukemia)

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5
Q

6-Mercaptopurine

A

Purine Antimetabolite

Mechanism: *Inhibits DNA and Purine Synthesis

Uses:

1) Leukemias
2) Lymphomas

Toxicity:

1) *Pancreatitis
2) *Hepatic Dysfunction

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6
Q

6-Thioguanine

A

Purine Antimetabolite

Mechanism: *Inhibits DNA and Purine Synthesis

Uses:

1) Leukemias
2) Lymphomas

Toxicity:

1) *Pancreatitis
2) *Hepatic Dysfunction

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7
Q

Hydroxyurea

A

Analog of Urea

Mechanism:
1) *Inhibits Ribonucleotide Reductase
(enzyme for conversion of ribonucleotides to deoxyribonucleotides)

2) *Inhibits DNA Synthesis

Uses:

1) Radiation Sensitization
2) Leukemias

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8
Q

Cyclophosphamide

A

Alkylating Agents:
_Not Cell-cycle Specific
_Not Substrates for MDR Pump

1) Mustards: Nitrogen Mustards:
(i) **Cyclophosphamide
(ii) *Melphalan
(iii) *Chlorambucil

2) Nitrosureas:
(i) *Carmustine (BCNU)
(ii) *Lomustine (CCNU)
(iii) Streptozotocin

3) Triazenes: *Temozolomide

________________________

Nitrogen and Sulfur Mustards:
=> Related to Mustard Gas.

**Nitrogen Mustards contain a *BischloroethylAMINE Group

(Sulfur mustards contain a bischloroethylsulfide group)

Mustards: Nitrogen Mustards:

(i) **Cyclophosphamide
(ii) *Melphalan
(iii) *Chlorambucil

Mechanism:

1) *Alkylates DNA (Cross-links DNA)
2) Inhibits DNA Synthesis

Resistance:
1) *Increased GSH/GSH Metabolic Enzymes
(GSH = Glutathione)

2) Increased Alkyltransferase Repair

Uses:
1) *CNS Tumors (*Nitrosureas)
2) Varies by Drug 
(lymphomas, leukemias, 
solid: breast, lung, ovarian)
Toxicity:
1) *Myelosuppression
2) *Secondary Neoplasias
3) *Hemorrhagic Cystitis
(cyclophosphamide metabolite; contains tear gas)

________________________

Nitrosureas

**Cross the BBB: **Used for Primary Brain Tumors!!

Nitrosureas:

1) *Carmustine (BCNU)
2) *Lomustine (CCNU)

3) Streptozotocin:
_Sugar group confers High Affinity for Pancreas.
=> *Tumors @ Islets of Langerhans (Pancreas)

________________________

Triazenes: *Temozolomide

Crosses BBB.

Uses:
_Gliomas

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9
Q

Carmustine (BCNU)

A

Alkylating Agents:
_Not Cell-cycle Specific
_Not Substrates for MDR Pump

1) Mustards: Nitrogen Mustards:
(i) **Cyclophosphamide
(ii) *Melphalan
(iii) *Chlorambucil

2) Nitrosureas:
(i) *Carmustine (BCNU)
(ii) *Lomustine (CCNU)
(iii) Streptozotocin

3) Triazenes: *Temozolomide

________________________

Nitrogen and Sulfur Mustards:
=> Related to Mustard Gas.

**Nitrogen Mustards contain a *BischloroethylAMINE Group

(Sulfur mustards contain a bischloroethylsulfide group)

Mustards: Nitrogen Mustards:

(i) **Cyclophosphamide
(ii) *Melphalan
(iii) *Chlorambucil

Mechanism:

1) *Alkylates DNA (Cross-links DNA)
2) Inhibits DNA Synthesis

Resistance:
1) *Increased GSH/GSH Metabolic Enzymes
(GSH = Glutathione)

2) Increased Alkyltransferase Repair

Uses:
1) *CNS Tumors (*Nitrosureas)
2) Varies by Drug 
(lymphomas, leukemias, 
solid: breast, lung, ovarian)
Toxicity:
1) *Myelosuppression
2) *Secondary Neoplasias
3) *Hemorrhagic Cystitis
(cyclophosphamide metabolite; contains tear gas)

________________________

Nitrosureas

**Cross the BBB: **Used for Primary Brain Tumors!!

Nitrosureas:

1) *Carmustine (BCNU)
2) *Lomustine (CCNU)

3) Streptozotocin:
_Sugar group confers High Affinity for Pancreas.
=> *Tumors @ Islets of Langerhans (Pancreas)

________________________

Triazenes: *Temozolomide

Crosses BBB.

Uses:
_Gliomas

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10
Q

Lomustine (CCNU)

A

Alkylating Agents:
_Not Cell-cycle Specific
_Not Substrates for MDR Pump

1) Mustards: Nitrogen Mustards:
(i) **Cyclophosphamide
(ii) *Melphalan
(iii) *Chlorambucil

2) Nitrosureas:
(i) *Carmustine (BCNU)
(ii) *Lomustine (CCNU)
(iii) Streptozotocin

3) Triazenes: *Temozolomide

________________________

Nitrogen and Sulfur Mustards:
=> Related to Mustard Gas.

**Nitrogen Mustards contain a *BischloroethylAMINE Group

(Sulfur mustards contain a bischloroethylsulfide group)

Mustards: Nitrogen Mustards:

(i) **Cyclophosphamide
(ii) *Melphalan
(iii) *Chlorambucil

Mechanism:

1) *Alkylates DNA (Cross-links DNA)
2) Inhibits DNA Synthesis

Resistance:
1) *Increased GSH/GSH Metabolic Enzymes
(GSH = Glutathione)

2) Increased Alkyltransferase Repair

Uses:
1) *CNS Tumors (*Nitrosureas)
2) Varies by Drug 
(lymphomas, leukemias, 
solid: breast, lung, ovarian)
Toxicity:
1) *Myelosuppression
2) *Secondary Neoplasias
3) *Hemorrhagic Cystitis
(cyclophosphamide metabolite; contains tear gas)

________________________

Nitrosureas

**Cross the BBB: **Used for Primary Brain Tumors!!

Nitrosureas:

1) *Carmustine (BCNU)
2) *Lomustine (CCNU)

3) Streptozotocin:
_Sugar group confers High Affinity for Pancreas.
=> *Tumors @ Islets of Langerhans (Pancreas)

________________________

Triazenes: *Temozolomide

Crosses BBB.

Uses:
_Gliomas

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11
Q

Temozolomide

A

Alkylating Agents:
_Not Cell-cycle Specific
_Not Substrates for MDR Pump

1) Mustards: Nitrogen Mustards:
(i) **Cyclophosphamide
(ii) *Melphalan
(iii) *Chlorambucil

2) Nitrosureas:
(i) *Carmustine (BCNU)
(ii) *Lomustine (CCNU)
(iii) Streptozotocin

3) Triazenes: *Temozolomide

________________________

Nitrogen and Sulfur Mustards:
=> Related to Mustard Gas.

**Nitrogen Mustards contain a *BischloroethylAMINE Group

(Sulfur mustards contain a bischloroethylsulfide group)

Mustards: Nitrogen Mustards:

(i) **Cyclophosphamide
(ii) *Melphalan
(iii) *Chlorambucil

Mechanism:

1) *Alkylates DNA (Cross-links DNA)
2) Inhibits DNA Synthesis

Resistance:
1) *Increased GSH/GSH Metabolic Enzymes
(GSH = Glutathione)

2) Increased Alkyltransferase Repair

Uses:
1) *CNS Tumors (*Nitrosureas)
2) Varies by Drug 
(lymphomas, leukemias, 
solid: breast, lung, ovarian)
Toxicity:
1) *Myelosuppression
2) *Secondary Neoplasias
3) *Hemorrhagic Cystitis
(cyclophosphamide metabolite; contains tear gas)

________________________

Nitrosureas

**Cross the BBB: **Used for Primary Brain Tumors!!

Nitrosureas:

1) *Carmustine (BCNU)
2) *Lomustine (CCNU)

3) Streptozotocin:
_Sugar group confers High Affinity for Pancreas.
=> *Tumors @ Islets of Langerhans (Pancreas)

________________________

Triazenes: *Temozolomide

Crosses BBB.

Uses:
_Gliomas

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12
Q

Streptozotocin

A

Alkylating Agents:
_Not Cell-cycle Specific
_Not Substrates for MDR Pump

1) Mustards: Nitrogen Mustards:
(i) **Cyclophosphamide
(ii) *Melphalan
(iii) *Chlorambucil

2) Nitrosureas:
(i) *Carmustine (BCNU)
(ii) *Lomustine (CCNU)
(iii) Streptozotocin

3) Triazenes: *Temozolomide

________________________

Nitrogen and Sulfur Mustards:
=> Related to Mustard Gas.

**Nitrogen Mustards contain a *BischloroethylAMINE Group

(Sulfur mustards contain a bischloroethylsulfide group)

Mustards: Nitrogen Mustards:

(i) **Cyclophosphamide
(ii) *Melphalan
(iii) *Chlorambucil

Mechanism:

1) *Alkylates DNA (Cross-links DNA)
2) Inhibits DNA Synthesis

Resistance:
1) *Increased GSH/GSH Metabolic Enzymes
(GSH = Glutathione)

2) Increased Alkyltransferase Repair

Uses:
1) *CNS Tumors (*Nitrosureas)
2) Varies by Drug 
(lymphomas, leukemias, 
solid: breast, lung, ovarian)
Toxicity:
1) *Myelosuppression
2) *Secondary Neoplasias
3) *Hemorrhagic Cystitis
(cyclophosphamide metabolite; contains tear gas)

________________________

Nitrosureas

**Cross the BBB: **Used for Primary Brain Tumors!!

Nitrosureas:

1) *Carmustine (BCNU)
2) *Lomustine (CCNU)

3) Streptozotocin:
_Sugar group confers High Affinity for Pancreas.
=> *Tumors @ Islets of Langerhans (Pancreas)

________________________

Triazenes: *Temozolomide

Crosses BBB.

Uses:
_Gliomas

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13
Q

Cisplatin

A

Platinum Compounds

Alkylating-Like Agents

1) **Cisplatin
2) *Oxaliplatin

  • Not Cell-cycle Specific
  • Not Substrates MDR Pump

Mechanism:
1) *Form Intra-strand and Inter-strand DNA Cross-Links
=> Results in DNA Breaks
2) *Inhibits DNA Synthesis

(Only Cis form is active; trans platinum is inactive.)

(Activated when in contact with water.

(Was accidentally discovered to block bacterial cell division.)

Resistance:

1) *Increased GSH/GSH-Metabolic Enzymes
2) *Increased DNA Repair

Uses: *Solid Tumors:
1) *Testicular Cancers

Toxicity:

1) *Nephrotoxicity
2) *Ototoxicity

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14
Q

Oxaliplatin

A

Platinum Compounds

Alkylating-Like Agents

1) **Cisplatin
2) *Oxaliplatin

  • Not Cell-cycle Specific
  • Not Substrates MDR Pump

Mechanism:
1) *Form Intra-strand and Inter-strand DNA Cross-Links
=> Results in DNA Breaks
2) *Inhibits DNA Synthesis

(Only Cis form is active; trans platinum is inactive.)

(Activated when in contact with water.

(Was accidentally discovered to block bacterial cell division.)

Resistance:

1) *Increased GSH/GSH-Metabolic Enzymes
2) *Increased DNA Repair

Uses: *Solid Tumors:
1) *Testicular Cancers

Toxicity:

1) *Nephrotoxicity
2) *Ototoxicity

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15
Q

Mitoxantrone

A

DNA-Interacting Antibiotics

(Multi-ring Anthracyclines)

*Not Cell-cycle Specific.
_But G phases (Growth) is More Susceptible.

Rubicins:

(i) *Doxorubicin
(ii) *Daunorubicin

Mechanism:
1) *Intercalate into DNA
(Disrupts DNA and RNA synthesis)

2) *Topoisomerase II Inhibition
(Due to distortion of double-helix: DNA strand breaks and DNA-protein cross-links)

3) *Generate ROS

Resistance:
=> *Are Substrates for MDR Pump!
(Due to planar structure)

Toxicity:  (Ruby Red Cardiotox!)
*Cardiotoxicity:
1) *Acute: Arrhythmias
2) *Chronic: CHF
(b/c Heart is a major producer of ROS anyway)

____________________

*Mitoxantrone:
_Similar Structure and Mechanism to Anthracyclines

_However, *Reduced Cardiotoxicity!!

=> Due to *Reduced ROS Formation

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16
Q

Doxorubicin

A

DNA-Interacting Antibiotics

(Multi-ring Anthracyclines)

*Not Cell-cycle Specific.
_But G phases (Growth) is More Susceptible.

Rubicins:

(i) *Doxorubicin
(ii) *Daunorubicin

Mechanism:
1) *Intercalate into DNA
(Disrupts DNA and RNA synthesis)

2) *Topoisomerase II Inhibition
(Due to distortion of double-helix: DNA strand breaks and DNA-protein cross-links)

3) *Generate ROS

Resistance:
=> *Are Substrates for MDR Pump!
(Due to planar structure)

Toxicity:  (Ruby Red Cardiotox!)
*Cardiotoxicity:
1) *Acute: Arrhythmias
2) *Chronic: CHF
(b/c Heart is a major producer of ROS anyway)

____________________

*Mitoxantrone:
_Similar Structure and Mechanism to Anthracyclines

_However, *Reduced Cardiotoxicity!!

=> Due to *Reduced ROS Formation

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17
Q

Daunorubicin

A

DNA-Interacting Antibiotics

(Multi-ring Anthracyclines)

*Not Cell-cycle Specific.
_But G phases (Growth) is More Susceptible.

Rubicins:

(i) *Doxorubicin
(ii) *Daunorubicin

Mechanism:
1) *Intercalate into DNA
(Disrupts DNA and RNA synthesis)

2) *Topoisomerase II Inhibition
(Due to distortion of double-helix: DNA strand breaks and DNA-protein cross-links)

3) *Generate ROS

Resistance:
=> *Are Substrates for MDR Pump!
(Due to planar structure)

Toxicity:  (Ruby Red Cardiotox!)
*Cardiotoxicity:
1) *Acute: Arrhythmias
2) *Chronic: CHF
(b/c Heart is a major producer of ROS anyway)

____________________

*Mitoxantrone:
_Similar Structure and Mechanism to Anthracyclines

_However, *Reduced Cardiotoxicity!!

=> Due to *Reduced ROS Formation

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18
Q

Plant (Natural) Products

A

Microtubule Inhibitors:
(“Spindle Poisons”)

1) Stabilizers: Taxanes:
_Paclitaxel (Taxol)

2) Destabilizers: Vinca Alkaloids:
_Vincristine (Oncovin)
_*Vinblastine (Velban)

Microtubule Inhibitors
(“Spindle Poisons”)
_Active During Mitosis, where they perturb the Mitotic Spindle and Disrupt Proper Chromosome Segregation

____________________

Topoisomerase Inhibitors:

1) Topoisomerase II Inhibitors:
_*Epipodophyllotoxins:
(i) *Etoposide *(VM-16)
(ii) *Teniposide *(VM-26)

2) Topoisomerase I Inhibitors:
_*Camptothecins: *Irinotecan

  • Topoisomerases Unwind Tangled DNA by cutting one strand so another can pass through the break:
    (1) Topo I: Relaxes Supercoils Ahead of DNA replication fork.
    (2) Topo II: Allows Daughter strands to pass THROUGH one another.
  • Topoisomerase Inhibitors Stabilize the DNA-Topo Intermediate in the Cut state, Leading to DNA Breaks.
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19
Q

Paclitaxel

A

Taxanes

Source: Yew Tree Bark
(FSU total synthesis: Taxol)

Microtubule Inhibitors
(“Spindle Poisons”)

*Paclitaxel (Taxol)

Mechanism:
*Stabilizes Microtubule;
= *Prevents Tubulin Depolymerization
= *Inhibits Microtubule Disassembly

Uses: *Solid Tumors
(ovarian, breast, lung)

Resistance:
*Substrate for MDR Pump

Toxicity:

1) *Peripheral Neuropathy
2) Cumulative Myelosuppression

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20
Q

Vinblastine

A

Vinca Alkaloids

(Looks Like Pacman eating Ghost)
(Complex Plant Derivatives)

Microtubule Inhibitors
(“Spindle Poisons”)

  • Specificity: *M Phase (Mitosis).
  • Vinblastine, *Vincristine

Mechanism:

1) *Destabilizes Microtubules
2) *Mitotic Arrest

Resistance: *MDR Efflux Pumps

Toxicity:
1) Neurotoxicity (Vincristine)
(*Muscle Weakness, *Peripheral Neuropathy)

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21
Q

Vincristine

A

Vinca Alkaloids

(Looks Like Pacman eating Ghost)
(Complex Plant Derivatives)

Microtubule Inhibitors
(“Spindle Poisons”)

  • Specificity: *M Phase (Mitosis).
  • Vinblastine, *Vincristine

Mechanism:

1) *Destabilizes Microtubules
2) *Mitotic Arrest

Resistance: *MDR Efflux Pumps

Toxicity:
1) Neurotoxicity (Vincristine)
(*Muscle Weakness, *Peripheral Neuropathy)

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22
Q

Etoposide

A

Epipodophyllotoxins

(Derived from Mayapple / American Mandrake)

Topoisomerase II Inhibitor

1) *Etoposide *(VP-16)
2) *Teniposide *(VM-26

Mechanism:

1) *Stabilizes Topo II-DNA Intermediate,
2) *Leading to DNA Breaks

(Mechanism and structure similar to Anthracyclines; S and G2 phases most sensitive)

Resistance:
1) *MDR Pump

2) *Decreased or *Mutant Topo II

3) *p53 Mutation
(p53 mediates response to DNA damage)

Toxicity:

1) *Leukopenia *(Dose-Limiting)
2) *Hepatotoxicity *(High-Dose)

____________________

  • Topoisomerases Unwind Tangled DNA by cutting one strand so another can pass through the break:
    (1) Topo I: Relaxes Supercoils Ahead of DNA replication fork.
    (2) Topo II: Allows Daughter strands to pass THROUGH one another.
  • Topoisomerase Inhibitors Stabilize the DNA-Topo Intermediate in the Cut state, Leading to DNA Breaks.
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23
Q

Teniposide

A

Epipodophyllotoxins

(Derived from Mayapple / American Mandrake)

Topoisomerase II Inhibitor

1) *Etoposide *(VP-16)
2) *Teniposide *(VM-26

Mechanism:

1) *Stabilizes Topo II-DNA Intermediate,
2) *Leading to DNA Breaks

(Mechanism and structure similar to Anthracyclines; S and G2 phases most sensitive)

Resistance:
1) *MDR Pump

2) *Decreased or *Mutant Topo II

3) *p53 Mutation
(p53 mediates response to DNA damage)

Toxicity:

1) *Leukopenia *(Dose-Limiting)
2) *Hepatotoxicity *(High-Dose)

____________________

  • Topoisomerases Unwind Tangled DNA by cutting one strand so another can pass through the break:
    (1) Topo I: Relaxes Supercoils Ahead of DNA replication fork.
    (2) Topo II: Allows Daughter strands to pass THROUGH one another.
  • Topoisomerase Inhibitors Stabilize the DNA-Topo Intermediate in the Cut state, Leading to DNA Breaks.
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24
Q

Irinotecan

A

Camptothecins

(Derived from Happy Tree)

Topoisomerase I Inhibitor

*Irinotecan

Mechanism:
1) *Stabilizes Topo I-DNA Intermediate

Resistance:

1) Reduced levels or Altered Affinity of Topo I (Mutant)
2) Weak Substrate for MDR Pump

Uses: *Solid Tumors
(ovarian, colon, small cell lung cancers: SCLC)

____________________

  • Topoisomerases Unwind Tangled DNA by cutting one strand so another can pass through the break:
    (1) Topo I: Relaxes Supercoils Ahead of DNA replication fork.
    (2) Topo II: Allows Daughter strands to pass THROUGH one another.
  • Topoisomerase Inhibitors Stabilize the DNA-Topo Intermediate in the Cut state, Leading to DNA Breaks.
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25
Q

Hormone-Targeted Chemotherapy

A

Goal: *Turn OFF Hormone Signaling

Uses:

1) *Endometrial
2) *Breast
3) *Prostate
4) (Sometimes Lung Cancer b/c Estrogen Receptor is expressed in Lung)

Approaches:

1) *Compete with Endogenous Hormone for Receptor Binding
2) *Block Production of Endogenous Hormone

**Toxicities are Much Milder than Other Chemotherapeutics
_B/c Not actually Killing the cells

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26
Q

Flutamide

A

Anti-Androgenic Agents

1) Anti-Androgens: *Flutamide

Mechanism:
*Competitive Antagonist of Androgens

Use: *Prostate Cancer

2) LHRH Agonists: *Leuprolide

Mechanism:
*Inhibits Androgen Release via Downregulation
(with chronic administration)

Use: *Prostate Cancer

(and GnRH antagonist)

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27
Q

Leuprolide

A

Anti-Androgenic Agents

1) Anti-Androgens: *Flutamide

Mechanism:
*Competitive Antagonist of Androgens

Use: *Prostate Cancer

2) LHRH Agonists: *Leuprolide

Mechanism:
*Inhibits Androgen Release via Downregulation
(with chronic administration)

Use: *Prostate Cancer

(and GnRH antagonist)

28
Q

Tamoxifen

A

Anti-Estrogenic Agents

1) Anti-Estrogens: *Tamoxifen

Mechanism:
*Competitive Antagonist of Estrogen

Use:
_Prevents or Slows Growth of Estrogen-Dependent Tumors:
*Breast Cancer

2) Aromatase Inhibitors: *Anastrazole

Mechanism:

1) *Inhibits Aromatase,
2) *Blocking Estrogen Synthesis

Use:
_Breast Cancer in Post-Menopausal Women

29
Q

Anastrazole

A

Anti-Estrogenic Agents

1) Anti-Estrogens: *Tamoxifen

Mechanism:
*Competitive Antagonist of Estrogen

Use:
_Prevents or Slows Growth of Estrogen-Dependent Tumors:
*Breast Cancer

2) Aromatase Inhibitors: *Anastrazole

Mechanism:

1) *Inhibits Aromatase,
2) *Blocking Estrogen Synthesis

Use:
_Breast Cancer in Post-Menopausal Women

30
Q

Corticosteroids

Glucocorticoids

A

Mechanism:
_*Lyse Malignant T lymphocytes

Use:

1) *Lymphomas
2) *Acute Lymphocytic Leukemia

31
Q

Bleomycin

A

Miscellaneous Agent

Mechanism:
*Breaks DNA via *Free Radicals

Toxicity:
_*Minimal Marrow Toxicity

32
Q

Aspariginase

A

Miscellaneous Agent

Mechanism:
_*Inhibits Protein Synthesis

Resistance:
_*Increase Asparagine Synthetase Activity in Tumor cell

Use: *Childhood Acute Leukemia

Toxicity: *Hypersensitivity Reactions

33
Q

Targeted Therapies of Cancer:

“New Wave”

A

**Target Specific Molecular Pathways or Mediators of the Malignant Phenotype.

Efficacy:
_More Effective than conventional therapies,
_But only in cases where target is a prominent factor in the disease

Toxicities:
_Less than conventional therapies
_Infusion Reactions are common for most IV agents.

1) Tyrosine Kinase Inhibitors
(-Tinibs)

2) Disruptors of Gene Expression, Protein Translation, Proteolysis
3) Monoclonal Antibodies (-Mabs)
4) Cytokines and Immunomodulators
5) Differentiating Agents
6) Other

34
Q

Imatinib

A

Tyrosine Kinase Inhibitors
= Analogs of ATP

Designed Against Kinases that Activate Pro-Growth, Pro-Survival Pathways.

Use is guided by known frequent Deregulation of a Receptor-Pathway in a given cancer.

Mechanisms:

1) *Promote Apoptosis
2) *Inhibit Growth Factors
3) *Inhibit Angiogenesis
4) *Inhibit Proliferation

Usually Given *p.o. (orally)

Adverse Effects:

1) *Skin and *Mucosal Effects
2) *Fatigue

___________________

1) *Imatinib:

Mechanism: *Inhibits Abl Kinase
*(ABL-BCR Fusion Gene)
(Philadelphia Chromosome)

Use: *Drug of Choice!:
*Chronic Myelogenous Leukemia
___________________

2) Gefetinib:

Mechanism: *Inhibits EGFR
(Epidermal Growth Factor Receptor)

Use: *Oral Treatment of NSCLC
(Non-small cell lung cancer)

(Most effective in Never-Smoker Females and Asians)
___________________

3) Lapatinib:

Mechanism: *Inhibits HER-2

Use:
*Advanced/Metastatic Breast Cancer
___________________

4) Sunitinib (not bold this yr)

Mechanism: Blocks VEGFR
(Vascular Endothelial Growth Factor Receptor)

Use: Renal Cancer

Not as selective for desired kinases
(good or bad?)

35
Q

Gefetinib

A

Tyrosine Kinase Inhibitors
= Analogs of ATP

Designed Against Kinases that Activate Pro-Growth, Pro-Survival Pathways.

Use is guided by known frequent Deregulation of a Receptor-Pathway in a given cancer.

Mechanisms:

1) *Promote Apoptosis
2) *Inhibit Growth Factors
3) *Inhibit Angiogenesis
4) *Inhibit Proliferation

Usually Given *p.o. (orally)

Adverse Effects:

1) *Skin and *Mucosal Effects
2) *Fatigue

___________________

1) *Imatinib:

Mechanism: *Inhibits Abl Kinase
*(ABL-BCR Fusion Gene)
(Philadelphia Chromosome)

Use: *Drug of Choice!:
*Chronic Myelogenous Leukemia
___________________

2) Gefetinib:

Mechanism: *Inhibits EGFR
(Epidermal Growth Factor Receptor)

Use: *Oral Treatment of NSCLC
(Non-small cell lung cancer)

(Most effective in Never-Smoker Females and Asians)
___________________

3) Lapatinib:

Mechanism: *Inhibits HER-2

Use:
*Advanced/Metastatic Breast Cancer
___________________

4) Sunitinib (not bold this yr)

Mechanism: Blocks VEGFR
(Vascular Endothelial Growth Factor Receptor)

Use: Renal Cancer

Not as selective for desired kinases
(good or bad?)

36
Q

Lapatinib

A

Tyrosine Kinase Inhibitors
= Analogs of ATP

Designed Against Kinases that Activate Pro-Growth, Pro-Survival Pathways.

Use is guided by known frequent Deregulation of a Receptor-Pathway in a given cancer.

Mechanisms:

1) *Promote Apoptosis
2) *Inhibit Growth Factors
3) *Inhibit Angiogenesis
4) *Inhibit Proliferation

Usually Given *p.o. (orally)

Adverse Effects:

1) *Skin and *Mucosal Effects
2) *Fatigue

___________________

1) *Imatinib:

Mechanism: *Inhibits Abl Kinase
*(ABL-BCR Fusion Gene)
(Philadelphia Chromosome)

Use: *Drug of Choice!:
*Chronic Myelogenous Leukemia
___________________

2) Gefetinib:

Mechanism: *Inhibits EGFR
(Epidermal Growth Factor Receptor)

Use: *Oral Treatment of NSCLC
(Non-small cell lung cancer)

(Most effective in Never-Smoker Females and Asians)
___________________

3) Lapatinib:

Mechanism: *Inhibits HER-2

Use:
*Advanced/Metastatic Breast Cancer
___________________

4) Sunitinib (not bold this yr)

Mechanism: Blocks VEGFR
(Vascular Endothelial Growth Factor Receptor)

Use: Renal Cancer

Not as selective for desired kinases
(good or bad?)

37
Q

Sunitinib

A

Tyrosine Kinase Inhibitors
= Analogs of ATP

Designed Against Kinases that Activate Pro-Growth, Pro-Survival Pathways.

Use is guided by known frequent Deregulation of a Receptor-Pathway in a given cancer.

Mechanisms:

1) *Promote Apoptosis
2) *Inhibit Growth Factors
3) *Inhibit Angiogenesis
4) *Inhibit Proliferation

Usually Given *p.o. (orally)

Adverse Effects:

1) *Skin and *Mucosal Effects
2) *Fatigue

___________________

1) *Imatinib:

Mechanism: *Inhibits Abl Kinase
*(ABL-BCR Fusion Gene)
(Philadelphia Chromosome)

Use: *Drug of Choice!:
*Chronic Myelogenous Leukemia
___________________

2) Gefetinib:

Mechanism: *Inhibits EGFR
(Epidermal Growth Factor Receptor)

Use: *Oral Treatment of NSCLC
(Non-small cell lung cancer)

(Most effective in Never-Smoker Females and Asians)
___________________

3) Lapatinib:

Mechanism: *Inhibits HER-2

Use:
*Advanced/Metastatic Breast Cancer
___________________

4) Sunitinib (not bold this yr)

Mechanism: Blocks VEGFR
(Vascular Endothelial Growth Factor Receptor)

Use: Renal Cancer

Not as selective for desired kinases
(good or bad?)

38
Q

HDAC Inhibitors

A

Transcription, Translation, and Proteolysis Disruptors

HDAC Inhibitors:
_*Prevent Histone Deacetylation

Rapamycins (Sirolimus):

1) *Block New Protein Synthesis
2) *Stimulate Autophagy

Proteasome Inhibitors:
_Bortezomib
_*Block Protein Turnover by the Proteasome; Induce Apoptosis
Use: *Multiple Myeloma (1st line)

39
Q

Sirolimus

A

Transcription, Translation, and Proteolysis Disruptors

HDAC Inhibitors:
_*Prevent Histone Deacetylation

Rapamycins (Sirolimus):

1) *Block New Protein Synthesis
2) *Stimulate Autophagy

Proteasome Inhibitors:
_Bortezomib
_*Block Protein Turnover by the Proteasome; Induce Apoptosis
Use: *Multiple Myeloma (1st line)

40
Q

Bortezomib

A

Transcription, Translation, and Proteolysis Disruptors

HDAC Inhibitors:
_*Prevent Histone Deacetylation

Rapamycins (Sirolimus):

1) *Block New Protein Synthesis
2) *Stimulate Autophagy

Proteasome Inhibitors:
_Bortezomib
_*Block Protein Turnover by the Proteasome; Induce Apoptosis
Use: *Multiple Myeloma (1st line)

41
Q

Rituximab

A

Monoclonal Antibodies

*All Must be Given by Infusion
Can Cause Infusion Reactions:
_Rash, *Edema, *Hypotension, Bronchospasms;
_Rarely, Anaphylaxis

1) *Rituximab:
_Antigen: *CD20
_Use: *B cell Lymphoma
_Mechanism: ADCC

2) *Alemtuzumab:
Antigen: *CD52
Use: *T cell Lymphoma
Mechanism: ADCC

3) *Trastuzumab:
Antigen: *HER-2/Neu Tyrosine Kinase
Use: *Breast Cancer
Mechanism: Block Receptor and Deliver Toxic species

4) *Cetuximab:
Antigen: *EGFR Tyrosine Kinase
Use: *Colorectal
Mechanism: Block Receptor

5) *Bevacizumab: 
Antigen: *VEGF 
(Reduces Angiogenesis)
Use: *Colorectal Cancer
Mechanism: Absorb Ligand

___________________

Mechanisms:

1) Recruit immune cells to Trigger
*Antibody-Dependent Cell-Mediated Toxicity (ADCC):
_Rituximab
_Alemtuzumab

2) *Absorb a Ligand for a Receptor:
_Bevacizumab

3) *Block Activation of a Receptor:
_Trastuzumab
_Cetuximab

4) *Deliver a Toxic Species to Cancer Cells:
_Trastuzumab-emtansine

42
Q

Alemtuzumab

A

Monoclonal Antibodies

*All Must be Given by Infusion
Can Cause Infusion Reactions:
_Rash, *Edema, *Hypotension, Bronchospasms;
_Rarely, Anaphylaxis

1) *Rituximab:
_Antigen: *CD20
_Use: *B cell Lymphoma
_Mechanism: ADCC

2) *Alemtuzumab:
Antigen: *CD52
Use: *T cell Lymphoma
Mechanism: ADCC

3) *Trastuzumab:
Antigen: *HER-2/Neu Tyrosine Kinase
Use: *Breast Cancer
Mechanism: Block Receptor and Deliver Toxic species

4) *Cetuximab:
Antigen: *EGFR Tyrosine Kinase
Use: *Colorectal
Mechanism: Block Receptor

5) *Bevacizumab: 
Antigen: *VEGF 
(Reduces Angiogenesis)
Use: *Colorectal Cancer
Mechanism: Absorb Ligand

___________________

Mechanisms:

1) Recruit immune cells to Trigger
*Antibody-Dependent Cell-Mediated Toxicity (ADCC):
_Rituximab
_Alemtuzumab

2) *Absorb a Ligand for a Receptor:
_Bevacizumab

3) *Block Activation of a Receptor:
_Trastuzumab
_Cetuximab

4) *Deliver a Toxic Species to Cancer Cells:
_Trastuzumab-emtansine

43
Q

Trastuzumab

A

Monoclonal Antibodies

*All Must be Given by Infusion
Can Cause Infusion Reactions:
_Rash, *Edema, *Hypotension, Bronchospasms;
_Rarely, Anaphylaxis

1) *Rituximab:
_Antigen: *CD20
_Use: *B cell Lymphoma
_Mechanism: ADCC

2) *Alemtuzumab:
Antigen: *CD52
Use: *T cell Lymphoma
Mechanism: ADCC

3) *Trastuzumab:
Antigen: *HER-2/Neu Tyrosine Kinase
Use: *Breast Cancer
Mechanism: Block Receptor and Deliver Toxic species

4) *Cetuximab:
Antigen: *EGFR Tyrosine Kinase
Use: *Colorectal
Mechanism: Block Receptor

5) *Bevacizumab: 
Antigen: *VEGF 
(Reduces Angiogenesis)
Use: *Colorectal Cancer
Mechanism: Absorb Ligand

___________________

Mechanisms:

1) Recruit immune cells to Trigger
*Antibody-Dependent Cell-Mediated Toxicity (ADCC):
_Rituximab
_Alemtuzumab

2) *Absorb a Ligand for a Receptor:
_Bevacizumab

3) *Block Activation of a Receptor:
_Trastuzumab
_Cetuximab

4) *Deliver a Toxic Species to Cancer Cells:
_Trastuzumab-emtansine

44
Q

Cetuximab

A

Monoclonal Antibodies

*All Must be Given by Infusion
Can Cause Infusion Reactions:
_Rash, *Edema, *Hypotension, Bronchospasms;
_Rarely, Anaphylaxis

1) *Rituximab:
_Antigen: *CD20
_Use: *B cell Lymphoma
_Mechanism: ADCC

2) *Alemtuzumab:
Antigen: *CD52
Use: *T cell Lymphoma
Mechanism: ADCC

3) *Trastuzumab:
Antigen: *HER-2/Neu Tyrosine Kinase
Use: *Breast Cancer
Mechanism: Block Receptor and Deliver Toxic species

4) *Cetuximab:
Antigen: *EGFR Tyrosine Kinase
Use: *Colorectal
Mechanism: Block Receptor

5) *Bevacizumab: 
Antigen: *VEGF 
(Reduces Angiogenesis)
Use: *Colorectal Cancer
Mechanism: Absorb Ligand

___________________

Mechanisms:

1) Recruit immune cells to Trigger
*Antibody-Dependent Cell-Mediated Toxicity (ADCC):
_Rituximab
_Alemtuzumab

2) *Absorb a Ligand for a Receptor:
_Bevacizumab

3) *Block Activation of a Receptor:
_Trastuzumab
_Cetuximab

4) *Deliver a Toxic Species to Cancer Cells:
_Trastuzumab-emtansine

45
Q

Bevacizumab

A

Monoclonal Antibodies

*All Must be Given by Infusion
Can Cause Infusion Reactions:
_Rash, *Edema, *Hypotension, Bronchospasms;
_Rarely, Anaphylaxis

1) *Rituximab:
_Antigen: *CD20
_Use: *B cell Lymphoma
_Mechanism: ADCC

2) *Alemtuzumab:
Antigen: *CD52
Use: *T cell Lymphoma
Mechanism: ADCC

3) *Trastuzumab:
Antigen: *HER-2/Neu Tyrosine Kinase
Use: *Breast Cancer
Mechanism: Block Receptor and Deliver Toxic species

4) *Cetuximab:
Antigen: *EGFR Tyrosine Kinase
Use: *Colorectal
Mechanism: Block Receptor

5) *Bevacizumab: 
Antigen: *VEGF 
(Reduces Angiogenesis)
Use: *Colorectal Cancer
Mechanism: Absorb Ligand

___________________

Mechanisms:

1) Recruit immune cells to Trigger
*Antibody-Dependent Cell-Mediated Toxicity (ADCC):
_Rituximab
_Alemtuzumab

2) *Absorb a Ligand for a Receptor:
_Bevacizumab

3) *Block Activation of a Receptor:
_Trastuzumab
_Cetuximab

4) *Deliver a Toxic Species to Cancer Cells:
_Trastuzumab-emtansine

46
Q

Interleukin-2 (IL-2)

A

Cytokines:

*Interleukin-2 (IL-2)

Mechanism:
=> *Produces Tumor-Cytolytic Lymphocytes

Uses:

1) *Renal Cell Carcinoma (RCC)
2) *Metastatic Melanoma

47
Q

Colony Stimulating Factors

A

Differentiating Agents

(Inducing Differentiation should stop cancer cells from dividing)

Effects: @ Level of Gene Transcription

1) *Colony Stimulating Factors:

Mechanism:
=> Act on Cells @ Various Stages of Hematopoietic Hierarchy

Use:
=> Replenish RBCs suppressed by chemotherapy

2) *Retinoic Acids:
(Vitamin A Derivatives)

_Tretinoin (All trans-retinoic Acid)

_*Accutane

Rarely used, but effective against Acute Pro-Myelocytic Leukemias

(=> Reduce likelihood of transformation into Leukemia)

48
Q

Accutane

A

Differentiating Agents

(Inducing Differentiation should stop cancer cells from dividing)

Effects: @ Level of Gene Transcription

1) *Colony Stimulating Factors:

Mechanism:
=> Act on Cells @ Various Stages of Hematopoietic Hierarchy

Use:
=> Replenish RBCs suppressed by chemotherapy

2) *Retinoic Acids:
(Vitamin A Derivatives)

_Tretinoin (All trans-retinoic Acid)

_*Accutane

Rarely used, but effective against Acute Pro-Myelocytic Leukemias

(=> Reduce likelihood of transformation into Leukemia)

49
Q

Cyclosporine

A

ImmunoSuppressors

Calcineurin Inhibitors:

1) Cyclosporine
2) Tacrolimus

Mechanism:
1) Blocks Calcineurin;
=> Blocking Cell Proliferation

Uses:
1) Organ Transplant
2) Autoimmune:
Rheumatoid Arthritis

Toxicity:

1) Nephrotoxic
2) CYP450 Drug Interactions

50
Q

Tacrolimus

A

ImmunoSuppressors

Calcineurin Inhibitors:

1) Cyclosporine
2) Tacrolimus

Mechanism:
1) Blocks Calcineurin;
=> Blocking Cell Proliferation

Uses:
1) Organ Transplant
2) Autoimmune:
Rheumatoid Arthritis

Toxicity:

1) Nephrotoxic
2) CYP450 Drug Interactions

51
Q

Sirolimus

Immuno

A

ImmunoSuppressors

Target of Rapamycin (mTOR) Inhibitors:
_Sirolimus

Mechanism:
1) Inhibits mTOR;
=> Blocking Cell Proliferation

Uses:

1) Transplant Rejection
2) Reduce Proliferation in Stents

Toxicity:

1) CYP450 Drug Interactions
2) Elevated Blood Lipids
3) Risk of Cancer
4) Myelosuppression
5) Risk of Infections

52
Q

Methotrexate

Immuno

A

ImmunoSuppressors

Anti-Proliferative Agents:
=> Anti-Metabolites:
1) Methotrexate (Folate Analog)
2) Azathioprine (Purine Analog)
3) Mycophenolate Mofetil 
(Purine Analog)

Mechanism:

1) Interfere with Nucleic Acid Synthesis
2) Affects Cellular Immunity More than Humoral

Uses:

1) Organ Transplant: *RENAL
2) Some Autoimmune

Toxicity:

1) Myelosuppression
2) GI: Nausea, Vomiting

53
Q

Azathioprine

A

ImmunoSuppressors

Anti-Proliferative Agents:
=> Anti-Metabolites:
1) Methotrexate (Folate Analog)
2) Azathioprine (Purine Analog)
3) Mycophenolate Mofetil 
(Purine Analog)

Mechanism:

1) Interfere with Nucleic Acid Synthesis
2) Affects Cellular Immunity More than Humoral

Uses:

1) Organ Transplant: *RENAL
2) Some Autoimmune

Toxicity:

1) Myelosuppression
2) GI: Nausea, Vomiting

54
Q

Mycophenolate Mofetil

A

ImmunoSuppressors

Anti-Proliferative Agents:
=> Anti-Metabolites:
1) Methotrexate (Folate Analog)
2) Azathioprine (Purine Analog)
3) Mycophenolate Mofetil 
(Purine Analog)

Mechanism:

1) Interfere with Nucleic Acid Synthesis
2) Affects Cellular Immunity More than Humoral

Uses:

1) Organ Transplant: *RENAL
2) Some Autoimmune

Toxicity:

1) Myelosuppression
2) GI: Nausea, Vomiting

55
Q

Cyclophosphamide

Immuno

A

ImmunoSuppressors

Alkylating Agents:
1) Nitrogen Mustards:
Cyclophosphamide

Mechanism:
1) Alkylates DNA (Cross-Links)
=> Inhibits DNA Synthesis

2) Humoral Immunity Affected More than Cellular Immunity

Uses:

1) Bone Marrow Transplant
2) Autoimmune

Toxicity:

1) Myelosuppression
2) Secondary Neoplasias
3) Hemorrhagic Cystitis
4) GI: Nausea, Vomiting

56
Q

Prednisone

A

ImmunoSuppressors

Corticosteroids (Glucocorticoids):

1) Prednisone
2) Hydrocortisone
3) Dexamethasone

Mechanism:

1) Reduce T Cell Function,
2) Reduce Chemotaxis,
3) Inhibit Production of Inflammatory Mediators

Uses:

1) Autoimmune
2) Inflammatory Diseases
3) Transplant Adjunct

Toxicity:
1) Fat Deposition Changes:
_Moon Face, Buffalo Hump
2) Diabetes, Hyperglycemia
3) Psychosis
4) Risk of Infection
5) (Discontinue Slowly to Avoid Adrenal Insufficiency
57
Q

Hydrocortisone

A

ImmunoSuppressors

Corticosteroids (Glucocorticoids):

1) Prednisone
2) Hydrocortisone
3) Dexamethasone

Mechanism:

1) Reduce T Cell Function,
2) Reduce Chemotaxis,
3) Inhibit Production of Inflammatory Mediators

Uses:

1) Autoimmune
2) Inflammatory Diseases
3) Transplant Adjunct

Toxicity:
1) Fat Deposition Changes:
_Moon Face, Buffalo Hump
2) Diabetes, Hyperglycemia
3) Psychosis
4) Risk of Infection
5) (Discontinue Slowly to Avoid Adrenal Insufficiency
58
Q

Dexamethasone

A

ImmunoSuppressors

Corticosteroids (Glucocorticoids):

1) Prednisone
2) Hydrocortisone
3) Dexamethasone

Mechanism:

1) Reduce T Cell Function,
2) Reduce Chemotaxis,
3) Inhibit Production of Inflammatory Mediators

Uses:

1) Autoimmune
2) Inflammatory Diseases
3) Transplant Adjunct

Toxicity:
1) Fat Deposition Changes:
_Moon Face, Buffalo Hump
2) Diabetes, Hyperglycemia
3) Psychosis
4) Risk of Infection
5) (Discontinue Slowly to Avoid Adrenal Insufficiency
59
Q

Rh0 Antibody

A

ImmunoSuppressors

Uses:
=> Prevents Hemolytic Disease of Rh+ Newborn born to Rh- Mother.

60
Q

Infliximab

A

ImmunoSuppressors

Binding Proteins:

1) Infliximab
2) Etanercept

Mechanism:
=> Bind to TNF-Alpha

Uses:

1) Rheumatoid Arthritis
2) Crohn’s Disease
3) Psoriasis

61
Q

Etanercept

A

ImmunoSuppressors

Binding Proteins:

1) Infliximab
2) Etanercept

Mechanism:
=> Bind to TNF-Alpha

Uses:

1) Rheumatoid Arthritis
2) Crohn’s Disease
3) Psoriasis

62
Q

Muromonab-CD3

A

ImmunoSuppressors

Binding Protein

Use:
=> Renal Transplant

63
Q

Immune Globulin

A

ImmunoStimulant

Natural Adjuvant

Mechanism:
(Prepared from pooled plasma)

Uses:
(Various ImmunoDeficiency States,
Agammaglobulinemia)

64
Q

Thalidomide

A

ImmunoStimulant

Synthetic

Toxicity:
=> Phocomelia!!
(Absent/Short Limbs)

65
Q

Interferon Alpha

A

ImmunoStimulant

Cytokines

Uses:
=> Various Neoplasms:
1) Kaposi’s Sarcoma
2) Hairy Cell Leukemia

66
Q

Interferon Beta-1b

A

ImmunoStimulant

Cytokines

Use:
=> Relapsing Multiple Sclerosis

67
Q

Interleukin-2

Immuno

A

ImmunoStimulant

Cytokines

Mechanism:
=> Produces Cytolytic Lymphocytes Against Tumor Cells

Uses:

1) Renal Cell Carcinoma (RCC)
2) Metastatic Melanoma

Pharm 2015 (22 decks)

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