Term
|
Definition
*Antibody HER-2(EGF) Receptor binder (not ligand site) leading to NK cell activation(ADCC). It does NOT prevent receptor dimerization
*Also increases internalization of receptors, blocks the ectodomain protease, and decreases angiogenesis(.
*
*Breast Cancer
*
*Increased Risk of CHF / cardiomyopathy |
|
|
Term
|
Definition
*Antibody HER-1(EGF) Receptor blocker. As opposed to trastuzumab, it DOES prevent ligand binding.
*Apoptosis is enhanced. MMP and VEGF release are inhibited.
*Widely Used
*
*
* |
|
|
Term
|
Definition
*Tyrosine Kinase Inhibitor (BCR-ABL specific)
*Treats Chronic Mylogenous Leukemia(CML) which is unique in that only one translocation has occured tp created Philadelphia Chromosome, creating a very specific BCR-ABL receptor that is targeted by Imatinib.
*
*
*
* |
|
|
Term
|
Definition
*Tyrosine Kinase Inhibitor
*Alternative to Imatinib to treat CML
*
*
*
* |
|
|
Term
|
Definition
*Tyrosine Kinase Inhibitor (EGF non-specific)
*
*
*
*
* |
|
|
Term
|
Definition
*Tyrosine Kinase Inhibitor (EGF non-specific)
*
*
*
*
* |
|
|
Term
|
Definition
*Tyrosine Kinase Inhibitor (VEGF, PDGF, Kit-Stem cell factor)
*The block of VEGF is useful in fighting cancers that require very high angiogenesis like RCC
*
*
*
* |
|
|
Term
|
Definition
*Tyrosine Kinase Inhibitor (VEGF, PDGF, Kit-Stem cell factor)
*The block of VEGF is useful in fighting cancers that require very high angiogenesis like RCC and GIST
*
*
*
* |
|
|
Term
|
Definition
*Tyrosine Kinase Inhibitor (ERB-1,2 and Her-2)
*
*
*Breast Cancer
*
* |
|
|
Term
|
Definition
*Antibody for VEGF, "sponging" up the ligand for the receptor.
*Used in combo with traditional Tx
*Widely used
*
*
*Bleeding toxicity because normal vessels can't repair as well |
|
|
Term
|
Definition
*DNA Demethylating to activate tumor suppressor genes like p53. Also inhibits tRNA function
*Is activated by triphosphorylation, is incorporated into DNA, and forms a complex with the DNA methyl transferase.
*
*
*
* |
|
|
Term
|
Definition
*Protease Inhibitor
*Results in the build up of phosphorylated IkB which results in cytotoxicity and apoptosis.
*
*
*
* |
|
|
Term
|
Definition
| *Antibody against CD20 of B-cells |
|
|
Term
Alemtuzumab
Gemtuzumab
Nimotuzumab
Ofatumumab |
|
Definition
-CD52 on T/B cells
-CD33
-EGF Receptor (like Cetuximab)
-CD20 (but binds closer and with greater recognition) |
|
|
Term
|
Definition
*Alkylating Agent (Cross Linking)
*Highly Reactive, requiring direct injection into tumor due to E- donating group. Part of the MOPP protocol. Antidote is Sodium Thiosulfate
*
*
*Not Cell Cycle Specific
* |
|
|
Term
|
Definition
*Alkylating Agent (Cross linking)
*Can be taken orally due to E- withdraw
*
*
*Not Cell Cycle Specific
* |
|
|
Term
|
Definition
*Alkylating Agent (Cross linking)
*Can be taken orally due to E- withdraw
*Widely used
*Breast Cancer
*Not Cell Cycle Specific
* |
|
|
Term
|
Definition
*Alkylating Agent (Cross linking)
*
*
*
*Not Cell Cycle Specific
* |
|
|
Term
|
Definition
*Alkylating Agent (Cross linking)
*Activated by CYP, deactivated by dehydrogenase. Acrolein toxicity can be reduced by combining with MESNA.
*
*Breast Cancer
*Not Cell Cycle Specific
*Bladder toxicity via Acrolein |
|
|
Term
|
Definition
*Alkylating Agent (Cross linking)
*Activated by CYP, deactivated by dehydrogenase.
*Widely Used
*
*Not Cell Cycle Specific
*Bladder toxicity via Chloroacetaldehyde (side chain oxidation) |
|
|
Term
|
Definition
*Alkylating Agent (Cross linking unless metabolized)
*If CYP or Hydrolysis, no cross linking. If neither, then cross linking.
*
*Breast Cancer
*Not Cell Cycle Specific
* |
|
|
Term
|
Definition
*Alkylating Agent (Cross linking)
*Can be used in hi dose for bone marrow transplant.
*
*
*Not Cell Cycle Specific
*Pulmonary Fibrosis/Bisulfan Lung |
|
|
Term
|
Definition
*Alkylating Agent (Intrastrand cross linking)
*
*Widely Used
*
*Not Cell Cycle Specific
*Neurotoxic and Nephrotoxic |
|
|
Term
|
Definition
*Alkylating Agent (Intrastrand cross linking)
*Decreased activity for increased selectivity vs. Cisplatin.
*Widely Used
*
*Not Cell Cycle Specific
* |
|
|
Term
|
Definition
*Alkylating Agent (Intrastrand cross linking)
*Decreased activity for increased selectivity vs. Cisplatin.
*
*
*Not Cell Cycle Specific
*Neurotoxicity |
|
|
Term
|
Definition
*Alkylating Agent (Cross linking)
*Lipophilicity allows treatment of Brain cancer
*
*
*Not Cell Cycle Specific
* |
|
|
Term
|
Definition
*Alkylating Agent (Cross linking)
*Lipophilicity allows treatment of Brain cancer
*
*
*Not Cell Cycle Specific
* |
|
|
Term
|
Definition
*Alkylating Agent (Methylating)
*Won't cross BBB
*
*
*Not Cell Cycle Specific
*Renal Toxicity |
|
|
Term
|
Definition
*Alkylating Agent (Methylating)
*Part of MOPP protocol. Methylates by formation of both carbocations and methyl radicals.
*
*
*Not Cell Cycle Specific
* |
|
|
Term
|
Definition
*Alkylating Agent (Methylating)
*This prodrug requires CYP activation. Methylates by forming a N2CH3+ which is equivalent to a carbocation.
*
*
*Not Cell Cycle Specific
* |
|
|
Term
|
Definition
*Alkylating Agent (Methylating)
*Unlike Dacarbazine, does not require CYP activation to work. Methylates by forming a N2CH3+ which is equivalent to a carbocation.
*
*
*Not Cell Cycle Specific
* |
|
|
Term
|
Definition
*Blocks Thymidylate Synthase. Can also disrupt DNA if incorporated
*Pyrimidine drug. Works by replacing an -H leaving group with -F which is stable. Inactivated by dihydropyridine dehydrogenase. Also used to inhibit inactivation of Tegafur, which is broken down by the same enzyme.
*
*Breast Cancer
*S-phase specific
* |
|
|
Term
|
Definition
*Essentially is 5-FU with the sugar already attached. (Blocks TS)
*Pyrimidine drug. Avoids some of the resistances to 5-FU.
*
*Breast Cancer?
*S-phase specific
* |
|
|
Term
|
Definition
*Prodrug to 5-FU (Blocks TS)
*Pyrimidine drug. Converted to 5-FU by phosphorylase, which cancer cells are thought to have more of.
*
*Breast Cancer?
*S-Phase specific
* |
|
|
Term
|
Definition
*Prodrug to 5-FU (Blocks TS)
*Pyrimidine Drug. 5-FU is given along with this to slow down the breakdown of Tegafur.
*
*Breast Cancer?
*S-phase specific
* |
|
|
Term
|
Definition
*Can be incorporated into DNA to inhibit chain elongation and can inhibit Ribonucleotide Reductase(RR)
*Pyrimidine drug
*
*
*S-phase specific
* |
|
|
Term
|
Definition
*Can be phosphorylated, incorporated into DNA, and cause chain termination
*Pyrimidine drug
*
*
*S-phase specific
* |
|
|
Term
|
Definition
| *A folate that is given prior to 5-FU to increase thymidylate synthase inactivation |
|
|
Term
|
Definition
*Converted to the monophosphate and inhibits the rate limiting step in purine biosynthesis. Can be triphosphorylated to inhibit DNA polymerase
*Purine drug. Can inhibit feedback inhibition
*
*
*S-phase specific
* |
|
|
Term
|
Definition
*Converted to the monophosphate and inhibits the rate limiting step in purine biosynthesis. Can be triphosphorylated to inhibit DNA polymerase
*Purine drug.
*
*
*S-phase specific
* |
|
|
Term
|
Definition
*Triphosphorylated to inhibit DNA polymerase
*Purine Drug. Inactivated by Adenosine Deaminase.
*
*
*S-phase specific
* |
|
|
Term
|
Definition
*Triphosphorylated to inhibit DNA polymerase
*Purine Drug. Halogenated, so resistant to inactivation by Adenosine Deaminase.
*
*
*S-phase specific
* |
|
|
Term
|
Definition
*Triphosphorylated to inhibit DNA polymerase
*Purine Drug. Halogenated, so resistant to inactivation by Adenosine Deaminase.
*
*
*S-phase specific
* |
|
|
Term
|
Definition
*Triphosphorylated to inhibit DNA polymerase
*Purine Drug. Halogenated, so resistant to inactivation by Adenosine Deaminase.
*
*
*S-phase specific
* |
|
|
Term
|
Definition
*Triphosphorylated to inhibit DNA polymerase
*Purine Drug. Actually an inhibitor of Adenosine Deaminase.
*
*
*S-phase specific
* |
|
|
Term
|
Definition
*Inhibits DHFR to decrease purine/pyrimidine synthesis.
*Anti-folate. Due to increased basicity, will protonate and form an irreversible ionic bond with DHFR. Increases the activity of 5-FU if given beforehand.
*
*Breast Cancer
*S-phase specific
*Renal and Skin toxicity |
|
|
Term
|
Definition
*Mainly inhibits DHFR/Thymidylate Synthase to decrease purine/pyrimidine synthesis.
*Anti-folate.
*
*
*S-phase specific
*Renal and Skin toxicity |
|
|
Term
|
Definition
*Mainly inhibits DHFR/Thymidylate Synthase to decrease purine/pyrimidine synthesis.
*Anti-folate.
*
*
*S-phase specific
*Renal and Skin toxicity |
|
|
Term
|
Definition
*Blocks Thymidylate Synthase. Can disrupt DNA if incorporated
*Works by replacing an -H leaving group with F, which is a bad leaving group. Inactivated by dehydrogenase. Can be used to increase t1/2 of Tegafur. (Pyrimidine)
*
*Breast Cancer
*S-phase specific
* |
|
|
Term
|
Definition
| *Is 5-FU with the sugar already attached. So can avoid some resistances to 5-FU. (Pyrimidine) |
|
|
Term
|
Definition
*Prodrug to 5-FU.
*(Pyrimidine)
*
*
*S-phase specific
* |
|
|
Term
|
Definition
*Phosphorylated and incorporated into DNA. Can decrease chain elongation and inhibit Ribonucleotide Reductase
*(Pyrimidine)
*
*
*S-phase specific
* |
|
|
Term
|
Definition
*Phosphorylated and incorporated into DNA. Results in chain termination.
*(Pyrimidine)
*
*
*S-phase specific
* |
|
|
Term
|
Definition
| *A folate which can be given prior to 5-FU to increase thymidylate synthase inactivation. |
|
|
Term
|
Definition
*Converted to monophosphate form. Inhibits rate limiting step to purine synthesis. Can be triphosphorylated to inhibit DNA polymerase.
*Can inhibit feedback inhibition.
*
*
*S-phase specific
* |
|
|
Term
|
Definition
*Converted to monophosphate form. Inhibits rate limiting step to purine synthesis. Can be triphosphorylated to inhibit DNA polymerase.
*
*
*
*S-phase specific
* |
|
|
Term
|
Definition
*Triphosphorylated and incorporated into DNA to inhibit DNA polymerase
*Inactivated by adenosine deaminase
*
*
*S-phase specific
* |
|
|
Term
|
Definition
*Triphosphorylated and incorporated into DNA to inhibit DNA polymerase
*Because halogenated, resistant to adenosine deaminase inactivation
*
*
*S-phase specific
* |
|
|
Term
|
Definition
*Triphosphorylated and incorporated into DNA to inhibit DNA polymerase
*Because halogenated, resistant to adenosine deaminase inactivation
*
*
*S-phase specific
* |
|
|
Term
|
Definition
*Triphosphorylated and incorporated into DNA to inhibit DNA polymerase
*Because halogenated, resistant to adenosine deaminase inactivation
*
*
*S-phase specific
* |
|
|
Term
|
Definition
*Triphosphorylated and incorporated into DNA to inhibit DNA polymerase
*Actually an inhibitor of adenosine deaminase
*
*
*S-phase specific
* |
|
|
Term
|
Definition
*Inhibits DHFR to ultimately decrease purines and pyrimidines
*Due to increased basicity, will protonate and form an irreversible ionic bond with DHFR.
*
*Breast Cancer
*S-phase specific
*Renal and skin toxicity |
|
|
Term
|
Definition
*Inhibits Thymidylate Synthase
*
*
*
*S-phase specific
*Renal and skin toxicity |
|
|
Term
|
Definition
*Inhibits Thymidylate Synthase
*
*
*
*S-phase specific
*Renal and skin toxicity |
|
|
Term
|
Definition
*Intercolator. Can inhibit RNA synthesis and topoisomerase II.
*Used in children
*
*
*G1 and S-phase specific
* |
|
|
Term
|
Definition
*Intercolator. Inhibits topoisomerase II.
*
*Widely used
*
*G1 and S-phase specific
*Cardiotoxicity from hydroxide radicals. |
|
|
Term
|
Definition
| *Similar to Doxorubicin but decreased spectrum |
|
|
Term
|
Definition
*Similar to Doxorubicin but decreased spectrum
*Increased topoisomerase II inhibition. Decreased cardiotoxicity |
|
|
Term
|
Definition
*Similar to Doxorubicin but decreased spectrum
*Increased topoisomerase II inhibition. Decreased cardiotoxicity |
|
|
Term
|
Definition
*Similar to doxorubicin
*An orphan drug for bladder cancer |
|
|
Term
|
Definition
| *Chelates iron to reduce the cardiotoxicity of the anthracyclines ("_rubicin") |
|
|
Term
|
Definition
*Intercolator. Inhibits topoisomerase II.
*Greatly reduced cardiotoxicity versus the anthracyclins
*Widely Used
*Breast Cancer
*S-phase specific
* |
|
|
Term
|
Definition
*Binds and Inhibits Topoisomerase II
*A derivative of podophyllotoxin
*Widely used
*Breast Cancer
*S and G2 phase specific
* |
|
|
Term
|
Definition
*Binds and Inhibits Topoisomerase II
*A derivative of podophyllotoxin. Can be given by IV due to phosphate
*
*
*S and G2 phase specific
* |
|
|
Term
|
Definition
*Binds and Inhibits Topoisomerase II
*A derivative of podophyllotoxin
*
*
*S and G2 phase specific
* |
|
|
Term
|
Definition
*Inhibits Topoisomerase I
*Camptothecin derivative
*
*
*
*Diarrhea in 2 phases (1st via AchE inhibition. 2nd via SN-38G metabolite) |
|
|
Term
|
Definition
*Inhibits Topoisomerase I
*Camptothecin derivative. Carboxyl esterase metabolite is 1000x more potent and causes the toxicity
*Widely Used
*
*
*Diarrhea in 2 phases (1st via AchE inhibition. 2nd via SN-38G metabolite) |
|
|
Term
|
Definition
*Intercolates DNA, drawing the part of the structure that chelates iron close to the DNA. This then binds O2 and results in hydroxide radicals which cleave DNA.
*Given as a mixture of two different forms of the drug. Lungs and skin have fewer enzymes of deactivation, giving the toxicity.
*
*
*G2 and M phases
*Pulmonary toxicity |
|
|
Term
|
Definition
*Tubuline Binder to block Dynamic Instability and Treadmilling
*Can be resisted by Pgp efflux (MDR)
*Widely used
*
*M-phase specific
* |
|
|
Term
|
Definition
*Tubuline Binder to block Dynamic Instability and Treadmilling
*Can be resisted by Pgp efflux (MDR)
*Widely used
*
*M-phase specific
*Neurotoxicity (peripheral neuritis) |
|
|
Term
|
Definition
*Tubuline Binder to block Dynamic Instability and Treadmilling
*Can be resisted by Pgp efflux (MDR)
*
*Breast Cancer
*M-phase specific
* |
|
|
Term
|
Definition
*Low concentration - Inhibition of microtubule depolymerization
Hi concentration - Microtubule depolymerization is enhanced.
*
*Widely Used
*Breast Cancer
*M-phase specific
* |
|
|
Term
|
Definition
*Low concentration - Inhibition of microtubule depolymerization
Hi concentration - Microtubule depolymerization is enhanced.
*Fluid retention(manageable) can occur.
*
*Breast Cancer
*M-phase specific
* |
|
|
Term
|
Definition
*Low concentration - Inhibition of microtubule depolymerization
Hi concentration - Microtubule depolymerization is enhanced.
*Resistant to Pgp efflux. Used after the taxanes fail to work.
*
*Breast Cancer
*M-phase specific
*Neurotoxicity (peripheral neuritis) |
|
|
Term
|
Definition
*Bioreductive Alkylating Agent (natural)
*Cross linking can occur. Stable until activated by reduction of the quinone to hydroquinone.
*Widely Used
*Breast Cancer
*
* |
|
|
