Term
| antimetabolite common features |
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Definition
-bine, -dine, -tine
S phase specific
myelosuppresion, diarrhea, mucusitis |
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Term
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Definition
Class: cancer, antimetabolite, folate analog
Mechanism: competitive inhibtion of DHFR, decrease resynthesis of THF, blocks purine synthesis, blocks DNA/RNA/protein synthesis; REQUIRES TRANSPORTER TO ENTER CELL; convertion to serioeus of POLYGLUTAMATES which is critical for therapeutic action
Indications: solid tumors, some blood; rheumatoid arthritis, psoriasis
Adverse effects: mucositis, diarrhea, myelosuppression, defective oogenesis/spermatogenesis
Pharmacokinetics:
Administration: IV or oral (F is erratic)
Elimination: renal, modify dose in renal dysfx |
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Term
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Definition
Class: cancer, antimetabolite, rescue
Mechanism: bypasses DHFR and serves as THF substitute, rescues normal cells from MTX effects
Indications: high dose MTX chemotherapy, accidental overdose |
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Term
| 6-mercaptopurine (6-MP, purinethol) |
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Definition
Class: cancer, antimetabolite, purine analog
Mechanism: analog of purine (A&G), inhibit de novo purine syntehsis and become incorporated into DNA/RNA; REQUIRES HGPRT ENZYME FOR CONVERSION TO ACTIVE FORM (resistance due to deficiency of HGPRT)
Indications: blood cancers (AML, ALL)
Adverse effects: myelosuppression, hepatotoxicity, hyperuricemia (allopurinol to decrease)
Pharmacokinetics:
Administration: oral (10-50%, first pass effect) and IV
Elimination: hepatic |
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Term
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Definition
Class: cancer, antimetabolite, pyrimidine analog
Mechanism: [DUAL] inhibits ribonucleotide reductase (RNR), depletes deoxyribonucleotides, inhibits incorportation of dCTP into DNA by DNA polymerase; active form dFdCTP/dFdCDP
Indication: solid tumorss, some blood cancers
Adverse effects: nausea, vomit, myelosuppression, pulmonary toxicity
Pharmacokinetics:
Administration: IV only |
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Term
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Definition
Class: cancer, antimetabolite, pyrimidine analog
Mechanism: inhibits thymidylate synthase (TS), inhibits conversion dUMP to TMP, thymidine depletion, inhibition of DNA synthesis, enhances incorporation of FdUTP into DNA (DNA dysfx), enhances FUTP into RNA causing RNA alteration
resisted by decreased activation of drug, increased TS activity, mutant TS
Indications: solid tumors
Adverse effects: TOXICITY ENHANCED WITH LEUCOVORIN, SIGNIFICANT MUCOSITIS AND DIARRHEA (ESP. IF DIHYDROPYRIMIDINE DEHYDROGENASE DEFICIENT); SKIN HYPERPIGMENTATION
Pharmacokinetics:
Administration: IV
Metabolism: extensively by liver, dihydropyrimidine dehydrogenase |
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Term
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Definition
Class: cancer, antimetabolite, pyrimidine analog
Mechanism: oral pro-drug of 5-FU, liver metabolizes to 5-FU (several enzymes), inhibits thymidylate synthase (TS)
Indication: solid tumors
Adverse effects: nothing special
Pharmacokinetics:
Administration: oral (70-80%) |
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Term
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Definition
Class: cancer, antimetabolite, pyrimidine analog
Mechanism: activated by kinases, incorporates into DNA and inhibits incorporation of dCTP into DNA by DNA polymerase, inhibits chain elongation/synthesis/repair, inhibits RNR
resisted by cytidine deaminase
Indications: blood cancers (AML, ALL, CLL in blast crisis); MOST COMMON ANTIMETABOLITE USED FOR AML
Adverse effects: nothing special
Pharmacokinetics:
Administration: IV (high cytidine deaminase in GI)
Distribution: taken into cell via carrier, must be phosphorylated for activity |
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Term
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Definition
Class: cancer, antimetabolite, pyrimidine analog
Mechanism: inhibition of RNR, prevents conversion to deoxyribonucleotides
resisted by increased RNR synthesis
Indication: CML, melanomas, sickle-cell disease
Adverse effects: nothing special
Pharmacokinetics:
Administration: oral (80-100%)
Elimination: renal, adjust dose for renal dysfx |
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Term
| alkylating agent common features |
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Definition
MOA: transfer alkyl group to N7 of guanine; causes miscoding (abnormal base pairing), depurination (DNA stran breaks), and DNA cross-linking
Best during G1 and S, but not specific to
Carcinogenic, inc. risk of 2* malignancies esp. AML |
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Term
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Definition
Class: cancer, akylating agent
Mechanism: akylates N7 of guanine; causes miscoding, DNA strand breaks and DNA cross-linking; bis-alkylates; PRO DRUG metabolized to active form by P450 system
Indication: solid tumor, blood cancer, severe rheumatoid arthritis, multiple sclerosis
Adverse effects: FANCOLI-LIKE SYNDROME IN KIDNEYS (DELAYED)
Pharmacokinetics:
Administartion: oral (high F) or IV |
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Term
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Definition
Class: cancer, organosulfur, akylating agent rescue
Mechanism: detoxifies urotoxic metabolites of cancer drugs (cyclophosphamide) by rxn of its sulfhydryl group with the toxic drugs vinyl group
Indication: reduce incidence of hemorrhagic cytsitis and hematuria in pt on chemo (cyclophosphamide) |
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Term
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Definition
Class: cancer, alkylating agent
Mechanism: alkylates N7 of guanine, causes cross link of DNA
Indication: multiple myeloma, breast cancer, ovarian cancer
Adverse effects: myelosuppression (dec. WBC, dec. platelet, 2* malignancy leukemia)
Pharmacokinetics:
Administration: oral or IV |
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Term
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Definition
Class: cancer, akylating-like agent, platinum analog
Mechanism: form intra- and inter-strand DNA cross-links; inhibits DNA synthesis and fx; bind N7 of guanine primarily also some N3 adenine and O6 cysteine
Indications: broad range of solid tumors
Adverse effects: NEPHROTOXICITY
Pharmacokinetics:
Administration: IV, w/ saline to hydrate
Elimination: renal, modify dose for renal dysfx |
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Term
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Definition
Class: cancer, alkylating-like agent, platinum analog
Mechanism: form intra- and inter-strand DNA cross-links; inhibit DNA synthesis and fx; bind N7 guanine primarily but also N3 adenine and O6 cysteine
Indication: broad range of solid tumors, refractory hematologic cancers
Adverse effects: MYELOSUPPRESION (dose-limiting), less renal toxicity |
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Term
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Definition
Class: cancer, alkylating-like agent, platinum analog
Mechanism: form intra- and inter-strand DNA cross-links; inhibits DNA synthesis and fx; binds N7 guanine primarily but also N3 adenine and O6 cysteine
Indications: broad range solid tumors
Adverse effects: myelosuppresion, peripheral sensory neuropathy, diarrhea |
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Term
| akylating-like agent common features |
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Definition
platinum analogs
synergize w/ akylating drugs, fluoropyrimidines, taxanes
MOA: form intra- and inter-strand DNA cross-links; inhibits DNA synthesis and function
binds to N7 of guanine but also can interact w/ N3 adenine and O6 of cysteine |
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Term
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Definition
Class: cancer, cytotoxic antibiotic
Mechanism: glycopeptide with DNA binding region and iron-binding domain at opposite ends, causes single and double strand breaks after free-radical formation, INTERCALATIVE BINDING of bithaizole helps breakage, CELL CYCLE SPECIFIC G2 accumulation
Indication: blood and solid tumors
Adverse effects: RAYNAUD'S PHENOMENON
Pharmacokinetics:
Administration: subq, IM, IV
Elimination: renal, adjust dosage for renal dysfx |
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Term
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Definition
Class: cancer, cytotoxic antibiotic
Mechanism: polypeptide abx, inhibit transcription by binding DNA at transcription initiation complex and prevent elongation of RNA chain by RNA polymerase; may be metabolized to free-radical and cause single strand breaks
Indication: Wilms', Ewings', rhabdomyosarcoma, gestational trophoblastic, malignant mole
Adverse effects: myelosuppression |
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Term
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Definition
Class: cancer, anthracycline
Mechanism: inhibit topoisomerase II; bind via intercalation to DNA causing block of synthesis of DNA/RNA and DNA strand scission; generates free radicals
Indication: solid and blood tumors
Adverse effects: cariotoxicity (thought to be due to the free radicals)
Pharmacokinetics:
Administration: IV, in comb with other anticancer drugs
Metabolism: hepatic (reduce dose in dysfx)
Excretion: 50% biliary, 50% renal; urine may turn bright red |
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Term
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Definition
Class: cancer, anthracycline
Mechanism: inhibit topoisomerase II; bind DNA via intercalation causing block of synthesis of DNA/RNA and DNA strand scission; generates free radicals
Indications: mainly AML and ALL (limited effect in solid tumors)
Adverse effects: cardiotoxicity |
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Term
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Definition
Class: cancer, microtubule inhibitor, vinca alkaloid
Mechanism: inhibit tubulin polymerization, disrupts assembly of microtubules, mitotic arrest in M phase
resisted by drug efflux
Indication: ALL, Hodgkin's and non-Hodgkin's, rhabdomyosarcoma, neuroblastoma, Wilms'
Adverse Effects: NEUROTOXICITY w/ peripheral neuropathy, VESICANT
Pharmacokinetics:
Metabolism: P450
Excretion: feces, dose modification if liver dysfx |
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Term
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Definition
Class: cancer, microtubule inhibitor, vinca alkaloids
Mechanism: inhibit tubulin polymerization, disrupts assembly of microtubules, mitotic arrest in M phase
resisted by drug efflux
Indications: Hodgkin's, non-Hodgkin's, germ cell cancer, breast, Kaposi's
Adverse effects: NEUROTOXICITY, vesicant, myelosuppresion
Pharmacokinetics:
Metabolism: P450
Excretion: feces, adjust dose in liver dysfx |
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Term
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Definition
Class: cancer, microtubule inhibitor, taxane
Mechanism: enhance tubulin polymerization and promote assembly, in absence of microtubule-assoc. proteins results in inhibition of mitosis and cell division
Indication: broad range of solid tumors
Adverse effects: HYPERSENSTIVITY, PERIPHERAL SENSORY NEUROPATHY, MYALGIA, ARTHALGIA, HAND-FOOT SYNDROME
Pharmacokinetics:
Metabolism: P450
Excretion: feces, dose adjustment in hepatic dysfx |
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Term
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Definition
Class: cancer, microtubule inhibitor, taxane
Mechanism: enhance tubulin polymerization and promote assembly, in absence of microtubule-assoc. proteins this causes inhibition of mitosis and cell division
Indication: breast cancer, other solid cancers
Adverse effects: NEUROTOXICITY
Pharmacokinetics:
Metabolism: P450
Excretion: feces, dose adjustment in liver dysfx |
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Term
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Definition
Class: cancer, topoisomerase I inhibitor
Mechanism: camptothecin analog, pro-drug, metabolite is 1000x more potent, inhibit topoisomerase I and cause single strands cuts in DNA (damage)
Indication: colorectal ca (w/ 5-FU and leucovorin), GE ca, non-small cell lung ca
Adverse effect: MYELOSUPPRESION AND DIARRHEA
Pharmacokinetics:
Excretion: bile and feces, dose reduction in liver dysfx |
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Term
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Definition
Class: drug, topoisomerase II inhibitor
Mechanism: inhibits topo II, results in double DNA strand cuts and damage
Indication: non-small cell ung, non-Hodgkin's, gastric ca, germ cell, breast and lymphomas
Adverse effects: MYELOSUPPRESSION, SECONDARY MALIGNANCIES
Pharmacokinetics:
Administration: IV and oral (50%)
Excretion: 30-50% urine, dose reduction in renal dysfx |
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Term
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Definition
Class: cancer, target therapy, chemical inhibitor, protein kinase inhibitor
Mechanism: inhibits BCR-ABL tyrosine kinase and other receptor kinase
Indication: CML, GI stromal tumor, Philadelophia chromosome ALL
Adverse effect: MYELOSUPPRESION, GI, SKIN, FLUID RETENTION W/ ANKLE AND PERIORBITAL EDEMA
Pharmacokinetics:
Administration: oral
Metabolism: liver, CYP3A4
Excretion: feces |
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Term
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Definition
Class: cancer, targeted therapy, chemical inhibitor, protein kinase inhibitor
Mechanism: small molecule inhibitor of tyrosine kinase domain assoc. with EGFR
Indication: non-small cell lung ca, pancreatic cancer
Adverse effects: nothing special
Pharmacokinetics:
Administration: oral
Metabolism: CYP3A4
Excretion: feces |
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Term
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Definition
Class: cancer, targeted therapy, chemical inhibitor, protein kinase inhibitor
Mechanism: competitive bind ATP-binding pocket of target protein kinases, active against ALK kinase activity of non-small cell lung ca
Indication: non small cell carcionoma
Adverse effects: Trails from lights in peripheral vision in low light conditions
Pharmacokinetics:
Administration: oral |
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Term
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Definition
Class: cancer, targeted, mTOR inhibitors
Mechanism: bind to its protein receptor FKBP12 which directly interacts with mTORC1 inhibiting its downstream signaling
Indication: RCC, ER+/HER2- breast cancer, immunosuppressant in organ transplants
Adverse effects: lung/breathing problems, nothing special
Pharmacokinetics:
Administration: oral
Metabolism: hepatic CYP3A4 |
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Term
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Definition
Class: cancer, targeted, chemical inhibitors, mTOR inhibitors
Mechanism: binds to FBKP12 which directly interacts with mTORC1 leading to inhibition of its down stream signaling
Indication: RCC, breast ca
Adverse effects: fatigue
Pharmacokinetics:
Administration: IV
Metabolism: hepatic, CYP3A4 |
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Term
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Definition
Class: cancer, targeted, chemical inhibitor, epigenetic pathway inhibition
Mechanism: incorporates into DNA, inhibits DNMT (DNA methyltransferases); incorporates into RNA, inhibits protein synthesis
Indication: MDS, HIV, HTLV
Adverse effects: nothing special
Pharmacokinetics:
Administration: IV or subq |
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Term
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Definition
ClasS: cancer, targeted, chemical inhibitor, epigenetic pathway inhibitor
Mechanism: deoxy derivative of azacitidine, incorporates to DNA only, inhibits DNMT
Indication: MDS, AML
Adverse effects: nothing special
Pharmacokinetics:
Administration: IV or subq |
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Term
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Definition
Class: cancer, targeted, chemical inhibitor, epigenetic pathway inhibitor
Mechanism: binds active site of HDAC (histone deacetylase) and inhibits its, chelates zinc found in active site of HDAC
Indication: cutaneous T cell lymphoma (CTCL) - first HDAC inhibitor approved
Adverse effects: edema, fatiue, GI, proteinuria
Pharamacokinetics:
Administration: oral w/ food 1x/d |
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Term
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Definition
Class: cancer, targeted, chemical inhibitors, proteasome inhibitor
Mechanism: boron atom binds to catalytic site of 26S proteasome (high affinity and specificity), prevents degradation of pro-apoptotic factors, thus more activation of cell death in cells that try to suppress it
Indication: MULTIPLE MYELOMA, MANTLE CELL LYMPHOMA
Adverse effects: PERIPHERAL NEUROPATHY, GI EFFECTS (C,N)
Pharmacokinetics:
Administration: IV only |
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Term
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Definition
Class: cancer, targeted, hormone therapy
Mechanism: pro-drug metabolized by P450 to more active form; SERM, antagonist (partial agonist) at estrogen receptor, prevents growth of hormone-denpendent cancers
Indication: ER+ breast cancer, McCune-Albright infertility, gynecomastia, bipolar disorder
Adverse effects: increased risk of endometrial cancer
Pharmacokinetics:
Administration: oral |
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Term
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Definition
Class: cancer, targeted, hormone therapy
Mechanism: SERM, partial agonist; antagonises estrogen activation; lowers growth signals to hormone-dependent cancer cells
Indication: ER+ breast cancer, prevent osteoporosis in post-menopausal women
Adverse effects: (no inc. risk of endo ca), nothing else special
Pharmacokinetics:
Administration: oral |
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Term
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Definition
Class: cancer, targeted, hormone therapy
Mechanism: reversible competitive inhibition of aromatase, inhibits conversion of androgens to estrogen in peripheral tissues, inhibits synthesis of estrogen
Indication: ER+ breast cancer (postmenopausal)
Adverse effects: joint pain, etc. LESS THAN TAMOX AND RALOX
Pharmacokinetics:
Administration: oral |
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Term
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Definition
Class: cancer, targeted, hormone therapy
Mechanism: non-steroidal, antagonist at androgen receptor, prevents testosterone from stimulating cancer cells to grow
Indication: prostate cancer, excess androgen levels in women (PCOS)
Adverse effects: gynecomastia, liver injury, GI stuff
Pharmacokinetics:
Administration: oral |
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Term
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Definition
Class: cancer, targeted, hormone therapy
Mechanism: GnRH and LH-RH analog; desensitizes GnRH receptors, downreuglates secretion of LH and FSH, causes reduction in estradiol and testosterone levels
Indication: Hormone responseive cancers (prostate, breast), estrogen-dependent conditions (endometriosis, fibroids), percocious puberty, control IVF; chronic adrenal disease, steroid abuse
Adverse effects: bone pain, gynecomastia, hematuria, impotence, testicular atrophy
Pharmacokinetics:
Administration: slow-release implant or subq/IM |
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Term
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Definition
Class: cancer, targeted, hormone therapy
Mechanism: prodrug, androgen production inhibitor, inhibits 17a-hydroxylase (CYP17A1) found in testicular/adrenal/prostatic tumors, decreases circulating levels of testosterone
Indication: castration resistant prostate cancer
Adverse effects: URINARY TRACT INFECTION
Pharmacokinetics:
Administration: oral w/ food
Metabolism: cleaved by plasma esterases to active form |
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Term
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Definition
Class: cancer, targeted, hormone therapy
Mechanism: prodrug, glucocorticoid receptor agonist, most commonly prescribed glucocorticoid in cancer, inhibits luekocyt infiltration of site of inflammation, suppresion of hormonal and inflammatory mediator responses
Indication: blood cancers, hormone sensitive cancers; asthma, rheumatic disorders, allergies, UC, crohn's, adrenocortical insufficiency
Adverse effects: CUSHING-LIKE SYNDROME
Pharmacokinetics:
Administration: oral
Metabolism: converted by liver to active form |
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Term
| ATRA (all-trans retinoic acid) |
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Definition
Class: cancer, targeted, hormone therapy
Mechanism: inhibits the binding of PML-RARAa (fusion protein) to DNA, thus promoting transcription and differentiation of granulocytes
Indication: APL with the PML-RARa fusioni protein (95% of cases); acne tx
Adverse effects: retinoid acid syndrome (fever, wt gain, resp distresss, pleural effusion, pulm infiltrates, rapid inc WBC)
Pharmacokinetics:
Administration: oral |
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Term
| sipuleucel-T (Dendreon's provenge) |
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Definition
Class: cancer, targeted, immunotherapy, cell-based
Mechanism: "canver vaccine", remove immune cells, activate cells specific to cancer, grow and return to patient [NK cells, lymphokine-activated killer cells, CTLs, dendritic cells]
Indication: prostate ca |
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Term
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Definition
Class: cancer, targeted, immunotherapy, antibody
Mechanism: monoclonal Ab that targets VEGF-A, binds and inhibits signaling, inhibits tumor vascular permeability, enhance blood floow and drug delivery
Indication: colorectal, breast, non-small cell lung, renal cell
Adverse effects: HTN, infusion rxn, arterial thromboembolic, GI perf, wound healing comp, proteinuria
Pharmacokinetics:
Administration: IV only |
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Term
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Definition
Class: cancer, targeted, immunotherapy, antibody
Mechanism: monoclonal Ab that interferes with HER2/neu receptor, and blocks growth signals from the receptor, reduces proliferation
Indication: HER-2(+) breast cancer (70% don't respond)
Adverse effects: CARDIAC DYSFUCTION IN 2-7%
Pharmacokinetics:
Administration: IV only |
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Term
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Definition
Class: cancer, targeted, immunotherapy, antibody
Mechanism: chimeric monoclonal Ab aginst extracellular domain of EGFR, inhibits downstream signaling and enhances response to chemo and radiation
Indication: wild-type KRAS, colorectal, head&neck, non-small cell
Adverse effects: SKIN RASH
Pharmacokinetics:
Administration: IV only |
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Term
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Definition
Class: cancer, targeted, immunotherapy, antibody
Mechanism: chimeric monoclonal Ab to CD20, forms cap and draws proteins to one side of cell, enhances NK killing of cancer cells
Indication: Blood Cancers, rheumatoid arthritis, anti-rejection for organ transplants
Adverse effects: SEVERE INFUSION REACTION
Pharmacokinetics"
Administration: IV only |
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Term
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Definition
Class: cancer, targeted, immunotherapy, antibody
Mechanism: monoclonal Ab that binds to CTLA4, blocks the inhibitory signal of CTLA4 and allows CTLs to destroy cancer cells
Indication: melanoma, small and non-small cell lung, prostate
Adverse effects: immune related - fever, rash, colitis
Pharmacokinetics:
Administration: IV only |
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Term
| T-DM1 (traxtuzumab emtansine) |
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Definition
Class: cancer, targeted, immunotherapy, conjugated antibody
Mechanism: targets HER2 protein attached to chemo drug (microtubule-destabilizing)
Indication: advanced HER2(+) breast cancer
Adverse effects: fever, chills, HA, nausea, vomit, diarrhea, rash
Pharmacokinetics:
Administration: IV only |
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Term
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Definition
Class: cancer, targeted, immunotherapy, cytokine
Mechanism: promotes anti-tumor effects of immune system, increases MHC expression and increase effector T and NK cells
Indication: hairy-cell leuk, AIDS Kaposi, follicular lymphoma, CML, melanoma
Adverse effects: flu-like symptoms
Pharmacokinetics:
Administration: IM or subq |
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Term
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Definition
Class: cancer, targeted, immunotherapy, cytokine
Mechanism: enhances T-cell response against tumor cells
Indication: renal cell, melanoma
Adverse effects: capillary leak syndrome, fever, renal/liver failure
Pharmacokinetics:
Administration: IV or subq |
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Term
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Definition
Class: cancer, combination therapy
Mechanism: cyclophosphamide, hydroxydaunorubicin, oncovin (vincristine), prenisone; MAXIMIZE KILLING, MINIMIZE RESISTANCE, MINIMIZE TOXICITY |
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