Know your oncology drugs

What type of anticancer agent, what drug class & important detail

Cytarabine

Chemotherapy

Antimetabolite

Interfere with DNA and RNA by acting as a substitute for the normal building blocks of DNA and RNA. When this happens, the DNA cannot make copies of itself, and cells cannot reproduce. Active in S phase (synthesis phase)

Cell-cycle-specific: S phase

Fludarabine

Chemotherapy

Antimetabolite

Interfere with DNA and RNA by acting as a substitute for the normal building blocks of DNA and RNA. When this happens, the DNA cannot make copies of itself, and cells cannot reproduce. Active in S phase (synthesis phase)

Cell-cycle-specific: S phase

Methotrexate

Chemotherapy

Antimetabolite

Interfere with DNA and RNA by acting as a substitute for the normal building blocks of DNA and RNA. When this happens, the DNA cannot make copies of itself, and cells cannot reproduce. Active in S phase (synthesis phase)

Cell-cycle-specific: S phase

Hydroxyurea

Chemotherapy

Antimetabolite

Interfere with DNA and RNA by acting as a substitute for the normal building blocks of DNA and RNA. When this happens, the DNA cannot make copies of itself, and cells cannot reproduce. Active in S phase (synthesis phase)

Cell-cycle-specific: S phase

Azacitidine

Chemotherapy

Antimetabolite

DNA-methyltransferase inhibitor that interferes with DNA and RNA by acting as a substitute for the normal building blocks of DNA and RNA. When this happens, the DNA cannot make copies of itself, and cells cannot reproduce. Active in S phase (synthesis phase)

Cell-cycle-specific: S phase

Vinblastine

Chemotherapy

Mitotic inhibitor - plant alkaloid - vinca alkaloid

Compound derived from natural products/plants. Works by stopping cells from dividing to form new cells. Active in M phase (mitosis or cell division phase)

Cell-cycle-specific: M phase

Vincristine

Chemotherapy

Mitotic inhibitor - plant alkaloid - vinca alkaloid

Compound derived from natural products/plants. Works by stopping cells from dividing to form new cells. Active in M phase (mitosis or cell division phase)

Cell-cycle-specific: M phase

Vinorelbine

Chemotherapy

Mitotic inhibitor - plant alkaloid - vinca alkaloid

Compound derived from natural products/plants. Works by stopping cells from dividing to form new cells. Active in M phase (mitosis or cell division phase)

Cell-cycle-specific: M phase

Docetaxel

Chemotherapy

Mitotic inhibitor - plant alkaloid - taxane

Compound derived from natural products/plants. Works by stopping cells from dividing to form new cells. Active in M phase (mitosis or cell division phase)

Cell-cycle-specific: M phase

Paclitaxel

Chemotherapy

Mitotic inhibitor - plant alkaloid - taxane

Compound derived from natural products/plants. Works by stopping cells from dividing to form new cells. Active in M phase (mitosis or cell division phase)

Cell-cycle-specific: M phase

Etoposide

Chemotherapy

Topoisomerase II inhibitor (Podophyllotoxin)

Interferes with topoisomerases, which help separate the strands of DNA. This blocks the ability of the cell to copy the DNA. Active in S (synthesis) and G2 phase

Cell-cycle-specific: S and G2 phases

Teniposide

Chemotherapy

Topoisomerase II inhibitor (Podophyllotoxin)

Interferes with topoisomerases, which help separate the strands of DNA. This blocks the ability of the cell to copy the DNA. Active in S (synthesis) and G2 phase

Cell-cycle-specific: S and G2 phases

Pegaspargase

Chemotherapy

Cause the chemical breakdown of amino acid “asparaginases” within cancerous cells. Active in G1 (preparatory phase)

Cell-cycle specific: G1 phase

Cyclophosphamide

Chemotherapy

Alkylating agent - nitrogen mustard

Stops the cell from reproducing (making copies of itself) by damaging its DNA. Because it damages DNA, they can affect the cells of the bone marrow, which make new blood cells.

Cell-cycle non-specific

Ifosfamide

Chemotherapy

Alkylating agent - nitrogen mustard

Stops the cell from reproducing (making copies of itself) by damaging its DNA. Because it damages DNA, they can affect the cells of the bone marrow, which make new blood cells.

Cell-cycle non-specific

Chlorambucil

Chemotherapy

Alkylating agent - nitrogen mustard

Stops the cell from reproducing (making copies of itself) by damaging its DNA. Because it damages DNA, they can affect the cells of the bone marrow, which make new blood cells.

Cell-cycle non-specific

Melphalan

Chemotherapy

Alkylating agent - nitrogen mustard

Stops the cell from reproducing (making copies of itself) by damaging its DNA. Because it damages DNA, they can affect the cells of the bone marrow, which make new blood cells.

Cell-cycle non-specific

Bendamustine

Chemotherapy

Alkylating agent - nitrogen mustard

Stops the cell from reproducing (making copies of itself) by damaging its DNA. Because it damages DNA, they can affect the cells of the bone marrow, which make new blood cells.

Cell-cycle non-specific

Carmustine

Chemotherapy

Alkylating agent - nitrosourea

Stops the cell from reproducing (making copies of itself) by damaging its DNA. Because it damages DNA, they can affect the cells of the bone marrow, which make new blood cells.

Cell-cycle non-specific

Lomustine

Chemotherapy

Alkylating agent - nitrosourea

Stops the cell from reproducing (making copies of itself) by damaging its DNA. Because it damages DNA, they can affect the cells of the bone marrow, which make new blood cells.

Cell-cycle non-specific

Busulfan

Chemotherapy

Alkylating agent

Stops the cell from reproducing (making copies of itself) by damaging its DNA. Because it damages DNA, they can affect the cells of the bone marrow, which make new blood cells.

Cell-cycle non-specific

Procarbazine

Chemotherapy

Alkylating agent

Stops the cell from reproducing (making copies of itself) by damaging its DNA. Because it damages DNA, they can affect the cells of the bone marrow, which make new blood cells.

Cell-cycle non-specific

Daunorubicin

Chemotherapy

Anti-tumour antibiotic - anthracycline

Anti-tumour antibiotic that binds with DNA so it cannot make copies of itself, and a cell cannot divide. Anthracyclines can cause significant and permanent cardiac damage if given in high doses. For this reason, lifetime dose limits (cumulative dose) are placed on these drugs.

Cell-cycle non-specific

Doxorubicin

Chemotherapy

Anti-tumour antibiotic - anthracycline

Anti-tumour antibiotic that binds with DNA so it cannot make copies of itself, and a cell cannot divide. Anthracyclines can cause significant and permanent cardiac damage if given in high doses. For this reason, lifetime dose limits (cumulative dose) are placed on these drugs.

Cell-cycle non-specific

Idarubicin

Chemotherapy

Anti-tumour antibiotic - anthracycline

Anti-tumour antibiotic that binds with DNA so it cannot make copies of itself, and a cell cannot divide. Anthracyclines can cause significant and permanent cardiac damage if given in high doses. For this reason, lifetime dose limits (cumulative dose) are placed on these drugs.

Cell-cycle non-specific

Bleomycin

Chemotherapy

Anti-tumour antibiotic

Anti-tumour antibiotic that binds with DNA so it cannot make copies of itself, and a cell cannot divide.

Cell-cycle non-specific

Cisplatin

Chemotherapy

Platinum agent

Stops the cell from reproducing (making copies of itself) by damaging its DNA. Because it damages DNA, they can affect the cells of the bone marrow, which make new blood cells.

Cell-cycle non-specific

Carboplatin

Chemotherapy

Platinum agent

Stops the cell from reproducing (making copies of itself) by damaging its DNA. Because it damages DNA, they can affect the cells of the bone marrow, which make new blood cells.

Cell-cycle non-specific

Oxaliplatin

Chemotherapy

Platinum agent

Stops the cell from reproducing (making copies of itself) by damaging its DNA. Because it damages DNA, they can affect the cells of the bone marrow, which make new blood cells.

Cell-cycle non-specific

Dactinomycin

Chemotherapy

Anti-tumour antibiotic

Complexes with DNA interfering with DNA-dependent RNA synthesis; also has immunosuppressant properties.

Cell-cycle non-specific

Apalutamide

Hormonal anticancer drug

Androgen receptor pathway inhibitor (ARPI) anti-androgen (second-generation)

Competitively inhibits the binding of androgen at androgen receptors, decreasing the production of testosterone and dihydrotestosterone and thus halting the growth of prostate cancer

Darolutamide

Hormonal anticancer drug

Androgen receptor pathway inhibitor (ARPI) anti-androgen (second-generation)

Competitively inhibits the binding of androgen at androgen receptors, decreasing the production of testosterone and dihydrotestosterone and thus halting the growth of prostate cancer

Enzalutamide

Hormonal anticancer drug

Androgen receptor pathway inhibitor (ARPI) anti-androgen (second-generation)

Competitively inhibits the binding of androgen at androgen receptors, decreasing the production of testosterone and dihydrotestosterone and thus halting the growth of prostate cancer

Bicalutamide

Hormonal anticancer drug

Androgen receptor pathway inhibitor (ARPI) anti-androgen (first-generation)

Competitively inhibits the binding of androgen at androgen receptors, decreasing the production of testosterone and dihydrotestosterone and thus halting the growth of prostate cancer; used as a ‘bridge’ to protect against testosterone flare during GnRH agonist ADT (Androgen Deprivation Therapy).

Anastrozole

Hormonal anticancer drug

Aromatase inhibitor

Prevents the conversion of testosterone and androstenedione to estriol and estradiol by inhibiting the action of aromatase enzymes, thus reducing the concentration of oestrogen

Exemestane

Hormonal anticancer drug

Aromatase inhibitor

Prevents the conversion of testosterone and androstenedione to estriol and estradiol by inhibiting the action of aromatase enzymes, thus reducing the concentration of oestrogen

Letrozole

Hormonal anticancer drug

Aromatase inhibitor

Prevents the conversion of testosterone and androstenedione to estriol and estradiol by inhibiting the action of aromatase enzymes, thus reducing the concentration of oestrogen

Goserelin

Hormonal anticancer drug

GnRH agonist (LHRH agonist)

Initially stimulates synthesis of FSH and LH, temporarily increasing serum testosterone in males or serum estrogen in females; continuous administration over time inhibits gonadotrophin production via over-stimulation, which ultimately suppresses testosterone and oestrogen to stop the growth of certain hormone-dependent tumours.

Leuprorelin

Hormonal anticancer drug

GnRH agonist (LHRH agonist)

Initially stimulates synthesis of FSH and LH, temporarily increasing serum testosterone in males or serum estrogen in females; continuous administration over time inhibits gonadotrophin production via over-stimulation, which ultimately suppresses testosterone and oestrogen to stop the growth of certain hormone-dependent tumours.

Triptorelin

Hormonal anticancer drug

GnRH agonist (LHRH agonist)

Initially stimulates synthesis of FSH and LH, temporarily increasing serum testosterone in males or serum estrogen in females; continuous administration over time inhibits gonadotrophin production via over-stimulation, which ultimately suppresses testosterone and oestrogen to stop the growth of certain hormone-dependent tumours.

Tamoxifen

Hormonal anticancer drug

Selective estrogen receptor modulator (SERM)

Estrogen antagonist in the breast (blocking the effects of estrogen), estrogen agonist in the endometrium, bone and lipids.

Abiraterone

Hormonal anticancer drug

CYP17 inhibitor androgen receptor pathway inhibitor (ARPI)

Inhibits CYP17, reducing androgen (testosterone and dihydrotestosterone) synthesis in testicular, adrenal and prostate tumour tissues

Degarelix

Hormonal anticancer drug

GnRH antagonist

Immediately inhibits gonadotrophin production, suppressing testicular androgen (testosterone and dihydrotestosterone) synthesis.

Relugolix

Hormonal anticancer drug

GnRH antagonist

Immediately inhibits gonadotrophin production, suppressing testicular androgen (testosterone and dihydrotestosterone) synthesis.

Fulvestrant

Hormonal anticancer drug

Anti-estrogen

Competitively binds to estrogen receptors resulting in their down-regulation. Inhibits the growth of estrogen receptor-positive tumours

Afatinib

Targeted therapy

Second-generation epidermal growth factor receptor (EGFR) inhibitor, human epidermal growth factor receptor (HER) 2 and 4 kinase inhibitor

Abemaciclib

Targeted therapy

Cyclin-dependent kinases (CDK) 4 and 6 inhibitor

Alectinib

Targeted therapy

Anaplastic lymphoma kinase (ALK) receptor inhibitor

Adverse effects include myalgia.

Binimetinib

Targeted therapy

Mitogen-activated extracellular kinases (MEK) 1 and 2 inhibitor

Brigatinib

Targeted therapy

Anaplastic lymphoma kinase (ALK) receptor inhibitor

Adverse effects include interstitial lung disease and other pulmonary events, managed by 7 day low dose lead-in titration to full dose, important to do again if the patient has taken a break from the drug and is to restart)

Capivasertib

Targeted therapy

AKT inhibitor

Cobimetinib

Targeted therapy

Mitogen-activated extracellular kinases (MEK) 1 and 2 inhibitor

Dabrafenib

Targeted therapy

BRAF inhibitor

Encorafenib

Targeted therapy

BRAF inhibitor

Entrectinib

Targeted therapy

ROS1, tropomyosin receptor kinases (TRK proteins; arise from the NTRK gene) and anaplastic lymphoma kinase (ALK) receptor inhibitor

Gefitinib

Targeted therapy

First-generation epidermal growth factor receptor (EGFR) inhibitor

Erlotinib

Targeted therapy

First-generation epidermal growth factor receptor (EGFR) inhibitor

Lapatinib

Targeted therapy

Epidermal growth factor receptor (EGFR) inhibitor and human epidermal growth factor receptor (HER) 2 kinase inhibitor

Vemurafenib

Targeted therapy

BRAF V600 E and V600 K inhibitor

Trametinib

Targeted therapy

Mitogen-activated extracellular kinases (MEK) 1 and 2 inhibitor

Sorafenib

Targeted therapy

VEGFR 2–3, PDGFR, c‑Kit, FLT‑3 and Raf kinase inhibitor

Selumetinib

Targeted therapy

Mitogen-activated extracellular kinases (MEK) 1 and 2 inhibitor

Ribociclib

Targeted therapy

Cyclin-dependent kinases (CDK) 4 and 6 inhibitor

Palbociclib

Targeted therapy

Cyclin-dependent kinases (CDK) 4 and 6 inhibitor

Osimertinib

Targeted therapy

Epidermal growth factor receptor (EGFR) inhibitor (including T790M mutation)

Lorlatinib

Targeted therapy

Anaplastic lymphoma kinase (ALK) receptor and ROS1 inhibitor

Adverse effects include hypercholesteremia and hypertriglyceridemia (monitor and manage with statins), cognition and mood deterioration

Ceritinib

Targeted therapy

Anaplastic lymphoma kinase (ALK) receptor inhibitor

Crizotinib

Targeted therapy

Anaplastic lymphoma kinase (ALK) receptor, mitogen-activated extracellular kinases (MEK) and ROS1 inhibitor

Sotorasib

Targeted therapy

KRAS G12C mutation inhibitor

Tepotinib

Targeted therapy

MET inhibitor

Midostaurin

Targeted therapy

FLT-3, VEGFR-2, PDGFR, c-Kit and protein kinase C inhibitorf

Ibrutinib

Targeted therapy

Bruton’s tyrosine kinase inhibitors

Inhibit Bruton tyrosine kinase, a receptor that chronic lymphocytic leukemia cells (cancerous B cells) rely on for survival and proliferation. Adverse effects include bleeding and hemorrhage, cardiovascular effects, and infections.

Acalabrutinib

Targeted therapy

Bruton’s tyrosine kinase inhibitors

Inhibit Bruton tyrosine kinase, a receptor that chronic lymphocytic leukemia cells (cancerous B cells) rely on for survival and proliferation. Adverse effects include bleeding and hemorrhage, cardiovascular effects, and infections.

Zanubrutinib

Targeted therapy

Bruton’s tyrosine kinase inhibitors

Inhibit Bruton tyrosine kinase, a receptor that chronic lymphocytic leukemia cells (cancerous B cells) rely on for survival and proliferation. Adverse effects include bleeding and hemorrhage, cardiovascular effects, and infections.

Venetoclax

Targeted therapy

B cell lymphoma 2 (BCL-2) inhibitor

Binds to and inhibits the B cell lymphoma 2 (BCL‑2) protein, which is an anti-apoptotic protein that is over-expressed in certain tumour cells, triggering cell death