Which medications in the drug class Antineoplastics are used in the treatment of Brain Metastasis?

Updated: Aug 01, 2018
  • Author: Victor Tse, MD, PhD; Chief Editor: Nicholas Lorenzo, MD, MHA, CPE  more...
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 Antineoplastic agents are employed to reduce tumor burden and induce remission. Some agents may also reduce angiogenesis, and metastasis. Selection and use depends on systemic disease, tumor type, and stage


Platinum coordination compound that inhibits DNA synthesis, cross-links and denatures strands of DNA and disrupts DNA function by covalently binding to DNA bases


Metabolites interfere with malignant cell growth by cross-linking tumor cell DNA; non-cell cycle specific with potent immunosuppressive activity

Ifosfamide (Ifex)

Synthetic analog of cyclophosphamide.  Exerts its cytotoxic effect via alkylation of DNA, leading to interstrand and intrastrand DNA crosslinks, DNA-protein crosslinks, and inhibition of DNA replication

Temozolomide (Temodar)

Imidazotetrazine derivative prodrug whose active metabolite, the reactive compound 5-(3-methyltriazen-1-yl),imidazole-4-carboxamide (MTIC), methylates guanine-rich areas of DNA that initiate transcription, which leads to DNA double strand breaks and apoptosis

Etoposide (Toposar)

A glycosidic derivative of podophyllotoxin that exerts a cytotoxic effect by stabilizing the normally transient covalent intermediates formed between the DNA substrate and topoisomerase II. The drug leads to single-stranded and double-stranded DNA breaks that arrest cellular proliferation in the late S or early G2 phase of cell cycle.

Teniposide (Vumon)

Semisynthetic podophyllotixin derivative which inhibits topoisomerase II to cause DNA strand breaks by inhibiting DNA strand-passing and DNA ligase activity.,  Prevents cells from entering mytosis by delaying the transit of cells through the S phase and causing arrest in late S or early G2 phase of the cell cycle.


Anthracycline antibiotic which crosslinks DNA,,primarily with guanine and cytosine, preventing replication and transcription. Cell-cycle nonspecific but acts primarily against cells in late G and early S phases.

Irinotecan (Camptosar)

 Semisynthetic derivative of camptothecin, an alkaloid extract from the Camptotheca acuminate tree. Inactive in its parent form. Converted by the carboxylesterase enzyme to its active metabolite from, SN-38.SN-38 binds to and stabilizes the topoisomerase I-DNA complex and prevents the relegation of DNA after it has been cleaved by topoisomerase I, inhibiting DNA replication.

Vinorelbine (Navelbine)

Semi-synthetic vinca alkaloid which inhibits mitosis at metaphase by depolymerizing microtubules. Disrupts the mitotic spindle, causing the cell to arrest at metaphase. It is specific for the M and S phase of the cell cycle. By blocking glutamic acid utilization may also interfere with nucleic acid and protein synthesis

Fluorouracil (Adrucil)

Fluoropyrimidine analog. Cell cycle-specific with activity in the S-phase as single agent and has for many years been combined with biochemical modulator leucovorin. Has activity as single agent that inhibits DNA replication and transcription. Classic antimetabolite anticancer drug with chemical structure similar to endogenous intermediates or building blocks of DNA or RNA synthesis.

Capecitabine (Xeloda)

  Fluoropyrimidine carbamate prodrug form of 5-fluorouracil (5-FU). Capecitabine itself is inactive. Undergoes hydrolysis in liver and tissues to form the active moiety (fluorouracil), inhibiting thymidylate synthetase, which in turn blocks methylation of deoxyuridylic acid to thymidylic acid. This step interferes with DNA and to a lesser degree with RNA synthesis.

Gefitinib (Iressa)

EGF receptor is present on normal and cancer cells and plays a role in cell growth and proliferation. Gefitinib reversibly inhibits the kinase activity of wild-type and certain activating mutations of epidermal growth factor receptor (EGFR) preventing autophosphorylation of tyrosine residues associated with the receptor, thereby inhibiting further downstream signaling and blocking of EGFR-dependent proliferation

Erlotinib (Tarceva)

Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor; may also block angiogenesis and cellular proliferation. Erlotinib exhibits higher binding activity for EGR exon 19 deletion or exon 21 L858R mutations than for the wild type receptor. Causes apoptosis by inhibiting intracellular phosphorylation, which in turn prevents downstream signaling

Sorafenib (Nexavar)

Multikinase inhibitor  of intracellular ((CRAF, BRAF, and mutant BRAF) and cell surface (KIT, FLT-3, RET, RET/PTC, vascular endothelial growth factor receptor [VEGFR]-1, VEGFR-2, VEGFR-3, and platelet-derived growth factor receptor-beta) kinases. which  are involved in tumor angiogenesis, cell signaling and apoptosis

Sunitinib (Sutent)

  Sunitinib inhibits cellular signaling by targeting multiple receptor tyrosine kinases, such as platelet-derived growth factor receptors, and vascular endothelial growth factor receptors, which play a role in both tumor angiogenesis and tumor cell proliferation

Lapatinib (Tykerb)

Tyrosine kinase inhibitor, blocking phosphorylation of EGF-receptor and HER2 kinase, which in turn blocks the activation of downstream second messengers responsible for cell proliferation and survival in ErbB- and ErbB-expressing tumors., Indicated in combination with capecitabine for patients with advanced or metastatic breast cancer whose tumors overexpress HER2 and who have received prior therapy including anthracycline, a taxane, and trastuzumab

Vemurafenib (Zelboraf)

Inhibitor of some mutated forms of BRAF serine-threonine kinase, including BRAF V600E, reducing cellular proliferation; Also inhibits other kinases in vitro (eg CRAF, ARAF, wild-type BRAF, SRMS, ACK 1, MAP4K5, FGR) at similar concentrations

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