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      News & Perspective Drugs & Diseases CME & Education Academy Video Decision Point
      Drugs & Diseases > Oncology

      Glioblastoma Medication

      Updated: Mar 07, 2023
      • Author: Jeffrey N Bruce, MD; Chief Editor: Herbert H Engelhard, III, MD, PhD, FACS, FAANS  more...
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      Medication

      Medication Summary

      The alkylating agent temozolomide is used for treatment of newly diagnosed glioblastoma, and the monoclonal antibody bevacizumab is used for treatment of recurrences. In addition, several medications are used for supportive care. Vasogenic cerebral edema is typically managed with corticosteroids (eg, dexamethasone), usually in combination with some form of antiulcer agent (eg, famotidine).

      For seizures, the patient usually is started on levetiracetam, phenytoin, or carbamazepine. Levetiracetam is often used because it lacks the effects on the P450 system seen with phenytoin and carbamazepine, which can interfere with antineoplastic therapy. A guideline from the Society for Neuro-Oncology (SNO) and European Society of Neuro-Oncology (EANO) recommends against routine prophylaxis with antiepileptic drugs (AEDs) in patients with newly diagnosed brain tumors and found insufficient evidence to recommend prescribing AEDs to reduce the risk of perioperative or postoperative seizures in patients undergoing surgery for brain tumors. [298]

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      Antineoplastic agents

      Class Summary

      Although the optimal chemotherapeutic regimen for glioblastoma is not yet defined, several studies have suggested significant survival benefit from adjuvant chemotherapy.

      Temozolomide (Temodar)

      Oral alkylating agent converted to MTIC (3-methyl-(triazen-1-yl)imidazole-4-carboximide) at physiologic pH; 100% bioavailable; approximately 35% crosses the blood-brain barrier. Indicated for glioblastoma combined with radiotherapy.

      Carmustine (BiCNU)

      Alkylates and cross-links DNA strands, inhibiting cell proliferation. Used in glioblastoma and other brain tumors (including brain-stem gliomas, medulloblastomas, astrocytomas, ependymomas, and brain metastases), multiple myeloma, Hodgkin’s lymphoma, and non-Hodgkin’s lymphoma. Carmustine is lipophilic and readily crosses the blood-brain barrier.

      Bevacizumab (Alymsys, Avastin)

      Binds to vascular endothelial growth factor A (VEGF-A), preventing its interaction with VEGF receptor tyrosine kinases, thus inhibiting tumor cell growth. Indicated in metastatic colorectal cancer, non-squamous non-small cell lung cancer, cervical cancer, and glioblastoma. As a result of promising phase II clinical trials, single-agent bevacizumab gained accelerated approval from the FDA in 2009 for recurrent glioblastoma in patients who had failed other therapeutic options. More recent trials have yielded less encouraging results, however, and there is no consensus on the best bevacizumab regimen in recurrent glioblastoma. Trials involving patients with newly diagnosed glioblastoma have demonstrated that bevacizumab has no significant effect on survival, health-related quality of life, or neurocognitive function but may reduce glucocorticoid requirements. [312]

      Erlotinib (Tarceva)

      Pharmacologically classified as a human epidermal growth factor receptor type 1/epidermal growth factor receptor (HER1/EGFR) tyrosine kinase inhibitor. EGFR is expressed on the cell surface of normal cells and cancer cells. Indicated for locally advanced or metastatic non-small cell lung cancer after failure of at least one prior chemotherapy regimen. While EGFR is overexpressed in most glioblastomas, and 30% of glioblastomas have mutations that lead to constitutively active mutant EGFRvIII, numerous phase II clinical trials have demonstrated that erlotinib alone is likely insufficient in the treatment of glioblastoma. [313]

      Gefitinib (Iressa)

      An anilinoquinazoline indicated as monotherapy to treat locally advanced or metastatic non-small cell lung cancer after failure of both platinum-based and docetaxel chemotherapies. The mechanism is not fully understood, but gefitinib is an EGFR inhibitor that blocks tyrosine kinases responsible for intracellular phosphorylation associated with transmembrane cell surface receptors. As with erlotinib, gefinitib has been extensively explored in glioblastoma due to the frequency of constitutively active EGFR vIII mutations within glioblastoma, but clinical trials have not shown significant efficacy. [313]

      Lomustine (CCNU, Gleostine)

      Although its mechanism of action is not completely understood, lomustine causes inhibition of DNA and RNA synthesis resulting from carbamylation of DNA polymerase, alkylation of DNA, and alteration of RNA proteins. Despite limited evidence, use of lomustine in recurrent glioblastoma is increasing; lomustine alone is now commonly used as a control arm in clinical trials. Lomustine anti-tumor activity may be restricted to patients with MGMT promoter methylation. [314]

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      Anticonvulsants

      Class Summary

      These agents are used to treat and prevent seizures.

      Levetiracetam (Keppra)

      Used as adjunct therapy for partial seizures and myoclonic seizures. Also indicated for primary generalized tonic-clonic seizures. Mechanism of action is unknown.

      Phenytoin (Dilantin)

      Acts to block sodium channels and prevent repetitive firing of action potentials. As such, it is a very effective anticonvulsant. First-line agent in patients with partial and generalized tonic-clonic seizures.

      Carbamazepine (Tegretol)

      Like phenytoin, acts by interacting with sodium channels and blocking repetitive neuronal firing. First-line agent in patients with partial and tonic-clonic seizures. Serum levels should be checked and should be approximately 4-8 mcg/mL.

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      Corticosteroids

      Class Summary

      These agents reduce edema around the tumor, frequently leading to symptomatic and objective improvement.

      Dexamethasone (Decadron)

      Postulated mechanisms of action in brain tumors include reduction in vascular permeability, cytotoxic effects on tumors, inhibition of tumor formation, and decreased CSF production. Numerous in vitro, in vivo, and clinical trials have yielded conflicting results about the effect of dexamethasone on glioblastoma aggressiveness, but dexamethasone remains the preferred glucocorticoid option for glioblastoma-induced cerebral edema. [257]

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