In recent years, there has been increasing evidence that chemotherapy for malignant gliomas has entered the “era of temozolomide”. Temozolomide, first synthesized by Steven, is an alkylating agent containing an imidazotetrazine ring as an antitumor drug. It is not active in itself, but is a precursor drug that must be converted to the active compound MITC (5-(3-methyltriazen-1-yl)imidazole-4-amide) by a non-enzymatic pathway at physiological levels of PH, which is further hydrolyzed to an active metabolite to show antitumor activity. Theoretically, the antitumor activity of MTIC is mainly produced by the action of alkylation with the sixth oxygen atom of guanine, as well as secondary additional alkylation with the seventh nitrogen atom of guanine, with subsequent cytotoxicity associated with the repair of these aberrant methyl compounds. Temozolomide has been used in the experimental treatment of gliomas since the early 1990s. A multicenter clinical trial summarized by Stupp et al. showed that radiotherapy + temozolomide resulted in a median survival of 14.6 months for patients with glioblastoma, a significant advantage compared to the efficacy of radiotherapy alone. Subsequently, Hegi et al. found that silencing of the DNA repair gene MGMT resulted in significantly longer survival in patients with glioblastoma treated with temozolomide, thus opening a new era of predicting temozolomide efficacy and tumor prognosis by targeted genetic testing. For patients whose MGMT gene is not silenced by methylation, another pathway is needed to improve the efficacy of chemotherapy; MGMT gene silencing does not prevent the development of tumor resistance and recurrence. Another rapidly advancing drug for malignant glioma is bevacizumab, a targeted agent for vasoactive endothelial factor (VEGF), and promising results were found in a 2005 Stark-Vance clinical trial combining bevacizumab and irinotecan for the treatment of recurrent malignant glioma. In several recent studies it was also possible to find that the combination of these two drugs could provide significant advantages over conventional chemotherapy regimens in terms of PFS6 and imaging changes. Notably, serious side effects such as intracranial hemorrhage, thrombosis and intestinal perforation have been reported in very few patients with this regimen. The anti-tumor mechanism of bevacizumab includes targeted inhibition of high VEGF expression in glioblastoma, anti-tumor angiogenesis disorder thus facilitating chemotherapeutic drug penetration and inhibition of tumor stem cell growth. The cytotoxic drug irinotecan also has a place in current chemotherapy regimens for malignant gliomas. It is a topoisomerase-1 inhibitor that was approved by the FDA in 1994 for use primarily in adjuvant combination chemotherapy for colon cancer. Since Friedman et al. first used irinotecan for malignant glioma in 1999, irinotecan has been used in combination with temozolomide and bevacizumab respectively, and the effects have been initially evaluated and confirmed. A better result was obtained in the same type of study by Zuniga et al. with a median PFS of 7.6 months, PFS6 of 63.7%, 6-month OS of 78% and 12-month OS of 42.6% in glioblastoma. Platinum agents also play a role in the adjuvant chemotherapy of malignant gliomas. Platinum agents in the 2010 NCCN guidelines refer mainly to cisplatin and carboplatin, both of which are rarely used alone in the chemotherapy of malignant gliomas, and there is evidence that platinum agents are not more effective than nitrosoureas. It is worth noting that the combination of platinum agents brings superimposed toxicity and should be evaluated for patient tolerability before application. There are reports of local chemotherapy with platinum encapsulation for glioblastoma with a median OS of 427.5 days, which is 1-fold more than the surgery+radiotherapy group alone, and a significant difference between the two; local agents are also more easily tolerated than systemic agents.