Small molecule tyrosine kinase inhibitors (TKIs) are being explored as potential treatments for glioblastoma (GBM), a highly aggressive brain cancer with poor prognosis. This review summarizes the latest research on TKIs targeting various kinases, including ALK, AXL, DDR1, IGF1R, MER, c-MET, EGFR, PDGFR, VEGFR, FAK, JAK, LCK, SYK, Src, and DYRK1A. These inhibitors have shown promising preclinical activity in GBM models, with some entering clinical trials. ALK inhibitors like crizotinib, alectinib, and ceritinib have demonstrated efficacy in GBM, while AXL inhibitors such as bemcentinib have shown potential in combination with temozolomide (TMZ). DDR1 inhibitors, including DDR1-IN-1, have shown radiosensitization effects. IGF1R inhibitors like linsitinib have shown some efficacy in GBM. MER inhibitors, such as MRX2843 and UNC2025, have shown potential in reducing GBM cell growth and survival. c-MET inhibitors like capmatinib and tivantinib have shown activity in GBM. EGFR inhibitors, including osimertinib, afatinib, erlotinib, and gefitinib, have shown promise in GBM, with osimertinib being the most effective. PDGFR inhibitors like CP-673451 have shown potential in GBM. VEGFR inhibitors, such as VGB and voacangine, have shown anti-angiogenic effects. FAK inhibitors like PF573228 have shown potential in reducing GBM cell adhesion. JAK inhibitors like AG490 and ruxolitinib have shown potential in modulating GBM growth. LCK inhibitors like A-770041 have shown potential in reducing GBM cell growth. SYK inhibitors like BAY61-3606, piceatannol, and NVP-QAB205 have shown anti-inflammatory and anti-proliferative effects. Src inhibitors like KX2-361 and Si306 have shown potential in reducing GBM cell proliferation and inducing apoptosis. DYRK1A inhibitors like VER-239353 have shown potential in inducing cell cycle arrest. These TKIs are being evaluated in clinical trials, with some showing promising results in improving survival and reducing tumor growth in GBM patients. The review highlights the importance of targeting specific kinases in GBM and the potential of TKIs as a new class of therapeutic agents for this aggressive cancer.Small molecule tyrosine kinase inhibitors (TKIs) are being explored as potential treatments for glioblastoma (GBM), a highly aggressive brain cancer with poor prognosis. This review summarizes the latest research on TKIs targeting various kinases, including ALK, AXL, DDR1, IGF1R, MER, c-MET, EGFR, PDGFR, VEGFR, FAK, JAK, LCK, SYK, Src, and DYRK1A. These inhibitors have shown promising preclinical activity in GBM models, with some entering clinical trials. ALK inhibitors like crizotinib, alectinib, and ceritinib have demonstrated efficacy in GBM, while AXL inhibitors such as bemcentinib have shown potential in combination with temozolomide (TMZ). DDR1 inhibitors, including DDR1-IN-1, have shown radiosensitization effects. IGF1R inhibitors like linsitinib have shown some efficacy in GBM. MER inhibitors, such as MRX2843 and UNC2025, have shown potential in reducing GBM cell growth and survival. c-MET inhibitors like capmatinib and tivantinib have shown activity in GBM. EGFR inhibitors, including osimertinib, afatinib, erlotinib, and gefitinib, have shown promise in GBM, with osimertinib being the most effective. PDGFR inhibitors like CP-673451 have shown potential in GBM. VEGFR inhibitors, such as VGB and voacangine, have shown anti-angiogenic effects. FAK inhibitors like PF573228 have shown potential in reducing GBM cell adhesion. JAK inhibitors like AG490 and ruxolitinib have shown potential in modulating GBM growth. LCK inhibitors like A-770041 have shown potential in reducing GBM cell growth. SYK inhibitors like BAY61-3606, piceatannol, and NVP-QAB205 have shown anti-inflammatory and anti-proliferative effects. Src inhibitors like KX2-361 and Si306 have shown potential in reducing GBM cell proliferation and inducing apoptosis. DYRK1A inhibitors like VER-239353 have shown potential in inducing cell cycle arrest. These TKIs are being evaluated in clinical trials, with some showing promising results in improving survival and reducing tumor growth in GBM patients. The review highlights the importance of targeting specific kinases in GBM and the potential of TKIs as a new class of therapeutic agents for this aggressive cancer.