Glioblastoma (GBM) research urgently requires a novel murine model for preclinical studies. The widely used GL261 cell line reliably forms glioma-like tumours when transplanted intracranially; however, these tumours do not accurately replicate human GBM, particularly as a model for immunotherapy. The tumour immune microenvironment (TIME) of GL261 tumours consistently responds to immune checkpoint inhibitors, yet these treatments have shown limited efficacy in multiple clinical trials. To address the limitations of GL261, we developed a new murine model of GBM. We introduced mutations into an immortalized eGFP astrocyte C57BL/6 cell line to create a genetic profile similar to that of human GBM cells. One version of these astrocytes models a classical GBM cell, featuring a Pten knockdown and stable transfection with RAS V12. Tumours formed reliably in both GL261 and Pten KD + RAS V12 models, with median survival times of 22.00 days. Notably, key histological differences were observed in H&E sections: GL261 tumours exhibited high vascularization and distinct borders with healthy tissue, while Pten KD + RAS V12 tumours displayed dense cell packing, clear invasion into the parenchyma, and signs of microvascular proliferation. Spectral flow cytometry revealed a significant increase in tumour associated macrophage (TAM) infiltration in Pten KD + RAS V12 tumours, whereas GL261 tumours contained a higher abundance of inflammatory monocytes. Furthermore, the new model demonstrated a decrease in functional antigen-presenting cells, particularly dendritic cells. These findings suggest a more suppressed and immunologically cold TIME in the Pten KD + RAS V12 tumours compared to GL261. Lastly, gene set enrichment analysis (GSEA) from RNA sequencing of whole tumours highlighted an enrichment of invasion and angiogenic pathways, alongside decreased expression of inflammatory interferon signalling. In conclusion, these results indicate that our new transplant model effectively recapitulates key histological and immunological phenotypes of glioblastoma, positioning it as a valid alternative for syngeneic models in preclinical research.