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temozolomide (SI 053 / Temodex / SI053)

✓ Approved

Double Bond Pharmaceutical · 小分子 · 小分子

什么是 temozolomide？

temozolomide 是一种小分子，由Double Bond Pharmaceutical研发。该药已获批，用于治疗相关适应症，给药途径：Intratumoral Injection。

药物档案

商品名SI 053, Temodex, SI053
公司Double Bond Pharmaceutical
药物类别小分子
给药途径Intratumoral Injection
状态Approved
来源： ClinicalTrials.gov, Double Bond Pharmaceutical

治疗适应症

temozolomide 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Brain neoplasm malignant✓ Approved

相关研究文献

PubMedCells2026-07-27

The Effect of the Combination of Temozolomide and Flubendazole on Glioblastoma Cells.

Kapickova Katerina K, Vitovcova Barbora B, Skarkova Veronika V, Havelek Radim R et al.

Glioblastoma multiforme (GBM) is a highly aggressive brain tumor characterized by rapid development of chemoresistance and poor patient survival. Due to the limited efficacy of current therapeutic protocols, alternative approaches are needed. One potential strategy is combined treatment with DNA-damaging and microtubule-targeting agents. This study investigated the biological effects of temozolomide (TMZ) and flubendazole (FLU) co-treatment in cultured GBM cells. Three GBM cell lines (A172, T98G, and U118MG) with different molecular profiles were treated with TMZ, FLU, or their combination. Treatment effects were evaluated using WST-1 assay, microscopy, flow cytometry, RT-PCR, and Western blotting. Drug accumulation in tumor and brain tissues was additionally analyzed in a nu-nu mouse model using LC/MS. Combined TMZ and FLU treatment reduced cell proliferation compared with untreated control and TMZ monotherapy in the tested GBM cell lines. FLU-containing treatments were associated with morphological alterations, caspase activation, altered microtubule organization, and G2/M cell cycle accumulation. In addition, co-administration of TMZ and FLU affected drug accumulation in vitro and in brain and tumor tissues in vivo. These findings suggest that the microtubule targeting may modulate the response of GBM cells to TMZ. However, the pharmacological interaction and potential relevance of TMZ + FLU co-treatment require further preclinical validation.

PMID 42505349
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PubMedMedical sciences (Basel, Switzerland)2026-07-27

When Surgical Innovation Outpaces Evidence: Does Modern Maximal Resection Require Re-Evaluation of Postoperative Radiotherapy in Glioblastoma?

Tykocki Tomasz T

Postoperative radiotherapy (RT) improves survival in glioblastoma, and its role in standard management is not disputed. The randomized trials establishing this benefit, however, were conducted before computed tomography, magnetic resonance imaging (MRI), molecular classification, and temozolomide (TMZ), in heterogeneous populations of "operated malignant glioma" treated with whole-brain or large-field RT versus best supportive care. Their pooled survival benefit (risk ratio 0.81; 95% CI 0.74-0.88) robustly answers the historical question they were designed to address. Since then, advances in surgery, imaging, molecular diagnostics, and systemic therapy have created a modern best-prognosis subgroup-young patients with excellent performance status, MRI-confirmed complete or supramaximal resection of an IDH-wildtype glioblastoma, and median survival approaching or exceeding three years-for whom no clearly defined historical counterpart exists. This perspective provides a structured appraisal of the directness of the landmark randomized evidence using GRADE concepts and translates that appraisal into a graded roadmap for future de-escalation trial designs. Across population, intervention, comparator, and outcomes, the historical trials exhibit substantial indirectness, while the only randomized RT-versus-no-RT evidence from the modern era derives from elderly patients representing the opposite prognostic extreme. This is not an argument against RT. The infiltrative biology of glioblastoma, predominantly in-field recurrence, and radioresistant stem-cell populations strongly support continued benefit. Rather, the unresolved question concerns the magnitude of benefit after maximal contemporary therapy and whether selected de-escalation strategies merit prospective evaluation. Our thesis is one of collective scientific equipoise regarding an unresolved evidence question rather than individual clinician equipoise or refutation of current standard care.

PMID 42506372
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PubMedCase reports in oncology2026-07-25

Achieving Stable Disease in an Adult with Malignant Gastrointestinal Tumor following Cabozantinib Treatment: Case Report.

Iverson Brianna Jo BJ, Milhem Mohammed M MM, Rieth John Markus JM

Malignant gastrointestinal neuroectodermal tumor (GNET) is a rare and aggressive neoplasm that is characterized by EWSR1 rearrangements. Most patients present with metastatic disease. There are no established treatment guidelines, and systemic therapy options remain poorly defined. A woman in her late 30s presented initially with right upper quadrant pain and bloating. Endoscopic biopsy of a duodenal mass revealed a SOX10-positive malignant neoplasm. Molecular testing identified an EWSR1:CREB1 fusion, confirming GNET. Initial treatment with ipilimumab and nivolumab resulted in disease progression. Subsequent therapies included a selective interleukin-2 agonist clinical trial, nivolumab/relatlimab, and temozolomide, all associated with continued progression. Cabozantinib was initiated after further radiographic progression. Follow-up imaging demonstrated tumor regression, and the patient maintained stable disease for 15 months before mild progression. Metastatic GNET has a poor prognosis and lacks standardized systemic therapy. This case demonstrates durable disease stabilization with cabozantinib after progression on immunotherapy and chemotherapy. Tyrosine kinase inhibition may represent a promising therapeutic strategy in GNET and warrants further investigation.

PMID 42499698
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PubMedFrontiers in oncology2026-07-25

Case Report: Supraorbital keyhole resection of IDH-mutant grade 3 astrocytoma of the medial orbitofrontal region.

Ashirov Nurali N, Pochivalov David D, Zhamoldin Daniyar D, Aleinikov Viktor V et al.

High-grade gliomas located in the medial orbitofrontal region present significant surgical challenges due to their deep location and proximity to critical neurovascular structures. While the supraorbital eyebrow approach is widely used for extra-axial skull base lesions, its application to intra-axial high-grade gliomas remains less frequently reported. We report the case of a 47-year-old female diagnosed with an isocitrate dehydrogenase (IDH)-mutant World Health Organization Grade 3 astrocytoma located in the medial orbitofrontal cortex. The patient underwent gross total resection via a minimally invasive supraorbital trans-eyebrow craniotomy. Early postoperative MRI performed within 72 hours confirmed gross total resection without residual contrast-enhancing tumor. Histopathological examination demonstrated microvascular proliferation consistent with Grade 3 astrocytoma, and molecular analysis confirmed IDH mutation. The patient subsequently received standard adjuvant radiochemotherapy with temozolomide. Follow-up demonstrated preserved neurological function and high cosmetic satisfaction. This case illustrates that, in carefully selected patients, the supraorbital keyhole approach can achieve oncologically adequate resection of medial orbitofrontal IDH-mutant high-grade gliomas while minimizing surgical morbidity and optimizing cosmetic outcomes.

PMID 42500282
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PubMedThe Tohoku journal of experimental medicine2026-07-23

DLK1-35 Contributes to Temozolomide Resistance in Glioblastoma Through the miR-140-3p/NHE1/ERK-MGMT Axis.

Guo Jianxiong J, Li Dan D, Sun Mingyang M, Wang Zhuo Z et al.

PMID 42486642
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PubMedThe Journal of biological chemistry2026-07-23

IGSF3 drives acquired temozolomide resistance in glioblastoma through ASNS-dependent asparagine biosynthesis.

Li Jie J, Lu Hongnian H, Xu Qianqian Q, Yin Ying Y et al.

Glioblastoma (GBM) is the most aggressive primary malignancy of the central nervous system, and acquired resistance to temozolomide (TMZ) is a major cause of tumor recurrence and poor clinical outcome. However, the tumor-intrinsic drivers and metabolic adaptations underlying this process remain incompletely understood. In this study, we integrated transcriptomic data from established TMZ-sensitive and TMZ-resistant models with public bulk and single-nucleus sequencing datasets, and validated candidate genes using clinical specimens, cell-based drug-sensitivity assays, xenograft models, metabolic measurements, luciferase reporter assays, chromatin immunoprecipitation, and small-molecule binding assays. Immunoglobulin superfamily member 3 (IGSF3) was consistently upregulated in TMZ-resistant cells, resistant xenografts, and recurrent GBM samples, and was mainly enriched in malignant glioma cells. Functionally, IGSF3 overexpression promoted resistance to TMZ-related treatment, whereas IGSF3 knockdown restored drug sensitivity. Mechanistically, IGSF3 was detected in the nucleus, where it enhanced the activity of the asparagine synthetase (ASNS) promoter. Additionally, IGSF3 was found to be enriched at the ASNS promoter, thereby increasing ASNS expression and asparagine production, reduced reactive oxygen species accumulation, preserved glutathione redox balance, and limited DNA damage induced by treatment. ASNS gain- and loss-of-function rescue experiments showed that ASNS was required for the pro-resistance effect of IGSF3. Finally, Tucatinib bound to IGSF3, suppressed the IGSF3-ASNS pathway, and enhanced TMZ efficacy in vitro and in vivo. These findings identify the IGSF3-ASNS axis as a tumor-intrinsic metabolic adaptation that drives acquired TMZ resistance in GBM and suggest a potential therapeutic strategy for recurrent GBM.

PMID 42486263
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