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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

PubMedCancer medicine2026-09-10

Spatial Omics in High-Grade Gliomas: Mapping Immune-Tumor Niches for Precision Therapy.

Shaikh Saniyah S, Raziq Thaabit T, Alfares Sulaf B SB, Raslan Touleen T TT et al.

High-grade gliomas (HGGs), particularly glioblastoma (GBM), remain among the most lethal human cancers despite decades of molecular profiling and therapeutic innovation. A primary reason for treatment failure is that HGG biology is spatial: malignant cell states, immune suppression, metabolic stress, and therapeutic resistance are organized into distinct anatomical and functional niches. Spatial omics technologies now enable high-dimensional mapping of gene expression, protein signaling, immune architecture, and metabolic activity within intact tumor tissue. These approaches reveal how proneural and mesenchymal transcriptional states coexist yet localize to distinct regions, alongside hypoxic, invasive, and stem-enriched niches. Spatial analyses show that key clinical determinants, including O6-methylguanine-DNA methyltransferase (MGMT)-associated temozolomide resistance, radiotherapy tolerance in hypoxic regions, and immunotherapy failure driven by myeloid-dominated immune exclusion, are influenced not only by molecular programs but also by cellular location. Beyond biological insight, spatial omics is reshaping clinical paradigms by enabling region-specific patient stratification, early assessment of treatment response, and identification of therapy-resistant reservoirs that seed recurrence. Prior bulk and single-cell studies defined HGG cell states and pathways but often treated resistance as tumor-wide. This review presents a spatially explicit framework that synthesizes spatial transcriptomic and immune-profiling studies to identify tumor-immune niches and spatial bottlenecks that drive therapeutic failure and recurrence.

PMID 42717555
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PubMedPharmacological reports : PR2026-09-09

Interactions of ACEA and WIN 55,212-2 mesylate with temozolomide and cisplatin in neuroblastoma and glioblastoma cell lines: an isobolographic analysis.

Załuska-Ogryzek Katarzyna K, Wróblewska-Łuczka Paula P, Góralczyk Agnieszka A, Chojnacki Michał M et al.

Glioblastoma is still the most aggressive primary brain tumor in adults. Recently, several advanced experimental treatment options have been proposed for glioblastoma patients, including the application of cannabinoids as an add-on therapy. In the MTT, LDH, and BrdU assays, the anti-proliferative effects of arachidonyl-2'-chloroethylamide (ACEA - a potent selective cannabinoid CB1 receptor agonist) and WIN 55,212-2 mesylate (a non-selective cannabinoid CB1 and CB2 receptor agonist) on neuroblastoma and glioblastoma cell lines (CHP-134, KELLY, U-87MG, T98G, and C6) were determined. The interaction profiles of ACEA and WIN 55,212-2 mesylate in combinations with cisplatin and temozolomide (two chemotherapeutic drugs) in CHP-134, KELLY, U-87MG, T98G, and C6 were assessed isobolographically in the MTT test. Additionally, the impact of ACEA and WIN 55,212-2 mesylate on cannabinoid CB1 receptors expressed on all the tested cell lines was examined with the Western blot technique. Pre-incubation with a selective cannabinoid CB1 receptor antagonist/invert agonist (AM281) and consecutive exposure of the neuroblastoma CHP-134 and glioblastoma T98G cell lines to ACEA or WIN 55,212-2 mesylate at various treatment times (24, 48, and 72 h) in the MTT assay was studied. Expression of Bax and Bcl-2 proteins in response to ACEA or WIN 55,212-2 mesylate treatment was examined with Western blot. ACEA and WIN 55,212-2 mesylate produced anti-proliferative effects on the tested cell lines. The selectivity index for ACEA ranged from 2.61 to 5.95, and that for WIN 55,212-2 mesylate ranged from 4.32 to 12.85. The combinations of ACEA with cisplatin (at the fixed ratio of 1:1) exerted additive interactions in all the tested cell lines. In contrast, WIN 55,212-2 mesylate, when combined with cisplatin, exerted a synergistic interaction in the CHP-134 cell line (p < 0.05) and additive interactions in the remaining (KELLY, U-87MG, T98G, and C6) cell lines in the MTT test. The combinations of ACEA with temozolomide (at the fixed-ratio of 1:1) exerted antagonistic interactions in two (CHP-134 at p < 0.05; and C6 at p < 0.0001) cell lines and additive interactions in three (KELLY, U-87MG, T98G) cell lines in the MTT assay. In contrast, WIN 55,212-2 mesylate, when combined with temozolomide, produced antagonistic interactions in three (KELLY at p < 0.05; T98G at p < 0.01, and C6 at p < 0.01) cell lines and additive interactions in the remaining (CHP-134 and U-87MG) cell lines in the MTT test. Western blot analysis confirmed that all the tested cell lines (CHP-134, KELLY, U-87MG, T98G, and C6) exposed to ACEA or WIN 55,212-2 mesylate changed the expression of cannabinoid CB1 receptors. Pre-incubation with AM281 and subsequent exposition of the CHP-134 and T98G cell lines to ACEA or WIN 55,212-2 mesylate revealed that the prior blockade of cannabinoid CB1 receptors reduced the anti-viability effects of the cannabinoid agonists in the MTT assay, confirming the involvement of cannabinoid CB1 receptors in this cellular response. Additionally, due to Western blot technique it was confirmed that neither Bax, nor Bcl-2 proteins were involved in the anti-proliferative effects of ACEA and WIN 55,212-2 mesylate in the tested CHP-134 and T98G cell lines. WIN 55,212-2 mesylate combined with cisplatin exerted the most desirable synergistic interaction in relation to the anti-proliferative effects in the neuroblastoma (CHP-134) cell line. In contrast, all the antagonistic interactions determined isobolographically for WIN 55,212-2 mesylate in combination with temozolomide in the KELLY, T98G, C6, and those of ACEA with temozolomide in the CHP-134, C6 cell lines in the MTT assay, should not be used clinically, due to the reduction of the anti-viability effects of the tested combinations.

PMID 42714782
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PubMedScience advances2026-09-09

Magnetically actuated nanoantennas for wireless glioblastoma therapy.

Saha Monochura M, Khan Ishaq N IN, Joy Baju B, Chen Shun-Ying SY et al.

Glioblastoma (GBM) remains a formidable clinical challenge, characterized by invasive growth, therapeutic resistance, and dismal patient survival. We report the development of HITMAN (highly localized electric field-induced tumor therapy using magnetically actuated nanoantennas), a wireless bioelectric therapy that selectively eradicates GBM cells with cellular precision. Magnetically actuated nanoantennas convert low-frequency (≤200 kHz), deep-brain-penetrant magnetic fields into localized electric fields, thereby triggering protein unfolding, membrane disruption, and ER stress. In vitro, HITMAN demonstrated superior efficacy compared to temozolomide (TMZ), significantly decreasing viability in drug-resistant, patient-derived GBM cells by 52.2%, versus 10% with TMZ while sparing neurons and astrocytes. Mechanistically, HITMAN activated the unfolded protein response and autophagy pathways, suppressed cell cycle and adhesion genes, reduced Ki-67 expression, disrupted cytoskeletal architecture, and elevated p53 levels, underscoring a multifaceted antitumor mechanism. In orthotopic mouse models, HITMAN significantly inhibited tumor growth, extended median survival by more than 50%, and exhibited no systemic toxicity. Thus, HITMAN offers a minimally invasive, spatially precise, and clinically translatable therapy for GBM.

PMID 42715333
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PubMedNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2026-09-09

Next-generation therapeutics for glioblastoma: Challenges and future directions.

Blaquier Juan B JB, Lim-Fat Mary Jane MJ, de la Fuente Macarena M

Glioblastoma (GBM) is the most common and aggressive primary malignant brain tumor in adults. Although recent World Health Organization classifications integrating molecular features have improved diagnostic precision, therapeutic outcomes for IDH-wild-type glioblastoma remain dismal. Standard treatment with radiotherapy and temozolomide has changed little over the past two decades, and most investigational therapies have failed to produce durable clinical benefit. Tumor heterogeneity, adaptive resistance mechanisms, a profoundly immunosuppressive tumor microenvironment, and limited drug delivery across the blood-brain barrier have collectively contributed to these failures. This review summarizes the evolving molecular landscape of glioblastoma and examines emerging therapeutic approaches designed to overcome these barriers. We discuss advances in molecularly targeted therapies, including strategies directed at BRAF and FGFR alterations, as well as continued efforts to address EGFR-driven disease. We also review immunotherapeutic approaches such as immune checkpoint inhibition, chimeric antigen receptor T-cell therapies, and oncolytic viruses, highlighting key clinical trial results and biological challenges. In parallel, we explore metabolic targeting strategies and novel technologies aimed at improving central nervous system drug delivery, including focused ultrasound and convection-enhanced delivery. Collectively, current evidence indicates that meaningful progress in glioblastoma will require biomarker-driven patient selection, rational combination strategies, and improved methods for intracranial drug delivery. While substantial challenges remain, ongoing translational and clinical efforts provide a framework for the development of more effective and personalized therapeutic strategies.

PMID 42715820
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PubMedNeuro-oncology2026-09-08

Association between temozolomide-related hematologic toxicity and health-related quality of life (HRQoL) in patients with newly diagnosed glioblastoma.

Machingura Abigirl A, Weller Johannes J, Koekkoek Johan A F JAF, Dirven Linda L et al.

Hematologic toxicity is a major adverse event of temozolomide chemoradiotherapy for newly diagnosed glioblastoma. Although severe hematologic toxicity occurs in approximately 10% of patients, its impact on HRQoL is unknown. This study evaluated the association between temozolomide-related hematologic toxicity and HRQoL in patients with newly diagnosed glioblastoma. Patients with newly diagnosed glioblastoma treated with temozolomide chemoradiotherapy and available HRQoL data from three clinical trials were included. Primary HRQoL outcomes were physical, social, and role functioning, pain, fatigue, nausea/vomiting, and global health status. Severe hematologic toxicity was defined grade 3-4 neutropenia, lymphopenia, thrombocytopenia, or anemia; febrile neutropenia; or prolonged (>30 days) grade 2 toxicity. Associations between severe hematologic toxicity and HRQoL were evaluated using linear mixed models. Clinical relevance was interpreted as glioma-specific minimally important difference thresholds. Among 1288 patients, 8% experienced severe hematologic toxicity during the concomitant phase, 6% during the maintenance and 1% during both. During the concomitant phase, severe hematologic toxicity was more frequent in females and in patients with MGMT promoter methylation. From baseline to week 6, global health mean scores declined by - 8.52 points in patients with severe toxicity and -4.78 points in those without, with a non-significant difference (p = 0.24). Similar patterns were observed for physical, social, and role functioning. Symptom scales were numerically worse in severe toxicity, but not significantly different. During maintenance phase, differences were minor. Severe temozolomide-related hematologic toxicity showed no statistically significant association with impaired HRQoL, suggesting limited impact on patient-reported functioning and symptoms. Possible effects on psychological functioning should be examined further.

PMID 42711275
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PubMedNature communications2026-09-08

MALT1 protease inhibition restrains glioblastoma progression by reversing tumor-associated macrophage-dependent immunosuppression in mice.

Hofstätter Azambuja Juliana J, Yerneni Saigopalakrishna S SS, Maurer Lisa M LM, Crentsil Hannah E HE et al.

MALT1 protease is an intracellular signaling molecule that promotes tumor progression via cancer cell-intrinsic and cancer cell-extrinsic mechanisms. MALT1 has been mostly studied in lymphocytes, and little is known about its role in tumor-associated macrophages. We show that MALT1 is expressed in glioblastoma (GBM)-associated macrophages. Mechanistically, GBM tumor cells induce a MALT1-NF-κB signaling axis in macrophages, leading to enhanced macrophage migration and polarization toward an immunosuppressive ('M2-like') phenotype. Inactivation of MALT1 protease promotes transcriptional reprogramming that reduces migration and restores a macrophage anti-tumor 'M1-like' phenotype. Preclinical in vivo analysis shows that MALT1 inhibitor treatment results in immuno-reactivity of GBM-associated macrophages and reduced GBM tumor growth. The addition of MALT1 inhibitor to temozolomide reduces immunosuppression in the tumor microenvironment, indicating that pharmacological inhibition of MALT1 protease may enhance the efficacy of chemotherapeutic. Thus, our findings suggest that MALT1 protease inhibition represents a promising macrophage-targeted immunotherapeutic strategy for the treatment of GBM.

PMID 42706275
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