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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

PubMedCurrent issues in molecular biology2026-10-27

Anticancer Effects of Genistein and Its Interaction with Temozolomide in Human Melanoma, Neuroblastoma and Glioblastoma Cells.

Wróblewska-Łuczka Paula P, Kwiatkowski Bartłomiej B, Kwieciński Maciej M, Góralczyk Agnieszka A et al.

(1) Background: Melanoma, glioblastoma, and neuroblastoma have distinct cellular origins, biological characteristics, and clinical behavior. Although these tumors differ in their origins, they exhibit aggressive biological features and may develop treatment resistance. New therapeutic options are constantly being sought. This study aimed to evaluate the anticancer potential of genistein, a soy-derived isoflavone, and investigate the pharmacodynamic interactions between genistein and temozolomide in human melanoma, neuroblastoma, and glioblastoma cell lines. (2) Methods: Genistein's potential for inhibiting cell viability, induction of cytotoxicity, and modulating apoptosis-related protein expression was assessed in eight cell lines. The interaction of the genistein + temozolomide combination (in a fixed 1:1 ratio) was assessed using isobolographic analysis. (3) Results: Genistein inhibited cell viability in a concentration-dependent manner. IC50 values ranged from approximately 40 to 110 μM in melanoma, 27 to 60 μM in neuroblastoma, and 37 to 83 μM in glioblastoma cell lines. Genistein treatment induced changes in apoptosis-related protein expression, including Bax and Bcl-2. The genistein + temozolomide combination produced additive interactions in the tested melanoma cell lines, whereas strong antagonism was observed in the neuroblastoma and glioblastoma models. These differences may reflect tumor-type-specific biological characteristics. (4) Conclusions: The findings provide comparative insights into genistein-temozolomide interactions across the investigated tumor models. Further studies are needed to clarify the underlying molecular mechanisms and evaluate the potential therapeutic relevance of this combination. Additional preclinical investigations are required to establish its efficacy, safety, and tolerability before clinical implications can be determined.

PMID 42939568
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PubMedInternational journal of molecular sciences2026-10-27

Reduced DDB2 Expression Is Associated with Temozolomide Resistance in Glioblastoma Cells.

Grávalos-Cano Inés I, Morales-Ruiz Teresa T, Ariza Rafael R RR, Roldán-Arjona Teresa T et al.

Glioblastoma (GBM) remains one of the most lethal primary brain tumours, and resistance to temozolomide (TMZ), the standard chemotherapeutic agent for GBM, represents a major obstacle to effective treatment. Although O6-methylguanine-DNA methyltransferase (MGMT) is a well-established determinant of TMZ response, MGMT status alone does not fully explain the heterogeneity of treatment outcomes, suggesting the involvement of additional DNA damage response mechanisms. Here, we investigated the contribution of different DNA repair pathways to TMZ sensitivity in a panel of GBM cell lines displaying distinct TMZ response profiles. Expression analysis of 84 DNA repair genes identified damage-specific DNA binding protein 2 (DDB2) as the only one consistently associated with TMZ sensitivity. We found that DDB2 expression was significantly reduced in TMZ-resistant cell lines and selectively induced following TMZ exposure in TMZ-sensitive cells. Proteomic profiling of representative sensitive and resistant cell models further revealed distinct responses to TMZ and identified enrichment of p53-associated DNA damage response pathways in sensitive cells, including altered expression of DDB2 and other canonical p53-regulated proteins. Importantly, siRNA-mediated depletion of DDB2 in the TMZ-sensitive A172 GBM cell line significantly reduced TMZ sensitivity. These findings provide functional evidence that DDB2 contributes to the cellular response to TMZ and extend the established roles of DDB2 in DNA repair and cancer biology to TMZ responsiveness in GBM.

PMID 42941718
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PubMedBiomedicines2026-10-27

Utility of Chemotherapy for Metastatic Melanoma in the Contemporary Era and Experience with Modified Vinblastine-Cisplatin-Temozolomide at a Tertiary Care Center.

Doolittle Woo Kyung Lee WKL, Rao Rohit R, Johnson Malena M, Tejawinata Felicia F et al.

Purpose: Chemotherapy can be a viable option for patients with relapsed-refractory melanoma (RRM) who do not have access to advanced treatments or clinical trials. We report our experience with a modified Vinblastine-Cisplatin-Temozolomide (mVCT) regimen in patients with RRM and barriers to their enrollment in clinical trials. Methods: We conducted a retrospective review of patients with RRM who received mVCT. The primary endpoint was overall response rate (ORR) following the last cycle. Secondary endpoints included the rate of complete response (CR), partial response (PR), stable disease (SD), clinical benefit rate (CBR), progression-free survival (PFS), intracranial (IC) PFS, (IC) CBR, (IC) RR, and toxicity. Results: Ten patients received mVCT for a median of 4.5 cycles (IQR: 3-6). Median follow-up was 20 months (IQR: 10.3-30.3). The ORR was 50% (CR-1, PR-4) and CBR was 70%. The median PFS was 7 months (IQR: 1.5-9.25). Among eight patients with brain metastasis, six underwent gamma-knife radiosurgery (GKRS); three achieved PR, and three had SD. Two patients without GKRS achieved CR, leading to an ICRR of 62.5% and an ICCBR of 100%. The median ICPFS was 7.5 months (IQR: 6-9.75). Median OS was 22 months (95% CI: 15.6-32.4). Four patients experienced grade ≥ 3 toxicities (fatigue in two, myelosuppression in two); two required dose reduction and one discontinued treatment. Two patients with PD later enrolled in phase 1 clinical trials. Brain metastasis (80%), immunotherapy-related toxicity (60%), acral/mucosal melanoma (50%), and social barriers (40%) were the major reasons for trial ineligibility. Conclusions: mVCT is an effective and well-tolerated regimen for patients with RRM and can serve as a bridge while they await access to advanced treatments or a clinical trial.

PMID 42940080
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PubMedMedicina (Kaunas, Lithuania)2026-10-27

Pretreatment Lactate Dehydrogenase-to-Albumin Ratio Identifies an Early Adverse Prognostic Profile in IDH-Wildtype Glioblastoma: A Real-World Cohort Study.

Kaya Hayrani H, Aydin Asim Armagan AA, Umit Abdullah A, Guven Ozan Deniz OD et al.

Background and Objectives: Clinical outcomes remain markedly heterogeneous in glioblastoma, isocitrate dehydrogenase (IDH)-wildtype, despite contemporary molecular classification and established clinicopathological risk factors. We investigated whether the pretreatment lactate dehydrogenase-to-albumin ratio (LAR), an accessible circulating index integrating systemic disease- and host-related information, provides complementary prognostic information. Materials and Methods: We retrospectively evaluated 134 patients with glioblastoma, IDH-wildtype, central nervous system (CNS) World Health Organization (WHO) grade 4. An exploratory, cohort-specific LAR threshold was derived for 12-month overall survival (OS) and retained without re-optimization across subsequent analyses. Associations with OS and progression-free survival (PFS) were evaluated using Cox regression, and incremental prognostic performance was assessed against a baseline clinicopathological model. Temporal and continuous associations with survival, internal model validation, and the relationship between LAR and treatment response during adjuvant temozolomide therapy were also examined. Results: The cohort-derived LAR threshold was 5.718. High pretreatment LAR was associated with shorter median OS (5.5 vs. 16.0 months) and PFS (5.2 vs. 10.6 months; both p < 0.001) and remained independently associated with OS (adjusted hazard ratio [HR], 4.51; 95% CI, 2.84-7.18) and PFS (adjusted HR, 3.60; 95% CI, 2.33-5.56). Adding LAR to the clinicopathological model increased Harrell's C-index from 0.699 to 0.760 for OS and from 0.690 to 0.759 for PFS (both likelihood ratios, p < 0.001), with optimism-corrected C-indices of 0.743 and 0.742, respectively. Prognostic discrimination and adjusted effect estimates were greatest early in the follow-up period and attenuated over time, whereas continuous LAR showed nonlinear associations with both endpoints. Among the 104 patients who received adjuvant temozolomide, a high LAR was independently associated with progressive disease (adjusted odds ratio, 3.72; 95% CI, 1.28-10.81). Conclusions: Pretreatment LAR identified patients with IDH-wildtype glioblastoma who experienced poorer survival, and the prognostic effect was concentrated predominantly in the early disease course. Its incremental contribution beyond conventional clinicopathological characteristics supports the further evaluation of LAR as an accessible component of baseline risk characterization. However, independent external validation is required before clinical application.

PMID 42942489
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PubMedCurrent issues in molecular biology2026-10-27

Melatonin Differentially Modulates Temozolomide Responses in Glioblastoma and Endothelial Cells: Associations with Global DNA Methylation and Cortistatin Levels.

Gundogan Gul Ipek GI, Yurttas Asiye Gok AG, Oltulu Yasemin Musteri YM, Ciraci Enver E et al.

Glioblastoma (GBM) is the most aggressive primary brain tumor in adults and remains highly resistant to current therapeutic strategies. Temozolomide (TMZ) is a standard chemotherapeutic agent used in GBM treatment; however, intrinsic and acquired resistance limits its efficacy. This study investigated treatment-associated response patterns to TMZ and melatonin in U87MG glioblastoma cells and human umbilical vein endothelial cells (HUVECs). Relative MTT metabolic activity was assessed using the MTT assay, and cell-cycle distribution was analyzed by flow cytometry. Global DNA methylation was evaluated using a 5-methylcytosine assay, with calibration-derived values expressed as %5-mC. CORT was assessed semi-quantitatively by ELISA, with background-corrected OD values normalized to the corresponding untreated control within each experimental run and expressed as relative CORT levels (% of control). Linear mixed-effects models were used to evaluate TMZ concentration, melatonin exposure, and the TMZ × melatonin interaction, with biological experiment included as a random effect. TMZ and melatonin produced treatment-condition- and cell-type-associated response patterns. In HUVECs, relative MTT metabolic activity remained comparatively high across most TMZ concentrations, whereas a more pronounced decrease was observed at 100 µM TMZ during melatonin co-treatment. U87MG cells showed a non-linear MTT response across TMZ concentrations, and the magnitude and direction of the melatonin-associated effect varied according to TMZ dose. Significant TMZ × melatonin interactions were identified for relative MTT metabolic activity in both cell types. Global DNA methylation-related measurements also showed treatment-associated differences, with distinct response patterns between HUVEC and U87MG cells; calibration-derived %5-mC values were used for quantitative presentation of global DNA methylation. Relative CORT levels likewise varied across treatment conditions, with larger relative changes observed in U87MG cells under several combination conditions. The observed findings should be interpreted as exploratory and hypothesis-generating. The present data do not establish therapeutic selectivity, pharmacological synergy, a causal epigenetic mechanism, or a CORT-mediated stress-response pathway. Further validation using additional glioblastoma models, non-malignant neural controls, fully quantitative and appropriately normalized CORT measurements, and targeted functional pathway analyses is required before mechanistic or clinical conclusions can be drawn.

PMID 42939522
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PubMedNeuro-oncology advances2026-10-27

Adult-onset giant cell glioblastoma with biallelic PMS2 inactivation in Lynch syndrome.

Onel Muhammed M, Gingell Luke L, Kasay Aysegul A, Chisti Mohammad Muhsin MM

Mismatch repair (MMR)-deficient glioblastomas represent a rare molecular subset with important hereditary and therapeutic implications. We report a 58-year-old man with adult-onset giant cell glioblastoma showing isolated PMS2 loss, microsatellite instability-high status, ultra-high tumor mutational burden, and confirmed biallelic PMS2 inactivation from a likely pathogenic germline PMS2 splice-site variant and somatic PMS2 nonsense mutation, revealing previously unrecognized Lynch syndrome. DNA methylation profiling classified the tumor as a high-grade glioma with MMR deficiency, with a methylation match to diffuse high-grade glioma, IDH-wildtype, subtype E. Given O⁶-methylguanine-DNA methyltransferase (MGMT) promoter unmethylation and MMR deficiency, temozolomide was omitted, and the patient received adjuvant radiation therapy with concurrent and maintenance pembrolizumab. Surveillance MRI at 5 months after gross total resection showed no evidence of recurrence. This case highlights giant cell morphology and ultra-high tumor mutational burden as potential clues to underlying MMR deficiency and supports consideration of reflex MMR immunohistochemistry, germline evaluation, and immune checkpoint inhibition in selected dMMR/MSI-H glioblastomas.

PMID 42936848
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