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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 reports (Hoboken, N.J.)2026-08-06

Harnessing Repurposed Drugs to Enhance Temozolomide Efficacy in Glioblastoma.

Nakhaei Ali A, Taghavi Atefeh A, Afshari Amir R AR, Davoudi Farzaneh F et al.

Glioblastoma (GB) is the most aggressive primary malignant brain tumor in adults and remains associated with poor survival despite surgical resection followed by radiotherapy and temozolomide (TMZ) chemotherapy. Intrinsic and acquired resistance to TMZ, including MGMT-dependent DNA repair and activation of pro-survival pathways, could decrease treatment efficacy. Drug repurposing offers an attractive strategy to identify agents that may enhance TMZ activity because these drugs already have known pharmacokinetic and safety profiles. This narrative review summarizes the available evidence on repurposed drugs investigated as potential modulators of TMZ response in GB. A range of repurposed agents, including chloroquine, valproic acid, levetiracetam, metformin, aspirin, amlodipine, atorvastatin, chlorpromazine, melatonin, disulfiram, bortezomib, and verteporfin, have been evaluated in GB models and selected clinical studies. Reported mechanisms include modulation of MGMT expression, autophagy, oxidative stress, apoptosis, DNA-damage responses, cancer stem-cell properties, and signaling pathways such as PI3K/AKT/mTOR, AMPK, EGFR, STAT3, ERK1/2, and NF-κB. Several agents have enhanced TMZ-associated cytotoxicity in cell culture and animal models. However, clinical evidence remains limited, and the results are inconsistent for some drugs. Blood-brain barrier penetration, achievable intratumoral drug exposure, toxicity, treatment scheduling, and molecular heterogeneity of GB remain major translational challenges. Repurposed drugs may provide useful candidates for improving TMZ-based therapy in GB. However, most evidence remains preclinical, and further studies are needed to clarify blood-brain barrier penetration, optimal dosing, toxicity, predictive biomarkers, and clinical efficacy. Well-designed prospective clinical trials are required before these combinations can be incorporated into routine GB treatment.

PMID 42557676
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PubMedJournal of neuroendocrinology2026-08-06

Can acromegaly be controlled in all cases?

Chiloiro Sabrina S, Sorrentino Francesco Padovano FP, Vicari Alessandra A, Giampietro Antonella A et al.

Acromegaly is a rare disease, due in most of the cases to a growth hormone (GH)-secreting pituitary adenoma (PA), namely neuroendocrine tumour (PitNET). The treatment of patients with acromegaly is multimodal and multi-step, including surgery, medical therapies, and radiotherapy. In the last 30 years, the therapeutic armamentarium for the treatment of acromegaly has progressively increased, and the therapeutic algorithm has been significantly modified through the identification of clinical, biochemical, and molecular biomarkers of treatment outcome. The personalization of acromegaly treatment has shifted the paradigm from a 'trial-and-error' to a 'target-to-treat' treatment approach to achieve early disease control and to reduce the risk of disease-related comorbidities that may lead to an increased mortality. Nevertheless, despite the numerous improvements in the treatment of patients with acromegaly, disease control is not achieved in all patients, according to the results of randomized clinical trials, interventional studies, and prospective and retrospective observational studies. In parallel, the normalization of GH and IGF-I levels may not be sufficient to control acromegaly related symptoms and prevent disease-related comorbidities. In this review, we will report on the most recent aims of treatment and cure in patients with acromegaly, on the efficacy and predictors of response to conventional treatments (such as first- and second-generation somatostatin receptor ligands and growth hormone receptor antagonist). A specific section will focus on the rarer aggressive disease pictures and on the treatment with systemic therapies (such as temozolomide and capecitabine) and on target therapies (such as neo-angiogenesis and immune checkpoint inhibitors).

PMID 42557589
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PubMedOncogene2026-08-06

TET2-driven demethylation of ANG promotes angiogenesis and malignant transformation in oligodendroglioma.

Jin Jiamin J, Yuan Zhenbo Z, Wu Hao H, Wei Yi Y et al.

Oligodendrogliomas (OG) are indolent yet inevitably progressive gliomas in which angiogenesis is tightly linked to malignant transformation, but the underlying epigenetic mechanisms remain unclear. By integrating public datasets of primary and malignant transformed OG specimens, patient-derived cell lines and orthotopic xenograft models, we identify angiogenin (ANG) as a key pro-angiogenic regulator whose high expression correlates with increased microvessel density, enhanced proliferation and poor overall survival. Promoter methylation analyses reveal that ANG is heavily methylated in low-grade tumors and that hypomethylation of three CpG-rich regions including the prognostic site e.g., cg10850001, associates with increased ANG expression, higher tumor grade and worse outcome. Functional studies show that ANG knockdown suppresses VEGFA and Ki67 expression, reduces endothelial tube formation and intratumoral microvessel density, and significantly prolongs survival in Oligodendroglioma PDOX mice, whereas pharmacologic demethylation with decitabine decreases methylation at the ANG CpG hotspot (CpG islands 5 and 6-7), upregulates ANG and accelerates malignant phenotypes. Among TET dioxygenases, TET2 is selectively upregulated in malignant oligodendroglioma, directly binds to the ANG upstream regulatory region, with enrichment at the ANG CpG hotspot, and enhances its activity; TET2 depletion increases methylation at the ANG CpG hotspot, downregulates ANG and pro-angiogenic markers, and impairs angiogenesis, effects that are rescued by ANG re-expression. The cell-permeable itaconate derivative 4-octyl itaconate (OI), an itaconate derivative reported to inhibit TET activity, restores methylation at the ANG CpG hotspot, suppresses TET2-ANG signaling and cooperates with Temozolomide (TMZ) to inhibit tumor growth and extend survival in PDOX models. These findings define a TET2-ANG-angiogenesis axis that promotes an angiogenic program associated with malignant progression in oligodendroglioma and support itaconate-based pharmacologic TET modulation as a promising but still preclinical potential therapeutic strategy. Schematic diagram. Proposed TET2-ANG axis in oligodendroglioma progression. Solid arrows indicate relationships directly supported by experimental evidence in this study, including TET2-dependent demethylation of the ANG promoter, increased ANG expression, and downstream changes in VEGFA expression, angiogenesis, and malignant progression. These downstream effects are also supported by our previous study6. Dashed arrows indicate proposed or indirectly supported steps that were not directly tested for causality here (e.g., VEGFA secretion/transfer to the extracellular space, VEGFA-mediated activation of endothelial cells, and the contribution of angiogenesis to malignant progression). The inhibitory bar denotes pharmacologic inhibition; a dashed inhibitory bar indicates putative target engagement inferred from downstream readouts.

PMID 42557305
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PubMedCureus2026-08-05

Ten-Year Disease Control of Metastatic Pancreatic Neuroendocrine Tumour Treated With Everolimus.

Machete Madalena M, Silva Bruno M BM, Simões Pedro P, Leal-Costa Luísa L et al.

Management of metastatic pancreatic neuroendocrine tumours remains challenging due to clinical heterogeneity and limited high-quality evidence, especially regarding treatment beyond first-line therapy. Optimal treatment strategies in the second-line setting are not well established. We report the case of a woman in her late 30s who presented with progressively debilitating back pain and was diagnosed with an intermediate-grade pancreatic neuroendocrine tumour with bone and liver metastases. Based on negative findings on somatostatin receptor-based imaging, she commenced first-line chemotherapy with capecitabine and temozolomide. In parallel, local therapy for bone metastases was administered through radiotherapy and surgical intervention. After eight months of therapy, there was significant disease progression, with numerous bone and lymph node metastases. At this point, treatment was switched to everolimus as second-line therapy. The patient experienced rapid functional improvement, a marked reduction in tumour burden, and only manageable side effects (stomatitis and hypertriglyceridaemia). Over time, she achieved sustained disease control with everolimus. This case illustrates a durable clinical response to second-line everolimus in a patient with metastatic pancreatic neuroendocrine tumour and adds to the growing clinical experience with this treatment. It also highlights the benefits of a multidisciplinary approach to the management of metastatic disease.

PMID 42553455
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PubMedJournal of oncology pharmacy practice : official publication of the International Society of Oncology Pharmacy Practitioners2026-08-05

Depatuxizumab mafodotin in glioblastoma: A systematic review of efficacy, safety, pharmacokinetics and biomarker stratification.

Matar Hasan H, Alrabadi Bassel B, Abu Ata Aseel A, Bahdar Zainab Z et al.

BackgroundGlioblastoma (GBM) is an aggressive primary brain tumor with a dismal prognosis. Alterations in the Epidermal Growth Factor Receptor (EGFR) in about half of the cases, represent a key therapeutic target. Depatuxizumab mafodotin (Depatux-M) is an antibody-drug conjugate (ADC) developed to deliver a cytotoxic payload specifically to EGFR-amplified tumor cells.AimThis systematic review aims to synthesize all available clinical evidence to evaluate the antitumor efficacy, safety profile, pharmacokinetics, and biomarker-based stratification for Depatux-M in the treatment of glioblastoma.MethodsA systematic literature search was conducted across PubMed, Scopus, Cochrane Library and Web of Science. After screening, 11 clinical studies involving a total of 1420 patients were included for analysis. Data on efficacy, safety, biomarkers, and pharmacokinetics were extracted and synthesized.ResultsThe review found that Depatux-M demonstrated modest antitumor activity, with objective responses and improved progression-free survival primarily observed in the molecular subgroup of patients with tumors harboring EGFR amplification and/or the EGFRvIII mutation. Pharmacokinetic data showed linear, predictable exposure with low potential for drug-drug interactions, notably with temozolomide (TMZ). Ocular toxicities were the most common adverse events, occurring in over 90% of patients; these were often reversible and manageable. The overall safety profile was considered acceptable.ConclusionDepatuxizumab mafodotin presents a targeted treatment option with a manageable safety profile for a molecularly defined subset of glioblastoma patients. Its clinical benefit remains limited, underscoring the disease's heterogeneity and therapeutic resistance. The findings support the continued investigation of biomarker-guided ADC therapy and highlight the critical need for future clinical trials to integrate comprehensive molecular profiling for optimal patient selection.

PMID 42554799
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PubMedAsian journal of pharmaceutical sciences2026-08-04

A barrier-crossing and immune checkpoint-blocking antibody fusion protein for enhanced glioma-targeted immunotherapy.

Bao Yanning Y, Yang Shengmin S, Ding Yuan Y, Zhou Jianfen J et al.

With low five-year survival estimates, poor prognosis, and high recurrence probabilities, glioma is considered one of the most intractable malignant tumors. Despite the discovery of lymphatic vascular system and immune system in the central nervous system (CNS), immune checkpoint blockade therapeutics, such as programmed death ligand 1 (PDL1, also called B7H1 or CD274) antibodies, are prevented from the CNS and glioma sites due to the existence of biological barriers including the blood-brain barrier (BBB) and blood-brain tumor barrier (BBTB). Herein, we constructed a BBB/BBTB-crossing recombinant antibody by fusing the PDL1 antibody (αPDL1) and the targeting moiety RAP22 peptide (RAP22) through a matrix metalloproteinase 2 (MMP2)-responsive cleavable linker, abbreviated as αPDL1-mRAP22. Not only was αPDL1-mRAP22 able to block PD1/PDL1 pathway, reduce T cell apoptosis, enhance T cell killing ability towards glioma cells in vitro, but also it showed higher accumulation in the glioma site, prolonged survival time, and potent immune responses as well as synergistic effects with temozolomide (TMZ) in vivo, offering a novel strategy for glioma immunotherapy.

PMID 42548860
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