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temozolomide (SI 053 / Temodex / SI053)

✓ Approved

Double Bond Pharmaceutical · Small Molecule · Small Molecule

What is temozolomide?

temozolomide is a small molecule developed by Double Bond Pharmaceutical. It is approved for therapeutic indications via intratumoral injection.

Drug Profile

Brand NamesSI 053, Temodex, SI053
CompanyDouble Bond Pharmaceutical
Drug ClassSmall Molecule
RouteIntratumoral Injection
StatusApproved
Sources: ClinicalTrials.gov, Double Bond Pharmaceutical

Therapeutic Indications

temozolomide is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Brain neoplasm malignant✓ Approved

Related Research Articles

PubMedCureus2026-07-17

Exceptional Long-Term Disease Stability Under Nivolumab in Recurrent High-Grade Glioma: A Case Report.

Santos Joana N JN, Batista Francisca S FS, Sanches Frederico F, Miranda Ana A et al.

Immune checkpoint inhibitors have not demonstrated a survival benefit in unselected high-grade glioma populations; however, a subset of patients may achieve durable disease control. We report the case of a 30-year-old male patient diagnosed with a right temporoparietal high-grade glioma, initially classified as anaplastic astrocytoma and later evolving to astrocytoma, isocitrate dehydrogenase (IDH)-mutant, grade 4 according to the 2021 World Health Organization classification. The patient underwent multiple surgical resections followed by radiotherapy with concomitant temozolomide and subsequent adjuvant temozolomide (Stupp protocol). Upon disease recurrence, he received second-line treatment with lomustine plus bevacizumab, with documented progression across successive lines of therapy. In the absence of standard therapeutic options, off-label nivolumab was initiated in November 2018 following further progression. The tumor harbored an IDH1 R132H mutation and O6-methylguanine-DNA methyltransferase (MGMT) promoter methylation. Corticosteroids were discontinued prior to immunotherapy initiation. Serial magnetic resonance imaging demonstrated sustained radiological stability, without evidence of nodular enhancement or increased perfusion suggestive of recurrence. The most recent imaging assessment (March 2026) confirmed ongoing disease stability of more than seven years after treatment initiation. Treatment was well tolerated, with only mild immune-related arthralgias reported. The patient remains functionally independent, with stable mild residual hemiparesis. This case highlights the potential for prolonged disease stability under anti-Programmed cell death protein 1 (PD-1) therapy in selected patients with high-grade glioma. Although immunotherapy has not shown benefit in unselected populations, molecular features such as IDH mutation and MGMT promoter methylation, as well as the absence of corticosteroid use, may contribute to enhanced treatment responsiveness and warrant further investigation.

PMID 42465174
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PubMedbioRxiv : the preprint server for biology2026-07-17

Expanding Microgel Parameters to Model the Tumor Microenvironment and Examine Temozolomide Resistance in Glioblastoma.

Payan Brittany A BA, Kattoor Joel J, Carrillo Diaz de Leon Annika A, Thompson Gunnar B GB et al.

Glioblastoma (GBM) is a highly aggressive brain tumor with a five-year survival rate of less than 5%. The current standard of care established 20 years ago includes maximal surgical resection and administration of alkylating agent temozolomide (TMZ). GBM is highly invasive, and GBM cells that evade surgical resection can become resistant to TMZ and develop new aggressive secondary tumors. Post-relapse there are few treatment options available to patients. Tissue engineering approaches suggest the opportunity to develop in vitro models of the GBM tumor microenvironment that may accelerate the discovery of novel therapies for GBM. Here, we report the adaptation of hydrogel microdroplets (microgels) to encapsulate GBM cells in a tailorable 3D matrix to assess patters of growth and to screen TMZ drug response using patient-derived xenograft (PDX) specimens. We exploit a unique aspect of the microgel system to account for the cellular heterogeneity within the tumor microenvironment (TME). We combine cell-laden microgels generated from TMZ-resistant and TMZ responsive variants of the same PDX specimens to create heterogeneous populations with varying levels of drug sensitivity. We demonstrate a range of drug resistance phenotypes as a function of the ratio of TMZ-responsive to resistance cells and identify the population required for TMZ-resistance to overtake take the response. We then investigate the influence of tumor mimetic shifts in hyaluronic acid bioavailability and hypoxia on patterns of TMZ resistance. We show exposure to matrix-bound hyaluronan increases TMZ resistance and the glioma stem cell population in both cell variants. Lastly, we report an increase in TMZ sensitivity but divergent changes in the GSC subfraction for TMZ resistant vs responsive GBM in the presence of hypoxia. Together, we demonstrate the versatility of cell-laden microgel approach to replicate heterogenous tumor populations, model shifts in the tumor microenvironment, and rapidly screen therapeutic response.

PMID 42465419
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PubMedFrontiers in immunology2026-07-17

The immunosuppressive tumor microenvironment in glioblastoma.

Yang Jing J, Li Jie J, Jin Ming M, Lu Yongping Y et al.

Glioblastoma (GBM) remains one of the most lethal primary brain tumors, with limited therapeutic improvement despite maximal surgical resection, radiotherapy, and temozolomide. A major barrier to durable treatment response is the profoundly immunosuppressive tumor microenvironment, which is characterized by immune exclusion, defective antigen presentation, myeloid dominance, and severe T-cell dysfunction. Tumor-associated macrophages, resident microglia, myeloid-derived suppressor cells, neutrophils, regulatory T cells, and glioma-derived extracellular vesicles collectively establish a suppressive niche through cytokine signaling, metabolic restriction, checkpoint ligand expression, impaired phagocytosis, and extracellular matrix remodeling. Key pathways, including TGF-β/SMAD, IL-10/STAT3, IDO-kynurenine metabolism, arginase-1-mediated amino acid depletion, adenosine signaling, hypoxia-HIF-1α activation, and VEGF-driven vascular dysfunction, converge to prevent effective antitumor immunity. This review summarizes the cellular and molecular mechanisms underlying immune suppression in GBM and discusses emerging therapeutic strategies, including myeloid reprogramming, phagocytosis checkpoint blockade, neutrophil and NET targeting, cellular immunotherapy, checkpoint blockade combinations, and metabolic intervention. Understanding these interconnected barriers may guide rational multimodal strategies to convert immune-excluded GBM into immune-responsive disease.

PMID 42465775
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PubMedmedRxiv : the preprint server for health sciences2026-07-17

Phase I dose escalation of the Exportin 1 inhibitor, Selinexor, in combination with chemoradiation in patients with newly diagnosed glioblastoma.

Mathen Peter P, Chaudhry Huma H, Mackey Megan M, Cooley-Zgela Theresa T et al.

Glioblastoma (GBM) remains associated with poor outcomes, with most recurrences occurring within the high-dose radiation field suggesting persistent radioresistance. Exportin 1 (XPO1) inhibition with Selinexor has demonstrated radiosensitizing effects in preclinical models. We conducted a phase I trial to evaluate the safety, tolerability, and preliminary efficacy of Selinexor in combination with standard chemoradiation for newly diagnosed GBM. This investigator-initiated phase I dose-escalation trial (3+3 design) enrolled adults with newly diagnosed GBM or gliosarcoma. Patients received standard radiotherapy (60 Gy in 30 fractions) with concurrent temozolomide and escalating doses of Selinexor. Three dose levels were evaluated: 80 mg weekly (weeks 1, 2, 4, 5); 60 mg twice weekly (weeks 1, 2, 4, 5); and 60 mg twice weekly (weeks 1-6) throughout radiotherapy. The primary endpoint was determination of the maximum tolerated dose (MTD) based on dose-limiting toxicities (DLTs). Secondary endpoints included progression-free survival (PFS), overall survival (OS), patterns of failure, and patient-reported outcomes (MDASI-BT). Eleven patients were enrolled. Median age was 58 years, and median KPS was 90. The MTD was established at Selinexor 60 mg twice weekly during weeks 1, 2, 4, and 5 of chemoradiation. Dose level 3 exceeded the MTD with two DLTs. Treatment compliance was high, with minimal missed radiotherapy fractions. Median PFS was 15.9 months (95% CI, 6.2-28.5), and median OS was 17.4 months (95% CI, 14.1-not reached). Most recurrences were central (5/6 evaluable patients). Notably, multiple cases of delayed pseudoprogression were observed at 5, 9, 10, and 23 months post-radiotherapy. Patient-reported symptom burden remained stable over time. Selinexor can be safely combined with standard chemoradiation in patients with newly diagnosed GBM, with an MTD of 60 mg twice weekly during select treatment weeks. Preliminary efficacy signals and an increased incidence of delayed pseudoprogression suggest a potential radiosensitizing effect. These findings support further investigation of Selinexor in larger, prospective studies.

PMID 42465896
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PubMedBiofabrication2026-07-17

Shape, shrink, spheroid: a DIY high-throughput spheroid generation device.

Mogha Pankaj P, Mukherjee Sourav S, Gangwar Tushar T, Roy Debjyoti D et al.

3D spheroids, which closely replicate three-dimensional cell-cell and cell-extracellular matrix interactions, offer superior predictive capabilities compared to conventional 2D monolayer cultures, positioning them as forward-looking platforms in drug testing, cancer biology, and regenerative medicine. However, high-throughput generation of uniform sized spheroids is still a technological challenge. In one hand, the use of conventional ultra-low attachment (ULA) multiwell plates for this purpose is labour intensive and complex. On the other hand, the use of microfabricated facilities demands cutting-edge infrastructure such as clean room, photolithography, and microfluidic setup which are often unavailable for the resource constrained laboratories. In this study, we addressed these problems by developing a low-cost Do-It-Yourself (DIY), polydimethylsiloxane (PDMS) and agarose-based spheroid generation device, capable of producing and maintaining hundreds of spheroids with minimal user intervention. We have demonstrated two variants based on their size, termed here as S1 and S2 devices which fit into 6-well and 12-well plates, and can generate 600 and 1200 uniform-sized spheroids respectively. We validated our device with various cell lines including primary and cancerous cell lines. We further demonstrated the drug testing capabilities of the device by estimating the IC50 value of the anticancer drug Temozolomide on U87-MG. The value was comparable with the same obtained from the spheroids generated using conventional ULA plates. Additional attachment of a perfusion system made the device suitable for long-term spheroid culture without much user intervention. Furthermore, the devices can also be used for the production of spheroids with gradually changing diameters in a controlled manner, resembling a size gradient. This feature is useful for checking the effect of drugs on different-sized spheroids and for co-culturing spheroids with varying cell densities, mimicking the disease architecture. We have co-cultured two types of the placental trophoblast cells, i.e., extravillous trophoblast (HTR-8) and syncytiotrophoblast (BeWo) with varying densities. In summary, this paper demonstrates a unique DIY method for a high-throughput uniform-sized spheroid generation at a fraction of cost which can be deployed to resource-constrained labs.

PMID 42462770
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PubMedActa clinica Belgica2026-07-16

Implementation of tumour treating fields for glioblastoma in Belgium: real-world outcomes from a Belgian tertiary centre.

Feyaerts Annelies A, Lambrecht Maarten M, De Vleeschouwer Steven S, Lambert Julie J et al.

Tumour treating fields (TTF) improve survival in newly diagnosed glioblastoma (GBM) in randomized trials, but real-world impact in Belgium remains unclear due to limited access and lack of reimbursement. This study evaluates progression-free survival (PFS) and overall survival (OS) in Belgian patients with newly diagnosed GBM treated with TTF alongside standard therapy. We conducted a retrospective single-centre cohort study at UZ Leuven including patients with histologically confirmed newly diagnosed GBM treated with TTF between April 2019 and July 2026. TTF was initiated during adjuvant temozolomide. Clinical, molecular and treatment data were extracted from institutional records. Primary outcomes were PFS and OS from diagnosis. Kaplan-Meier survival analyses were performed, including subgroup analyses by MGMT status, device adherence (>75%), and extent of resection. Twenty-eight patients were analysed (median age 52 years; 71% male). MGMT promoter methylation was present in 29% and gross total resection was achieved in 50%. Adherence exceeded 75% in 96%. Median PFS was 6.8 months and median OS 24.6 months, comparing favourably with EF-14 outcomes. ECOG status predicted survival (p = 0.04). Survival was not associated with MGMT status or adherence. Gross total resection showed a clinically meaningful association with improved OS (30.7 vs 8.2 months; p = 0.07). Treatment was well tolerated. In this real-world Belgian cohort, TTF with standard therapy yielded survival outcomes consistent with or exceeding pivotal trials. While clinical benefit appears evident, implementation remains challenged by financial costs. Further prospective Belgian studies are needed to assess cost-effectiveness and quality-of-life impact.

PMID 42460646
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