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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

PubMedGynecologic oncology reports2026-09-20

Temozolomide and olaparib for the treatment of an ARID1A-mutated uterine carcinosarcoma: A case report.

Liu Chrissy C, Abozenah Yasmin Y, Rutherford Thomas J TJ, Andikyan Vaagn V et al.

Pathogenic ARID1A mutations are common in uterine carcinosarcoma (UCS) and may confer vulnerability to the combination of temozolomide (TMZ) and a poly (ADP-ribose) polymerase inhibitor (PARPi) through synthetic lethality. Clinical experience with this regimen in gynecologic cancers is limited and has not been reported in UCS. A 54-year-old woman with stage IIIB UCS harboring a pathogenic ARID1A mutation developed isolated cavitating pulmonary metastases shortly after completing chemoradiation, surgery, and adjuvant carboplatin/paclitaxel with dostarlimab. She received off-label temozolomide and olaparib on a 21-day cycle. After four cycles, she achieved a complete radiographic response and has remained in clinical remission with normal CA-125 and negative circulating tumor DNA. Treatment was complicated by reversible grade 3-4 thrombocytopenia. This case suggests that TMZ/PARPi may produce durable responses in biomarker-selected UCS and supports prospective evaluation of this regimen in genomically characterized, ARID1A-defined gynecologic cancers.

PMID 42763538
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PubMedMolecular and cellular biochemistry2026-09-19

NRF2 signaling drives chemoresistance in NSCLC and glioblastoma.

de Souza Izadora I, Monteiro Linda Karolynne Seregni LKS, da Silva Teixeira Ana Beatriz AB, Guedes Camila Banca CB et al.

Although great advances have been made in cancer treatment, lung cancer and glioblastoma patients continue to present a dismal prognosis, mainly due to drug resistance. Evidence suggests that NRF2 and glutathione (GSH) play a fundamental role in chemotherapy resistance. Notably, GSH depletion by buthionine sulfoximine (BSO) has been demonstrated to sensitize human tumor cells to a wide variety of chemotherapeutic agents. However, the incorporation of BSO into standard chemotherapy regimens lacks a robust clinical rationale. In this study, we aimed to investigate the mechanisms governing differential sensitivity to chemotherapy in lung cancer and glioblastoma cells to identify novel strategies to enhance outcomes in these malignancies. For this purpose, we analyzed several cellular responses in cell lines exhibiting distinct sensitivities to temozolomide (TMZ) and cisplatin. Our findings indicate that the NRF2/GSH pathway plays a crucial role in TMZ and cisplatin resistance and that pharmacological GSH depletion enhances the sensitivity of NRF2-high, chemotherapy-resistant cells to these agents. Furthermore, BSO in combination with TMZ or cisplatin enhanced chemotherapy-induced cytotoxicity and engaged both apoptotic and ferroptosis-related responses in NSCLC cells. These findings provide preclinical evidence supporting further investigation of NRF2/GSH targeting as a strategy to overcome chemotherapy resistance.

PMID 42762415
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PubMedTranslational oncology2026-09-19

Paired bulk transcriptomic analysis of recurrent glioblastoma with primary single-cell reference mapping.

Kong Xuandong X, Zhao Ming M, Jin Qichao Q, Pan Bolin B

Glioblastoma (GBM) is the most aggressive primary brain tumor in adults, and virtually all patients relapse on standard temozolomide (TMZ) plus radiotherapy. The molecular mechanisms that allow residual tumor cells to survive treatment, reshape the microenvironment, and seed a drug-resistant recurrence remain incompletely understood. We analyzed paired bulk RNA-seq from 13 primary-recurrent patient pairs (GSE139533), used two published primary GBM single-cell/single-nucleus samples (GSE138794/GSM4119534 and GSE174554/GSM5319503; 5244 quality-controlled cells/nuclei) solely for cellular-context mapping, and evaluated an exploratory bulk-derived gene set in TCGA-GBM. Paired testing of 18,445 genes identified one significant gene at FDR 〈 0.05 and |log2FC| 〉 0.3: IL4I1 (log2FC = 1.49, FDR = 0.023). A 40-gene exploratory set was defined as the 40 positive paired-effect genes with the strongest paired-test evidence in the same 13 pairs and used descriptively; its mean paired score difference was 1.02 z-score units, but no independent significance test was assigned to this within-cohort score. In the primary single-cell references, the set scored highest in Myeloid-like cells, providing cellular context without constituting a primary-recurrent single-cell comparison. TCGA-GBM showed a weak, non-significant baseline survival association (Cox HR 1.30, 95% CI 0.91-1.87, P = 0.15). A TMZ-resistant U251 derivative had a higher TMZ IC50 than parental cells (612 vs 89 µM), and Western blotting showed increased MGMT, CD44, Vimentin, HIF-1α, OPN and PD-L1 across three biological experiments. Together, these data provide a paired bulk description of recurrence-associated expression and use primary single-cell references only to localize the exploratory signal.

PMID 42762693
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PubMedMedicine2026-09-19

Nasal NUT carcinoma with repeated responses during multimodal treatment incorporating radiotherapy: A case report.

An Qi Q, Tao Yuxuan Y, Wang Peiguo P, Wang Zhongqiu Z

Nuclear protein in testis (NUT) carcinoma, formerly referred to as NUT midline carcinoma, is an exceptionally rare and aggressive malignancy. Evidence guiding radiotherapy-based management is limited, especially for nasal primary tumors with neuroaxis and systemic dissemination. A 40-year-old woman was referred after resection of a nasal cavity malignancy. During the subsequent course, she experienced orbital pain, headache, visual impairment, severe lumbar and radicular pain, bilateral lower-limb paralysis, urinary retention, malignant pleural effusion, and widespread metastatic disease. Pathologic consultation supported nasal NUT carcinoma, with positive NUT immunostaining and a Ki-67 index of approximately 70%. External molecular testing was reported to confirm a NUTM1 rearrangement, although the original report could not be obtained for review, and the assay platform and fusion partner could not be independently verified. After surgery, the patient received postoperative VMAT/IMRT to 70 Gy in 35 fractions with concurrent cisplatin. Following leptomeningeal, cauda equina, and extensive osseous dissemination, she received palliative helical IMRT/Tomotherapy craniospinal irradiation to 15 Gy in 10 fractions. A later VMAT plan delivered 30 Gy in 10 fractions to one lumbar and 2 hepatic targets. Pembrolizumab, bevacizumab, temozolomide, pleural drainage, and intrapleural therapy overlapped with different treatment phases. During the first course, headache severity decreased from 8/10 to 2.5/10 on a visual analog scale, and clinically recorded Snellen visual acuity improved from 20/200 to 20/50. Pain relief was documented after craniospinal irradiation and after the third treatment course. Serial imaging was contemporaneously interpreted as indicating interval reduction in selected lesions after radiation-containing multimodal treatment phases, although uniform retrospective remeasurement was not feasible. According to telephone follow-up with the patient's family, the patient died approximately 12 months after surgery. Repeated clinical and imaging responses were observed following multiple phases of multimodal treatment incorporating radiotherapy. Because systemic therapies were administered during overlapping periods, the independent contribution of radiotherapy could not be isolated. Radiotherapy may provide clinically meaningful local or palliative benefit as part of individualized multimodal treatment in selected patients.

PMID 42760727
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PubMedPhotodiagnosis and photodynamic therapy2026-09-18

Safety and Efficacy of Sonodynamic Therapy Combined with Stupp Regimen in Controlling Postoperative Residual Lesions of Glioblastoma: A Prospective Pilot Phase I Study.

Wang Long L, Ding Jiayin J, Liu Xiaohao X, Li Tianqi T et al.

Postoperative residual disease in glioblastoma (GBM) drives early recurrence due to the blood-brain barrier (BBB), local hypoxia, and normal brain tissue dose constraints. Sonodynamic therapy (SDT) utilizes transcranial low-intensity ultrasound to selectively activate sonosensitizers (e.g., hematoporphyrin), inducing non-invasive oxidative tumor ablation, BBB permeabilization, and hypoxia alleviation. We evaluated the safety, feasibility, and preliminary efficacy of multi-session transcranial SDT combined with standard chemoradiotherapy in newly diagnosed GBM patients with MRI-confirmed residual lesions. In this prospective, open-label Phase I trial (Ethics Approval No. 2024-KY-0621-002), 18 newly diagnosed IDH-wildtype GBM patients received a three-phase regimen: (1) Induction: pre-radiotherapy SDT (hematoporphyrin 3 mg/kg, 0.84 MHz, 1.5 W/cm², 50% duty cycle, twice daily for 5 days) with temozolomide (TMZ, 75 mg/m² daily); (2) Concurrent: intensity-modulated radiotherapy (60 Gy in 30 fractions) with daily TMZ (75 mg/m² for 6 weeks); and (3) Maintenance: adjuvant TMZ with optional concurrent SDT (hematoporphyrin 5 mg/kg, n = 9) or TMZ alone (n = 9). Primary endpoints were safety (NCI-CTCAE v5.0) and feasibility. Secondary endpoints included progression-free survival (PFS), overall survival (OS), and objective response rate (ORR) via RANO criteria. Over a median follow-up of 26.23 months (95% CI: 21.97-27.47), primary safety and feasibility endpoints were met. No treatment-related deaths or grade 4/5 toxicities occurred. Treatment-related adverse events were mostly mild-to-moderate (grade 1/2) and transient, including 1 grade 1 photosensitivity reaction and 2 grade 1 cerebral edema events managed with osmotic therapy. For the entire cohort (n = 18), median OS was 19.00 months (95% CI: 17.27-23.97; 12-month OS rate: 88.9%), median PFS was 10.53 months (95% CI: 8.67-18.23), ORR was 66.7% (12 PR, 6 SD), and Disease Control Rate was 100%. In maintenance subgroup analysis, patients receiving SDT + TMZ showed a higher ORR (88.9% vs. 44.4%) and extended median PFS (11.80 vs. 9.27 months; P = 0.599) compared with TMZ alone, with comparable OS (19.00 vs. 20.10 months; P = 0.740). Integrating transcranial SDT with standard chemoradiotherapy and maintenance temozolomide is safe, feasible, and well tolerated in newly diagnosed GBM with residual disease. Encouraging preliminary efficacy signals warrant further evaluation in multi-center Phase II trials.

PMID 42759826
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PubMedACS omega2026-09-18

Design and Evaluation of PLGA-Based Hybrid Nanoparticles for Nasal Paclitaxel Delivery: Formulation Optimization, Barrier Transport, and Cytotoxicity Assessment.

Sousa Anna Carolina da Silva ACDS, Oda Caroline Mari Ramos CMR, Branco de Barros André Luis AL, de Freitas Marques Maria Betânia MB et al.

Paclitaxel (PTX) is a potent antiglioma agent, but its clinical use is limited by poor penetration across the blood-brain barrier (BBB). This study developed and evaluated a nose-to-brain delivery strategy using paclitaxel-loaded hybrid nanoparticles (HNP-PTX) for intranasal administration. A full 22 factorial design was employed to optimize the formulation, yielding an HNP-PTX system with a monodisperse distribution (<200 nm) and spherical morphology. The impact of chitosan coating was evaluated, revealing changes in surface charge and spray properties; but this did not significantly enhance transport across RPMI-2650 cells cultured at the air-liquid interface. Importantly, all HNP-PTX formulations preserved nasal epithelial barrier integrity while significantly increasing PTX permeation relative to the free drug. Cytotoxicity assays in U87-MG glioblastoma cells showed that HNP-PTX reduced cell viability more than both taxol and temozolomide (TMZ). These in vitro findings suggest HNP-PTX is a promising candidate for further in vivo evaluation as an intranasal formulation for glioblastoma treatment.

PMID 42756828
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