Delving into the Latest Updates on Temozolomide with Synapse

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

3,4-dihydro-3-methyl-4-oxoimidazo(5,1-d)-1,2,3,5-tetrazine-8-carboxamide, 3,4-dihydro-3-methyl-4-oxoimidazo(5,1-d)-as-tetrazine-8-carboxamide, 3-methyl-4-oxo-3,4-dihydroimidazo(5,1-d)(1,2,3,5)tetrazine-8-carboxamide

+ [29]

Target

DNA

Action

inhibitors

Mechanism

DNA inhibitors(DNA inhibitors), DNA alkylating agents

Therapeutic Areas

NeoplasmsNervous System DiseasesSkin and Musculoskeletal Diseases+ [10]

Active Indication

Ewing SarcomaMalignant glioma of brainMalignant melanoma, metastatic+ [75]

Inactive Indication

Acoustic Neuromaacute leukemiaAcute myeloid leukaemia with 11q23 abnormality+ [115]

Originator Organization

Merck Sharp & Dohme Corp.

Active Organization

Sun Pharmaceutical Industries (Europe) BV

Novartis AG

medac Gesellschaft für klinische Spezialpräparate mbH

+ [32]

Inactive Organization

Hexal AG

Duke University

The Vanderbilt-Ingram Cancer Center

+ [37]

License Organization

Double Bond Pharmaceutical International AB

Institut Gustave Roussy EURL

Belarusian State University

+ [1]

Drug Highest PhaseApproved

First Approval Date

European Union (26 Jan 1999),

AstrocytomaGlioblastoma MultiformeGlioma

RegulationAccelerated Approval (United States), Orphan Drug (United States), Orphan Drug (European Union), Priority Review (China)

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Structure/Sequence

Molecular FormulaC6H6N6O2

InChIKeyBPEGJWRSRHCHSN-UHFFFAOYSA-N

CAS Registry85622-93-1

The goal of this clinical trial is to: 1) evaluate the safety, tolerability, and recommended dose of dexbrompheniramine when combined with metronomic temozolomide for adults with recurrent high-grade glioma who have been previously treated with standard of care chemoradiation therapy and 2) determine the efficacy of the combination therapy in adults with glioblastoma who progressed during the first six cycles of adjuvant standard dose temozolomide.
The main questions it aims to answer are:
* What medical problems to participants have when taking dexbrompheniramine together with temozolomide?
* What is the correct dose of dexbrompheniramine to use when evaluating the safety and efficacy of the combination therapy?
* Is the combination therapy more effective at delaying disease progression compared to temozolomide alone?
Participants will take dexbrompheniramine and temozolomide every day at night.

Start Date01 Jun 2027

Sponsor / Collaborator

University of Nebraska

NCT07807878

/ Not yet recruitingPhase 2IIT

Phase II Trial of Temozolomide in BAP1 Mutated Patients With Advanced or Metastatic Cutaneous Melanoma

BAP1, or BRCA1-associated protein 1, is a gene involved in DNA repair via homologous recombination and is considered a tumor suppressor gene. It is lost or inactivated in a large number of tumors, and the presence of germline BAP1 mutations is associated with a syndrome of tumor predisposition.
Following our team's observation of two exceptional responses to temozolomide in patients who had reached a therapeutic impasse-one of which lasted 11 months and involved both intracerebral and extracerebral tumors-we hypothesize that this mutation may lead to increased susceptibility to chemotherapy.

Start Date01 Jun 2027

Sponsor / Collaborator

Assistance Publique Hôpitaux de Marseille

100 Clinical Results associated with Temozolomide

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100 Translational Medicine associated with Temozolomide

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100 Patents (Medical) associated with Temozolomide

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13,402

Literatures (Medical) associated with Temozolomide

01 Feb 2027·BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE

Lipid-autophagy crosstalk in glioblastoma: A context-dependent stress-adaptation interface under temozolomide pressure

Review

Author: Eshraghi, Mehdi ; Barzegar Behrooz, Amir ; Iurchenko, Ivan

Glioblastoma (GB) is characterized by aggressive progression and frequent recurrence despite temozolomide (TMZ)-based therapy. Although resistance is commonly linked to DNA repair mechanisms, these pathways do not fully explain tumor persistence under therapeutic stress. Accumulating evidence suggests that metabolic reprogramming, particularly crosstalk between lipid metabolism and autophagy, may contribute to GB adaptation under TMZ-induced stress. We discuss how this lipid-autophagy interface may enable tumor cells to reconfigure energy production, maintain redox balance, and remodel membranes in response to therapy. Although the available evidence remains predominantly preclinical, convergent findings from lipidomic analyses and functional perturbation studies support lipid-autophagy crosstalk as an emerging contributor to TMZ resistance. This review presents this interaction as a testable conceptual framework for understanding metabolic adaptation to TMZ and discusses its potential therapeutic relevance.

01 Feb 2027·BRAIN BEHAVIOR AND IMMUNITY

Melatonin ameliorates behavioral deficits in 5xFAD mice through modulation of neurogenesis, neuroimmune responses, neurotransmission, and metabolic pathways

Article

Author: Wong, Kah Hui ; Fung, Man Lung ; Aquili, Luca ; Tse, Vera ; Lu, Zhiliang ; Wong, Kan Yin ; Mihardja, Mazel ; Au, Ching ; Lim, Lee Wei ; Temel, Yasin ; Tsui, Ka Chun ; Roy, Jaydeep ; Lai, Yunfan ; Kocabicak, Ersoy ; Ng, Jonah ; Poon, Chi Him ; Zhang, Jingyi ; Li, Pui Ching

Alzheimer's disease (AD) is a neurodegenerative disorder with limited disease-modifying treatment options. Melatonin, an endogenous hormone, has been shown to have therapeutic effects on amyloid deposition, oxidative stress, and neuroinflammation in AD. However, the mechanisms of its neuroprotective effects in the hippocampus remain largely unknown. This study aimed to investigate the multi-mechanistic neuroprotective effects of melatonin in AD. Eight-month-old female 5xFAD transgenic mice were treated with melatonin (10 mg/kg) for 4 weeks. Temozolomide and bromodeoxyuridine were used to block neurogenesis and to label proliferating neurons, respectively. Our results showed that 5xFAD mice treated with melatonin exhibited improved exploratory behavior, enhanced memory performance, reduced depressive-like symptoms, and decreased levels of stress hormones. At the molecular level, melatonin reduced amyloid-beta (Aβ) plaque accumulation, elevated hippocampal neurogenesis markers (DCX and BrdU), increased Trem2 expression and anti-inflammatory microglial activation, restored serotonergic, dopaminergic, catecholaminergic, and GABAergic neurotransmission, and partially normalized broader hippocampal metabolic pathways. Notably, temozolomide treatment abrogated the beneficial effects of melatonin on memory performance and depressive-like behavior in 5xFAD mice, indicating a neurogenesis-dependent mechanism. Collectively, these findings suggest that melatonin ameliorates behavioral deficits in 5xFAD mice through both neurogenesis-independent (reduced Aβ plaque accumulation, Trem2-microglial activation, neurotransmission restoration, and metabolic remodeling) and hippocampal neurogenesis-dependent mechanisms. Overall, melatonin holds therapeutic potential for attenuating the neuropathology and behavioral deficits in AD.

01 Feb 2027·BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE

Loss of PIMREG impairs double-strand break signaling and repair

Article

Author: Mamede, Mariana Siqueira Lacerda ; Dias, Isabela Spido ; Greif, Philipp A ; de Almeida, Giovanna Gonçalves ; Heinzlmeir, Stephanie ; Kuster, Bernhard ; Cardoso, Isabela David ; Hojo, Elza Tiemi Sakamoto ; Archangelo, Leticia Fröhlich ; do Carmo, Laís ; Arfelli, Vanessa Cristina ; Black, Jennifer Ann ; de Rizzo Gasparini, Maria Vitória ; Chang, Yun-Chien ; Sardinha, Lígia Arantes

Glioblastoma (GBM) is the most common primary brain tumor in adults. It is an aggressive type of tumor with an average overall survival of 12-15 months post-diagnosis. Standard treatment involves surgical resection, followed by radiotherapy and chemotherapy with temozolomide (TMZ). However, resistance to treatment is frequently observed. PIMREG is a marker of proliferation highly expressed across different tumor types, with particularly elevated levels in GBM. Our previous study revealed that PIMREG silencing sensitizes GBM cells to TMZ treatment and affects ATM activation, a key apical kinase involved in DNA damage signaling. Given the emerging significance of PIMREG in the DNA damage response, we sought to explore PIMREG's role in DNA damage repair and signaling in GBM cells exposed to genotoxic agents. Here we assessed the functionally enriched pathways associated with high PIMREG expression in GBM patient samples, analyzed the interactome of PIMREG upon treatment of GBM cells with TMZ and evaluated the impact of PIMREG loss on DNA damage signaling, DNA break formation and the repair of double-strand breaks. Our findings reveal that PIMREG functions as a direct substrate for ATM/ATR kinases, interacts with key DNA repair proteins upon TMZ treatment and actively facilitates the cellular response to chemotherapy- and radiotherapy-induced DNA damage. Taken together, PIMREG may function in the DNA damage response, particularly in the signaling and repair of double strand breaks via homologous recombination in GBM cells. In all, our data suggested high PIMREG expression may affect resistance of GBM cells to treatment.

455

News (Medical) associated with Temozolomide

02 Nov 2026

·www.biospace.com

Nuvation Bio to Present Additional Updated Phase 2 Results at 2026 Society for Neuro-Oncology Annual Meeting

Nuvation Bio will present four posters: one will showcase updated long-term Phase 2 results; three posters highlight trial in progress overviews for ongoing safusidenib studies Poster featuring Phase 2 results to be presented at SNO includes additional data beyond topline results previously announced in July 2026 NEW YORK , Nov. 2, 2026 /PRNewswire/ -- Nuvation Bio Inc. (NYSE: NUVB), a global oncology company focused on tackling some of the toughest challenges in cancer treatment, today announced that additional updated results from the Phase 2 J201 study and three posters on ongoing studies of safusidenib, its selective investigational inhibitor of mutant IDH1, will be presented at the Society for Neuro-Oncology (SNO) Annual Meeting taking place November 12–15, 2026, in Philadelphia, PA. Positive topline Phase 2 J201 results were announced in July ; additional key data will be featured in the SNO poster. "Patients with IDH1 -mutant glioma are often diagnosed in their 30s and 40s and may live with their disease for many years, underscoring the importance of targeted treatments that can deliver durable responses with a consistent safety profile," said David Hung, M.D., Founder, President and Chief Executive Officer of Nuvation Bio. "We look forward to sharing updated Phase 2 results that speak to that need, as well as progress across our expanded safusidenib development program, with the clinicians and patient community working to advance care for people living with IDH1 -mutant glioma." Presentations Overview: Title: Updated efficacy and safety results from a Phase 2 study of safusidenib in patients with chemotherapy- and radiotherapy-naïve Grade 2 isocitrate dehydrogenase 1 (IDH1)-mutant glioma Presenter: Yoshiki Arakawa, Kyoto University Graduate School of Medicine, Kyoto, Japan Date: Friday, November 13, 2026 Session Time: 7:30-9:30 p.m. ET Title: SIGMA: A Phase 3 study evaluating maintenance safusidenib vs placebo following radiotherapy (RT) or chemoradiotherapy (CRT) and adjuvant temozolomide (TMZ) in patients with isocitrate dehydrogenase 1 (IDH1)-mutant astrocytoma with high-risk features Presenter: Katherine B. Peters, Duke University Medical Center, Durham, USA Date: Friday, November 13, 2026 Session Time: 7:30-9:30 p.m. ET Title: Open-label, single-arm, exploratory cohort evaluating safusidenib in chemotherapy (CT)- and radiotherapy (RT)-naïve patients with Grade 3 isocitrate dehydrogenase 1 (IDH1)-mutant oligodendroglioma Presenter: Fabio Iwamoto, Columbia University Irving Medical Center, New York, USA Date: Friday, November 13, 2026 Session Time: 7:30-9:30 p.m. ET Title: A Phase 2 study evaluating the efficacy and safety of safusidenib in Grade 2 or 3 isocitrate dehydrogenase 1 (IDH1)-mutant glioma after disease progression (PD) on vorasidenib Presenter: Macarena de la Fuente, Sylvester Comprehensive Cancer Center, University of Miami, Miami, USA Date: Friday, November 13, 2026 Session Time: 7:30-9:30 p.m. ET The materials will be made available in the Publications section of Nuvation Bio's website after the presentations. To meet representatives from Nuvation Bio, visit Booth #126. About IDH1 -mutant Glioma Gliomas are the most common type of brain cancer in adults worldwide. In the U.S., nearly 2,500 people are diagnosed with IDH -mutant gliomas each year, of which more than 95% harbor a mutation in the IDH1 gene. Most patients are diagnosed in their 30s and 40s. While patients with IDH1 mutations generally have longer survival times than those with wild-type IDH1 , gliomas are not currently curable and prognosis worsens for those with high-risk features, including high grade tumors. About Safusidenib Safusidenib is an investigational, oral, brain-penetrant, selective inhibitor of mutant IDH1. It is being studied in patient populations with significant unmet medical need, including settings where there are limited or no approved targeted treatment options. In Phase 1 and Phase 2 clinical studies, safusidenib demonstrated encouraging clinical activity, including delayed disease progression and durable responses across a range of tumor grades and risk groups, with a favorable risk-benefit profile. These early findings support further investigation of safusidenib in the currently enrolling Phase 3 SIGMA study, as well as in the Phase 3 G307 study in regions where vorasidenib is not yet approved or accessible and the Phase 2 G209 study in patients whose cancer has progressed on vorasidenib. In August 2026, the FDA granted Fast Track Designation to safusidenib for the treatment of IDH1-mutant glioma. About the SIGMA (G203) Study SIGMA is a pivotal Phase 3 study that will evaluate safusidenib compared to placebo as a maintenance therapy after standard-of-care in IDH1 -mutant astrocytoma with high-risk features. The pivotal portion of the study will enroll approximately 300 patients. A separate, exploratory, non-pivotal cohort will evaluate safusidenib in participants with grade 3 IDH1 -mutant oligodendroglioma who have not yet received chemotherapy or radiotherapy. The primary endpoint is objective response rate. This cohort is expected to enroll approximately 40 patients. About Nuvation Bio Nuvation Bio is a global oncology company focused on tackling some of the toughest challenges in cancer treatment with the goal of developing therapies that create a profound, positive impact on patients' lives. Our diverse pipeline includes taletrectinib (IBTROZI ® ), a next-generation ROS1 inhibitor; safusidenib, a brain-penetrant IDH1 inhibitor; and an innovative drug-drug conjugate (DDC) program. Nuvation Bio was founded in 2018 by biopharma industry veteran David Hung, M.D., who previously founded Medivation, Inc., which brought to patients one of the world's leading prostate cancer medicines. Nuvation Bio has offices in New York, San Francisco, Boston, and Shanghai. For more information, visit or follow the company on LinkedIn and X ( @nuvationbioinc ). Media and Investor Contacts Nuvation Bio Investor Contact JR DeVita ir@nuvationbio.com Nuvation Bio Media Contact Kaitlyn Nealy media@nuvationbio.com View original content to download multimedia: SOURCE Nuvation Bio Inc.

Phase 2Fast TrackPhase 3ASCOPhase 1

02 Nov 2026

·www.biospace.com

NeOnc Technologies to Present Data from Its NEO100 and NEO212 Programs at the 31st Annual Meeting of the Society for Neuro-Oncology

CALABASAS, Calif., Nov. 02, 2026 (GLOBE NEWSWIRE) -- NeOnc Technologies Holdings, Inc. (Nasdaq: NTHI) (“NeOnc” or the “Company”), a clinical-stage biopharmaceutical company developing therapies for central nervous system (CNS) cancers, today announced that data from its intranasal NEO100 and oral NEO212 programs will be presented in two posters on Friday, November 13, at the 31st Annual Meeting and Education Day of the Society for Neuro-Oncology (SNO), held November 12 to 15, 2026, at the Pennsylvania Convention Center in Philadelphia. “We look forward to presenting data from both of our clinical programs at SNO,” said Amir F. Heshmatpour, Executive Chairman, President and Chief Executive Officer of NeOnc. “These presentations reflect the progress we are making in bringing new approaches to patients with brain cancer.” Presentation Details Title: Durable Radiographic Remission and Prolonged Survival with Intranasal NEO100 in Recurrent WHO Grade III/IV IDH1-Mutant Astrocytoma: Updated Results from a Phase 1/2a Study and Compassionate Use Experience Abstract Number: CTNI-26 Presentation Type: Poster Session: Poster Session Presenter: Thomas C. Chen, MD, PhD, University of Southern California and NeOnc Technologies Holdings, Inc. Date and Time: Friday, November 13, 2026, 7:30 to 9:30 p.m. EST Location: Exhibit Halls D and E, Second Floor, Pennsylvania Convention Center, Philadelphia Title: Oral NEO212 in TMZ-Resistant Recurrent GBM and Brain Metastases: Phase 1 Safety, PK, and Early Signals of Activity Abstract Number: CTNI-27 Presentation Type: Poster Session: Poster Session Presenter: Josh Neman, PhD, University of Southern California and NeOnc Technologies Holdings, Inc. Date and Time: Friday, November 13, 2026, 7:30 to 9:30 p.m. EST Location: Exhibit Halls D and E, Second Floor, Pennsylvania Convention Center, Philadelphia About NEO100 NEO100 is a highly purified form of perillyl alcohol administered intranasally. Its delivery approach is designed to provide a non-invasive route to the brain. NEO100 remains investigational, and its safety and efficacy have not been established. About NEO212 NEO212 is an investigational oral conjugate of temozolomide and NEO100. It is being studied for CNS cancers, including recurrent glioblastoma. Preclinical studies support further evaluation of its potential activity and delivery characteristics; clinical efficacy and safety have not been established. NEO212 is being developed under an FDA investigational new drug application. About NeOnc Technologies Holdings, Inc. NeOnc Technologies Holdings, Inc. is a clinical-stage biopharmaceutical company developing therapies for central nervous system cancers. Its investigational programs include intranasal NEO100 and oral NEO212. NEO212 has completed Phase 1 dose escalation and is advancing toward Phase 2 development. NeOnc exclusively licenses a worldwide portfolio of issued patents and pending applications from the University of Southern California related to NEO100, NEO212 and other drug candidates and delivery approaches. For more information, visit . Forward-Looking Statements This press release contains forward-looking statements, including statements regarding the Company’s clinical development programs and the clinical potential of NEO100. Forward-looking statements in this release also include statements regarding the clinical potential of NEO212 and the planned presentation of data at the Society for Neuro-Oncology Annual Meeting. These statements reflect current expectations and involve risks and uncertainties. NEO100 is investigational and has not been approved by any regulatory authority; future studies may not demonstrate safety or efficacy; clinical development remains subject to applicable clinical, regulatory and institutional requirements; and no regulatory pathway or marketing approval is assured. NEO212 is also investigational and has not been approved by any regulatory authority. Actual results may differ materially. Readers should consider the risk factors described in the Company’s most recent filings with the Securities and Exchange Commission. These statements speak only as of the date of this release. The Company undertakes no obligation to update forward-looking statements except as required by law. “NEO100” and “NEO212” are registered trademarks of NeOnc Technologies Holdings, Inc. Contacts Company Contact: info@neonc.com Investor Contact: Jon Nugent Jon Nugent Communications jon@jonnugent.com 205-566-3026 This press release was published by a CLEAR® Verified individual.

Phase 1

01 Nov 2026

·www.biospace.com

Glioblastoma Foundation’s Genomic Testing & Research Laboratory Now Accepting Patient Samples for Genomic Testing

The Foundation's CLIA-certified laboratory combines DNA methylation profiling, MGMT status, copy-number variation analysis and glioblastoma subtype characterization in a single assay DURHAM, NC / ACCESS Newswire / October 31, 2026 / Gliolab, the Glioblastoma Foundation's new CLIA-certified Genomic Testing & Research Laboratory, today announced that it is accepting patient tumor samples for Whole-Genome DNA Methylation Profiling using the Epignostix Classifier, expanding access to one of the most comprehensive molecular characterization approaches currently available in neuro-oncology. The launch reflects a growing recognition that molecular profiling is increasingly essential for understanding glioblastoma biology. As molecular information assumes a greater role in brain tumor classification, clinicians and researchers are seeking more sophisticated tools to support diagnosis, characterize glioblastoma subtypes and inform future research efforts. "The field has made significant progress in understanding the molecular biology of glioblastoma, yet access to advanced testing remains inconsistent," said Gita Kwatra, PharmD, MBA, Co-Founder and Chief Executive Officer of the Glioblastoma Foundation. "Our goal is to help ensure that physicians, researchers and patients can benefit from the scientific advances that are reshaping neuro-oncology." Whole-Genome DNA Methylation Profiling using the Epignostix Classifier is an advanced genomic test currently available at only a handful of institutions in the United States. The test measures DNA methylation at hundreds of thousands of sites across the tumor genome and uses machine-learning and AI-based approaches to classify the tumor and confirm the diagnosis of glioblastoma. In addition, it provides important molecular information about the individual tumor, including MGMT promoter methylation, glioblastoma class and subclass, such as RTK1 and RTK2, and copy-number alterations involving 29 genes relevant to glioblastoma. Evidence supporting methylation-based classification continues to expand. In a landmark study published in Nature involving more than 1,000 central nervous system tumors, incorporation of methylation profiling altered or refined the diagnosis in approximately 12% of cases. Additional research from the U.S. National Cancer Institute found that methylation profiling influenced clinical management in approximately 15% of diagnostically challenging tumors. These findings underscore the growing role of molecular classification in supporting integrated diagnosis and improving understanding of tumor biology. Despite advances in genomic understanding, treatment options for glioblastoma remain limited. Standard therapy continues to rely primarily on surgery, radiation and temozolomide-based chemotherapy, with frontline treatment approaches remaining largely unchanged since 2005. As a result, there remains a significant need for research focused on understanding tumor heterogeneity, identifying biologically distinct patient populations and supporting future therapeutic development. Gliolab was established not only to expand access to molecular testing, but also to accelerate future discovery. Broad participation in molecular testing programs allows generations of large datasets needed to better understand glioblastoma biology and uncover new therapeutic opportunities. With appropriate patient consent and governance practices, molecular information generated through testing will support translational research, biomarker discovery, molecular subtype analysis and future clinical trial development. "Every sample has the potential to contribute to a larger understanding of this disease," said Kwatra. "The more comprehensively we can characterize glioblastoma biology, the better positioned the field will be to identify new research opportunities and, ultimately, develop future therapeutic approaches." Researchers, physicians and treatment centers are encouraged to consider submission of eligible patient samples to confirm and refine an initial diagnosis, characterize glioblastoma subtypes and inform future research efforts. The methylation assay represents the first phase of Gliolab's broader genomic testing program. Additional testing capabilities, including comprehensive genomic profiling with PGDx elio™ tissue complete and gene fusion testing, are expected to become available by mid-2027. About Gliolab Gliolab is the Glioblastoma Foundation's CLIA-certified Genomic Testing & Research Laboratory focused on expanding access to precision medicine for glioblastoma patients. The laboratory is believed to be the first nonprofit, CLIA-certified genomic testing laboratory in the United States dedicated exclusively to glioblastoma. Through advanced genomic testing and research, Gliolab helps physicians better understand tumor biology while generating insights that may advance future discoveries and more personalized treatment approaches. For more information, visit . About Glioblastoma Foundation Founded in 2016 and headquartered in Durham, North Carolina, Glioblastoma Foundation is a nonprofit organization dedicated to transforming glioblastoma therapy through research, education, precision medicine, and therapeutic development. The Foundation operates a CLIA-certified genomic testing laboratory focused on advancing genomic testing for glioblastoma patients, and supports the clinical development of lisavanbulin, an investigational therapy for glioblastoma. The Glioblastoma Foundation is committed to improving outcomes for patients and families affected by this disease. For more information, visit glioblastomafoundation.org . Media Contact: Kaplow Communications GF@kaplow.com SOURCE: Glioblastoma Foundation View the original press release on ACCESS Newswire

Clinical Study

100 Deals associated with Temozolomide

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External Link

KEGG	Wiki	ATC	Drug Bank
D06067	Temozolomide	L01AX03	DB00853

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Ewing Sarcoma	Japan	Ohara Pharmaceutical Co., Ltd.	21 Feb 2019
Ewing Sarcoma	Japan	MSD KK (Tokyo)	21 Feb 2019
Malignant glioma of brain	European Union	Teva Pharmaceuticals Europe BV	28 Jan 2010
Malignant glioma of brain	Iceland	Teva Pharmaceuticals Europe BV	28 Jan 2010
Malignant glioma of brain	Liechtenstein	Teva Pharmaceuticals Europe BV	28 Jan 2010
Malignant glioma of brain	Norway	Teva Pharmaceuticals Europe BV	28 Jan 2010
Malignant melanoma, metastatic	Australia	Merck Sharp & Dohme (Australia) Pty Ltd.	13 Nov 2009
Glioblastoma	China	Jiangsu Tasly Diyi Pharmaceutical Co., Ltd.	30 Apr 2004
Astrocytoma	European Union	Merck Sharp & Dohme BV	26 Jan 1999
Astrocytoma	Iceland	Merck Sharp & Dohme BV	26 Jan 1999
Astrocytoma	Liechtenstein	Merck Sharp & Dohme BV	26 Jan 1999
Astrocytoma	Norway	Merck Sharp & Dohme BV	26 Jan 1999
Glioblastoma Multiforme	European Union	Merck Sharp & Dohme BV	26 Jan 1999
Glioblastoma Multiforme	Iceland	Merck Sharp & Dohme BV	26 Jan 1999
Glioblastoma Multiforme	Liechtenstein	Merck Sharp & Dohme BV	26 Jan 1999
Glioblastoma Multiforme	Norway	Merck Sharp & Dohme BV	26 Jan 1999
Glioma	European Union	Merck Sharp & Dohme BV	26 Jan 1999
Glioma	Iceland	Merck Sharp & Dohme BV	26 Jan 1999
Glioma	Liechtenstein	Merck Sharp & Dohme BV	26 Jan 1999
Glioma	Norway	Merck Sharp & Dohme BV	26 Jan 1999

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Neuroblastoma	NDA/BLA	European Union	ORPHELIA Pharma SAS	14 Nov 2024
Glioblastoma, IDH-Wildtype	Phase 3	United States	NRG Oncology	16 Jul 2026
Uterine Leiomyosarcoma	Phase 3	United States	Alliance for Clinical Trials in Oncology	30 Mar 2022
Brain Stem Glioma	Phase 3	United States	National Cancer Institute	26 Jan 2011
Brain Stem Glioma	Phase 3	Canada	National Cancer Institute	26 Jan 2011
Cerebral Astrocytoma, Adult	Phase 3	United States	National Cancer Institute	26 Jan 2011
Cerebral Astrocytoma, Adult	Phase 3	Canada	National Cancer Institute	26 Jan 2011
High grade glioma	Phase 3	United States	National Cancer Institute	26 Jan 2011
High grade glioma	Phase 3	Canada	National Cancer Institute	26 Jan 2011
Pediatric Cerebellar Astrocytoma	Phase 3	United States	National Cancer Institute	26 Jan 2011

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Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


ESMO2026	Not Applicable	Thyroid Cancer, Medullary Second line RET	293	temozolomide (TMZ) or dacarbazine (DTIC)-based chemotherapy	josrwxfqxr(robkucnxwi) = ofqkxjkxqe gawegpjgva (hbbksxzakh ) View more	Negative	23 Oct 2026
ESMO2026	Not Applicable	Thyroid Cancer, Medullary Second line RET	293	vandetanib (V) or cabozantinib (C) multikinase inhibitor therapy	josrwxfqxr(robkucnxwi) = razooebxnh gawegpjgva (hbbksxzakh ) View more	Negative	23 Oct 2026
NCT05413304 (Abemaciclib Neuropharmacokinetics of Diffuse Midline Glioma Using Intratumoral Microdialysis, CTgov)	Phase 1	Diffuse Midline Glioma	5	Abemaciclib (Arm 1 Cortical High-Grade Glioma: Abemaciclib + Surgery)	eqbvfxufdx = ztebxvpkbs pvevatunjc (dxyoxapscz, xkvdgzmycd - nnzhdzxvei) View more	-	06 Oct 2026
	Phase 1	Diffuse Midline Glioma	5	Temozolomide+Abemaciclib (Arm 1 Cortical High-Grade Glioma: Abemaciclib + Surgery + Temozolomide & Maintenance Therapy)	eqbvfxufdx = qspcrcgwrv pvevatunjc (dxyoxapscz, gcusqqxzyo - mxqoytxswl) View more	-	06 Oct 2026
CTIS2025-520814-78-00 (FIDES, EANO2026)	Phase 2	Diffuse Midline Glioma H3K27-altered	20	Temozolomide (Focused ultrasound-mediated blood-brain barrier opening)	pwjjrbajby(vldihqhljb) = ewjfsvzelc cmaryjvtxu (dssfivztae ) View more	Positive	24 Sep 2026
EANO2026	Not Applicable	High grade glioma CHEK2 mutation \| MGMT promotor methylation	97	Temozolomide	hxehybdcxr(teqemmrxhd) = The most limiting adverse event for patients with TIAA seems to be thrombocytopenia. Eltrombopag lead to limited efficacy with ongoing need of platelets substitution. ifqxloiiny (qvnvhdslad )	Positive	24 Sep 2026
EANO2026	Not Applicable	Astrocytoma	31	Chemotherapy	vfaqlggmxf(pyaugoneak) = xigajzznpa jntfvkqfan (oreezeujtp ) View more	Positive	24 Sep 2026
EANO2026	Not Applicable	-	12	Radiotherapy + Nimotuzumab/Vinorelbine regimen (NV)	zweicxohes(zhrrgjfkbx) = tzqafvztdd rsakxbdxjv (svkcwuvygb, 0 - 43) View more	Negative	24 Sep 2026
EANO2026	Not Applicable	Astrocytoma First line BRAF V600E	18	Radiochemotherapy with concurrent and adjuvant temozolomide (TMZ)	ksrpgzockv(apaahivqry) = ynvqmsouqo cunzrhjdub (nxkfszxuta ) View more	Positive	24 Sep 2026
CSCO2026	Not Applicable	Melanoma BRAFV600 突变	28	达拉非尼联合曲美替尼联合替莫唑胺及仑伐替尼	xhhtomkbjr(xuquocwapr) = aopymmschh fcljgmxlgh (uodordlkwq ) View more	Positive	11 Sep 2026
NCT02179086 (CTgov)	Phase 2	Glioblastoma	624	Photon Beam Radiation Therapy+Temozolomide (Group 1 - Standard RT (Photon) (Arm A1))	wrknnpaczr(zggdgfithe) = triglmltnk cymxniucxw (jyjavbkcos, vqskjopzjm - helnenzggu) View more	-	28 Aug 2026
NCT02179086 (CTgov)	Phase 2	Glioblastoma	624	Photon Beam Radiation Therapy+Temozolomide (Group 1 - Intensified RT (Photon) (Arm B))	wrknnpaczr(zggdgfithe) = wzqiwuvlho cymxniucxw (jyjavbkcos, phydsyzmed - mpzqidrqok) View more	-	28 Aug 2026
NCT04019327 (CTgov)	Phase 1/2	Metastatic castration-resistant prostate cancer \| Adenocarcinoma of prostate	16	Tala+TMX (Dose Level 1 Tala 1mg, TMX 37.5 mg/m^2)	palmzvqjgs = stlflserji iuyoygwgdd (lddfbgufjh, omfrrvqidh - xndyiroqtn) View more	-	24 Aug 2026
NCT04019327 (CTgov)	Phase 1/2		16	Tala+TMX (Dose Level 1A Tala 0.75mg, TMX 50 mg/m^2)	palmzvqjgs = ggdpthxfsg iuyoygwgdd (lddfbgufjh, vyauhjgyzq - smoccwvaim) View more	-	24 Aug 2026