temozolomide

P1/2, N=64, Suspended, National Cancer Institute (NCI) | Trial completion date: Dec 2026 --> Dec 2027 | Recruiting --> Suspended | Trial primary completion date: Feb 2026 --> Dec 2026

P2, N=62, Active, not recruiting, Pediatric Brain Tumor Consortium | Trial completion date: Oct 2030 --> Sep 2027 | Trial primary completion date: Oct 2029 --> Mar 2026

P1/2, N=18, Active, not recruiting, Cantex Pharmaceuticals | Trial completion date: Dec 2025 --> Dec 2026 | Trial primary completion date: Dec 2024 --> Dec 2026

P=N/A, N=16, Active, not recruiting, Michigan State University | Trial completion date: Jun 2026 --> Jun 2027 | Trial primary completion date: Jun 2026 --> Jun 2027

Here, we investigated the effects of SM on proliferation, clonogenic survival, morphology and migration of IDH-wildtype GB cell lines (U-87MG, U-251MG and T98-G) and non-tumoral astrocytes under normoxic and hypoxic conditions, as well as its interaction with temozolomide (TMZ)...However, cleaved caspase-3 and p53 were not detected, suggesting a predominantly non-apoptotic mode of cell death. Together, these findings support SM as a promising candidate for IDH-wildtype GB therapy and underscore the need for further studies to clarify its mechanisms of action and optimize its therapeutic use.

In the NEN cell lines BON-1, QGP-1, and MS-18, we applied cisplatin, etoposide, streptozotocin, 5-fluorouracil, temozolomide, and everolimus- all systemic agents used in highly proliferative NEN. These findings might have an impact on the optimal therapy sequence and patient selection for future CXCR4-targeted approaches. Further, the decreased CXCR4 expression could represent a new mechanism of action of the established drugs Cisplatin, Temozolomide, and Everolimus.

P3, N=132, Recruiting, Ono Pharmaceutical Co. Ltd | Not yet recruiting --> Recruiting

P2/3, N=73, Active, not recruiting, National Cancer Institute (NCI) | N=190 --> 73 | Trial completion date: Mar 2030 --> Jan 2027

P3, N=406, Recruiting, University Hospital Heidelberg | Trial completion date: Mar 2031 --> Mar 2033 | Trial primary completion date: Mar 2031 --> Mar 2033

Cystathionine γ-lyase (CTH) is markedly enriched in glioblastoma (GBM) and is associated with poor patient survival, enhanced temozolomide (TMZ) resistance, and aggressive phenotypes; however, effective CTH inhibitors for GBM therapy are currently lacking...In addition, TKL002 inhibits GBM cell migration and invasion by upregulating E-cadherin and downregulating N-cadherin and vimentin. Collectively, these findings demonstrate that TKL002 exerts potent antiglioblastoma activity via modulation of the CTH/H2S/NF-κB/EMT signaling axis, highlighting its potential as a quinoline-based therapeutic candidate to overcome intrinsic GBM resistance and invasiveness.

P3, N=306, Suspended, NRG Oncology | Recruiting --> Suspended

P1, N=40, Active, not recruiting, Novartis Pharmaceuticals | Recruiting --> Active, not recruiting