ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
A Novel Class of Multi-substituted Diaryl Scaffold Derivatives Inhibit Glioblastoma Progression by Targeting CD155.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- Structural Optimization of Pterostilbene, a Promising Lead Molecule, and Evaluation of Its Derivatives via ADMET Prediction and In Vitro/In Vivo Anti-Cerebral Ischemic Activity.International journal of molecular sciences · 2026Article
- Review
- A Novel Class of Multi-substituted Diaryl Scaffold Derivatives Inhibit Glioblastoma Progression by Targeting CD155.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Clofoctol as a novel senolytic drug eliminating therapy-induced senescent glioma cells.Neuro-oncology advancesArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Glioblastoma (GBM) is the most formidable malignancy in the brain, characterized by a significant resistance to treatment. The immune targeting of glioblastoma stem cells (GSCs) holds great promise. In this study, structural modifications of the lead compound clofoctol is conducted and structure-activity relationship analyses are performed against GBM, yielding a novel blood-brain barrier-permeable compound, B7, featuring a pivotal multi-substituted diaryl scaffold. B7 demonstrates potent anti-GBM effects, significantly inhibiting GSC proliferation, migration, and invasion. Notably, B7 inhibits tumor progression, specifically bolstered natural killer (NK) cell-mediated cytotoxicity, and mitigates the immunosuppressive microenvironment in intracranial xenograft mice implanted with GBM cells and GSCs, as well as in cocultures of GSCs and NK-92 cells. Mechanistically, these anti-GBM effects of B7 are abolished by overexpression of poliovirus receptor cell adhesion molecule (CD155), both in vitro and in vivo. Further exploration reveals that B7 targets CD155 via interaction at five crucial binding sites, namely, L47, L108, L142, M110, and V115 residues. These interactions collectively contribute to the hydrophobic interaction energies within the B7-CD155 complex, modulating the CD155/T cell immunoreceptor with Ig and ITIM domains/CD226 axis to reshape the NK cell-mediated tumor immune microenvironment. In conclusion, this study establishes the therapeutic potential of B7 for glioma, synergistically targeting GSC biology and NK cell immunity for the treatment of GBM.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.