Dual-targeting pharmacological UFMylation inhibition reprograms tumor and immune microenvironments to achieve long-term glioblastoma regression.
A novel approach targeting tumor cells' stress response achieved tumor-free survival in two-thirds of brain cancer mice with lasting immune protection against recurrence.
UFMylation E3 ligase inhibition via osimertinib (novel covalent mechanism, EGFR-independent) and CP-24 achieved tumor-free outcomes in 65% of immunocompetent GBM mice with durable immune memory; mechanism: ER stress induction + macrophage M1 polarisation + PD-1 reduction. This record was retained from the prior triage attempt for PubMed pipeline handoff.
What the study was
- Study design
- preclinical_experimental
- Category
- novel_therapeutics
- Maturity
- Exploratory
- Journal
- Signal Transduction and Targeted Therapy
Why it surfaced
Novel mechanism (UFMylation inhibition) with exceptional preclinical efficacy in GBM (65% tumor-free, immune memory); osimertinib off-label repurposing angle has near-term translational relevance; Signal Transduct Target Ther is a high-impact journal.
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