EXTH-107. Effective targeting of EGFR-driven diffuse midline glioma with BLU5082, a novel brain-penetrant EGFR-targeting tyrosine kinase inhibitor (TKI) Article Swipe

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Robert Doherty , Krista C.J. Wink , Kallen Schwark , Sunjong Ji , A Gera , Dana Messinger , David C. Martin , Truman Knowles , Bavani Subramaniam , Yves Millet , Sebastian M. Waszak , Joanna Phillips , David H. Solomon , Javad Nazarian , Sabine Mueller , Alexander Beck , Jean Philippe Coppé , Carl Koschmann ·

YOU? · · 2025 · Open Access · · DOI: https://doi.org/10.1093/neuonc/noaf201.1440

Diffuse midline gliomas (DMGs) are lethal pediatric high-grade brain tumors with a prognosis of less than two years from diagnosis, the majority of which harbor the H3K27M histone mutation. A subgroup of DMGs harbor alterations in epidermal growth factor receptor (EGFR), including wildtype amplification (WT) and mutations in the extracellular domain (exon 7, e.g. A289T) or kinase domain (exon 20, e.g. 767delins). EGFR-targeting TKIs have shown limited efficacy against brain tumors but have not been developed to address the unique biology and EGFR alterations specific to H3K27M-DMG. Further, EGFR alterations are being validated as a biomarker of resistance to ONC201 suggesting that targeting EGFR may have broad utility for H3K27M-DMG. To this end, we established multiple human and murine models of H3K27M-DMG tumor cells with isogenic EGFR alterations (WT/A289T/767delins) and systematically evaluated the efficacy of the novel TKI BLU5082 (Blueprint Medicines). BLU5082 was uniquely effective in vitro at nanomolar concentrations against human H3K27M-DMG cells that express these EGFR alterations. Notably, the IC50 value of <0.2 µM against 767delins distinguished BLU5082. In cell-free kinase inhibition assays BLU5082 reduced EGFR WT and T790M activity by 50% at ~1 nM. We applied high-throughput kinase-activity mapping (HT-KAM) to detect the catalytic activity of >900 kinase-substrate nodes in EGFR-driven H3K27M-DMG cells. BLU5082 induced significant modulation of key oncogenic pathways in EGFR-767delins cells, including decreased MAPK family activity but persistence of AKT-driven metabolic pathways, denoting possible combinatorial partners which are being studied. In vivo testing demonstrated that daily 50 mg/kg BLU5082 treatment resulted in tumor eradication of isogenic EGFR-mutant (A289T/767delins) human H3K27M-DMG flank xenograft models within four weeks without any signs of toxicity. Pharmacokinetic analysis of 50 mg/kg BLU5082 resulted in peak brain concentrations of ~2 µM. Further assessment of the efficacy of BLU5082 against multiple intracranial H3K27M-DMG models is ongoing. Collectively, these preclinical studies highlight the potential of BLU5082 as a novel, targeted TKI therapeutic for EGFR-driven H3K27M-DMGs.

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Type: article
Language: en
Landing Page: https://doi.org/10.1093/neuonc/noaf201.1440
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DOI: https://doi.org/10.1093/neuonc/noaf201.1440

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Title: EXTH-107. Effective targeting of EGFR-driven diffuse midline glioma with BLU5082, a novel brain-penetrant EGFR-targeting tyrosine kinase inhibitor (TKI)

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Publication year: 2025

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Publication date: 2025-11-01

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Authors: Robert Doherty, Krista C.J. Wink, Kallen Schwark, Sunjong Ji, A Gera, Dana Messinger, David C. Martin, Truman Knowles, Bavani Subramaniam, Yves Millet, Sebastian M. Waszak, Joanna Phillips, David H. Solomon, Javad Nazarian, Sabine Mueller, Alexander Beck, Jean Philippe Coppé, Carl Koschmann

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Landing page: https://doi.org/10.1093/neuonc/noaf201.1440

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publication_date	2025-11-01
publication_year	2025
referenced_works_count	0
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abstract_inverted_index.WT	179
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abstract_inverted_index.~1	186
abstract_inverted_index.~2	280
abstract_inverted_index.20,	60
abstract_inverted_index.50%	184
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abstract_inverted_index.any	264
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abstract_inverted_index.vivo	238
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abstract_inverted_index.µM.	281
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abstract_inverted_index.T790M	181
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abstract_inverted_index.novel,	307
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abstract_inverted_index.unique	80
abstract_inverted_index.within	260
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abstract_inverted_index.BLU5082	139, 142, 176, 207, 245, 273, 288, 304
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abstract_inverted_index.BLU5082.	170
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citation_normalized_percentile