About GLIOBREAK

Glioblastoma is the most common and aggressive primary brain tumour in adults. Diffuse growth, extensive intratumoural heterogeneity, early resistance, and an immunosuppressive microenvironment leave patients with very limited treatment options.^{5, 6, 7}

BEA-17 is a small-molecule degrader that binds LSD1, disrupts its interaction with CoREST, and destabilises both proteins. GLIOBREAK is evaluating its effects on tumour immune signalling in preclinical GBM models while developing a predictive biomarker strategy to identify the patients most likely to respond. Predictive performance in patients has not yet been established.¹²⁸

GLIOBREAK aims to advance BEA-17, a first-in-class investigational small-molecule degrader that binds LSD1, disrupts its interaction with CoREST, and destabilises both proteins, from validated laboratory stage toward clinical readiness in glioblastoma.^{1, 2, 9}

GLIOBREAK builds on tumour-host biology and single-cell multi-omics expertise associated with the ongoing EU-funded GLIOMATCH project at KU Leuven. GLIOMATCH is developing spatial and imaging-informed approaches to glioma patient stratification; it is not presented here as clinical validation of BEA-17.³

GLIOBREAK aligns with European goals for personalised therapies, improved access to innovative treatments for rare cancers, and stronger translational oncology research.

Beactica leads programme management and core development work packages covering BEA-17 manufacturing process, analytical characterisation, formulation, pharmacokinetics, toxicology, and regulatory dossier preparation.¹

The Eclipsor platform supports discovery of allosteric modulators and protein-degrading small molecules. BEA-17 is a non-PROTAC small-molecule degrader: it binds LSD1, disrupts the LSD1/CoREST interaction, and destabilises both proteins. Beactica reports oral availability and blood-brain-barrier penetration in preclinical models; these properties have not been established in humans.^{2, 8}

The GLIOBREAK team includes leadership across discovery, operations, preclinical development, and CMC. Beactica reports that BEA-17 received FDA Orphan Drug Designation for glioblastoma in 2023; orphan designation is not marketing approval.^{2, 5}

FREDERIK DE SMET · CHIARA CAPRIOLI

LPCM leads the predictive biomarker and tumour-biology work, using clinically annotated material and patient-derived models to identify candidate markers of BEA-17 response. Its Leuven Living Tissue Bank provides curated cell lines from high-grade brain tumours.

AN COOSEMANS · ANNA MEYER · MATTEO RIVA · KATJA VANDENBRANDE

LTII leads the preclinical evaluation of BEA-17 in syngeneic mouse models of glioblastoma, bringing translational tumour-immunology and immunotherapy expertise to the project.

THIERRY VOET

The laboratory enables spatial and single-cell profiling of mouse and human glioblastoma samples to uncover the action of BEA-17.