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Novel Small-Molecule Inhibitors Of The Protein Kinase Dyrk: Potential Therapeutic Candidates In Cancer

Venkataramani, P.; Elkayam, E.; Garg, A.; Cheng, K. F.; Altiti, A.; He, M.; Thakur, K.; Michalopoulou, E.; Gonzalez, C.; Van Aelst, L.; Pappin, D.; Joshua-Tor, L.; Al-Abed, Y.; Tonks, N. K.

2025-11-06 cancer biology
10.1101/2025.11.05.686653 bioRxiv
Show abstract

Dual-specificity tyrosine-regulated kinase 1A (DYRK1A) is crucial for normal brain development and its disruption has been linked to various cancers. DYRK1A drives glioblastoma (GBM) progression via stabilization of epidermal growth factor receptor (EGFR). Here we describe two, selective, benzothiazole-derived DYRK inhibitors, FC-2 and FC-3, obtained by structure-activity optimization of a natural product lead. Both compounds inhibit DYRK1A with nanomolar potency and display high selectivity across a kinase panel. The co-crystal structure of FC-3 with DYRK1A revealed ATP-competitive binding, with interactions at the hinge region and the DYRK-specific phenylalanine gatekeeper residue explaining target selectivity. Generation of inhibitor-resistant mutants confirmed DYRK1A as the primary cellular target. In GBM cell-models, FC-2 and FC-3 impaired neurosphere self-renewal, cell invasion, and EGFR stability, phenocopying DYRK1A loss. Both compounds crossed the blood-brain barrier and suppressed tumor growth, to prolong survival in intracranial xenografts. These findings identify FC-2 and FC-3 as selective small-molecule inhibitors of DYRK1A with potential therapeutic utility in GBM.

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