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The human Vaccinia-Related Kinase 1 (VRK1) is highly expressed in various tumor types and plays important roles in cell proliferation and the maintenance of genome integrity. While prior genetic studies indicate that VRK1 inhibition offers therapeutic potential, especially in cancers deficient in VRK2 expression or DNA damage repair, the current lack of suitable VRK1 inhibitors hampers the validation of this kinase as a therapeutic target and the translation of these findings to the clinic. Here, we developed novel VRK1 inhibitors based on BI-D1870, a pteridinone inhibitor of RSK kinases. Our optimized VRK1 inhibitor displays improved kinome-wide selectivity, and effectively mimic cellular outcomes of VRK1 depletion. Notably, VRK1 inhibition triggered severe mitotic errors and genome instability in p53-deficient cells. Together, our findings highlight the potential of VRK1 inhibition in treating p53-deficient tumors and possibly enhancing the efficacy of existing cancer therapies that target DNA stability or cell division.
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Gama et al. (2023) studied this question.