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In this large collaborative study with partners from DKFZ, Bayer and others, OmicScouts proteomic technologies helped to identify the target and mechanism of NCT02, a compound that emerged from a phenotypic screen in patient-derived colorectal cancer spheroids. Using chemical proteomics and thermal proteome profiling we found CDK12 and its interaction partner CCNK to be affected by NCT02 treatment. Mechanistic analysis revealed that NCT02 acts as a molecular glue to induce degradation of the CCNK/CDK12 complex that confers selective vulnerability in colorectal cancers with stem cell like tumor-initiating cells.
Read the full Cell Reports article here.