Cyclin K and CDK12 are promising drug targets to treat cyclin E1-overexpressing tumors of human tumorigenesis. Molecular glues trigger the polyubiquitination and subsequent degradation of CDK12 's partner protein CCNK through binding to CDK12 and recruiting CCNK to form ternary complexes. Several small molecules have been explored as molecular glues modulating CDK12 protein to bind DDB1 of DDB1-CUL4-RBX1. For example, CR8, gluing DDB1 to Cyclin K, induces cancer cell apoptosis and has neuroprotective effects (Table ). The pyridine moiety in CDK-bound form of CR8 induces the formation of a complex between CDK12-cyclin K and the CUL4 adaptor protein DDB1, resulting in ubiquitination and degradation of cyclin K. Other promising cyclin K degraders include a series of 5methylthiazol analogues (glue01 series, Table ) , dCeMM compounds (dCeMM2/3/4) 61 , and HQ005.