The results of a collaborative study with Tokyo Medical University and others have been published in Nature Chemical Biology. The study identified p63, a transcription factor of the p53 family, as a novel substrate protein for Cereblon (CRBN) E3 ubiquitin ligase, an intracellular target protein of thalidomide, and found that ubiquitination and degradation of the p63 protein by thalidomide/CRBN was This finding indicates that the ubiquitination and degradation of p63 protein by thalidomide/CRBN is one of the causes of thalidomide’s teratogenicity to the fetus. The identification of the substrates involved in thalidomide teratogenicity is an important step toward the development of new thalidomide-type drugs without teratogenicity. For detail, please also see the press release below.