Crbn I391V is sufficient to confer in vivo sensitivity to thalidomide and its derivatives in mice

Abstract

Key Points Crbn I391V mice degrade known thalidomide derivative targets and recapitulate thalidomide-induced cytopenias and teratogenicity. Degradation of Ck1α is sufficient to explain the in vivo therapeutic window of lenalidomide in del(5q) myelodysplastic syndrome.