Immunomodulatory drugs (IMiDs) and CELMoDs
Thalidomide and its descendants lenalidomide and pomalidomide, which work by hijacking a cellular waste-disposal tag (cereblon) to destroy two proteins myeloma cells depend on, while also revving up T and NK cells. Newer, more potent versions are called CELMoDs.
Thalidomide's return from the 1960s disaster as a myeloma drug (1999) and the discovery that it acts as a molecular glue degrader of IKZF1/3 via cereblon founded the whole field of targeted protein degradation. Lenalidomide is in nearly every myeloma induction and maintenance regimen and treats del(5q) MDS and some lymphomas; pomalidomide follows lenalidomide failure. CELMoDs (iberdomide, mezigdomide) bind cereblon more tightly and are active in lenalidomide-refractory disease (EXCALIBER). Class effects are cytopenias, thrombosis (prophylaxis required), rash, and secondary cancers; teratogenicity mandates pregnancy-prevention programmes.
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