BCL2 and acute myeloid leukemia: However, 753B showed single-agent potency in reducing both target proteins in AML models and senolytic activity through apoptosis induction.422 The capacity to also target BCL2 is given by the different ternary complex conformation compared to DT2216, allowing access to BCL2 surface lysines as ubiquitination sites.423 In small-cell lung cancer 753B was also more potent than DT2216 or ABT-263 in reducing cell viability and was well tolerated in mice.424 With PROTAC 753B as a starting point, the second-generation dual degrader WH244 was recently developed.