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Clinical trials employing small-molecule MDM2\/p53 interaction inhibitors have demonstrated limited activity, underscoring an unmet need for a better approach to target MDM2. KT-253 is a highly potent and selective heterobifunctional degrader that overcomes the MDM2 feedback loop seen with small-molecule MDM2\/p53 interaction inhibitors and induces apoptosis in a range of hematologic and solid tumor lines. A single intravenous dose of KT-253 triggered rapid apoptosis and sustained tumor regression in p53 wild-type acute myeloid leukemia and acute lymphoblastic leukemia xenograft models. Additionally, a single intravenous dose of KT-253 in combination with standard-of-care venetoclax overcame venetoclax resistance in an acute myeloid leukemia xenograft model. The data herein define the therapeutic potential of KT-253 and support its clinical development in a range of hematologic and solid p53 wild-type malignancies, as a monotherapy and in combination with standard-of-care agents.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1158\/1535-7163.mct-24-0306","type":"journal-article","created":{"date-parts":[[2024,12,9]],"date-time":"2024-12-09T01:25:41Z","timestamp":1733707541000},"page":"497-510","update-policy":"https:\/\/doi.org\/10.1158\/crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["KT-253, a Novel MDM2 Degrader and p53 Stabilizer, Has Superior Potency and Efficacy than MDM2 Small-Molecule Inhibitors"],"prefix":"10.1158","volume":"24","author":[{"ORCID":"https:\/\/orcid.org\/0009-0007-0531-8877","authenticated-orcid":false,"given":"Yogesh K.","family":"Chutake","sequence":"first","affiliation":[{"name":"Kymera Therapeutics, Inc., 500 North Beacon Street, Watertown, 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