All content on this site is intended for healthcare professionals only. By acknowledging this message and accessing the information on this website you are confirming that you are a Healthcare Professional. If you are a patient or carer, please visit Know AML.
The aml Hub website uses a third-party service provided by Google that dynamically translates web content. Translations are machine generated, so may not be an exact or complete translation, and the aml Hub cannot guarantee the accuracy of translated content. The aml and its employees will not be liable for any direct, indirect, or consequential damages (even if foreseeable) resulting from use of the Google Translate feature. For further support with Google Translate, visit Google Translate Help.
The AML Hub is an independent medical education platform, sponsored by Astellas, Daiichi Sankyo, Johnson & Johnson, Kura Oncology and Syndax, and has been supported through educational grants from Bristol Myers Squibb and the Hippocrate Conference Institute, an association of the Servier Group. The funders are allowed no direct influence on our content. The levels of sponsorship listed are reflective of the amount of funding given. View funders.
Now you can support HCPs in making informed decisions for their patients
Your contribution helps us continuously deliver expertly curated content to HCPs worldwide. You will also have the opportunity to make a content suggestion for consideration and receive updates on the impact contributions are making to our content.
Find out moreCreate an account and access these new features:
Bookmark content to read later
Select your specific areas of interest
View AML content recommended for you
On June 22, 2023, the U.S Food and Drug Administration (FDA) granted orphan drug designation to KT-253, a novel, highly potent, and selective MDM2 degrader, for the treatment of patients with acute myeloid leukemia (AML).1 MDM2 is a regulator of the tumor suppressor p53, with overexpression of MDM2 implicated in AML. Small molecule inhibitors can stabilize and upregulate p53; however, this can create a feedback loop that increases MDM2 protein levels and subsequently decreases p53. Preclinical studies have demonstrated that KT-253 can counteract the MDM2 feedback loop and induce cancer cell death.1
The safety, tolerability, pharmacokinetics, and clinical activity of KT-253 are currently being assessed in an open-label, multicenter, phase I study (NCT05775406) which began in March, 2023.1 This phase I study includes patients with relapsed/refractory myeloid malignancies, such as AML, acute lymphocytic leukemia and lymphoma, and solid tumors, and will be used to determine the recommended phase II dose.1
References
Please indicate your level of agreement with the following statements:
The content was clear and easy to understand
The content addressed the learning objectives
The content was relevant to my practice
I will change my clinical practice as a result of this content