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新型MDM2降解剂及p53稳定剂KT-253比MDM2小分子抑制剂具有更强的效力和疗效。

KT-253, a Novel MDM2 Degrader and p53 Stabilizer, Has Superior Potency and Efficacy than MDM2 Small-Molecule Inhibitors.

作者信息

Chutake Yogesh K, Mayo Michele F, Dumont Nancy, Filiatrault Jessica, Breitkopf Susanne B, Cho Patricia, Chen Dapeng, Dixit Vaishali S, Proctor William R, Kuhn Eric W, Bollinger Martinez Sarah, McDonald Alice A, Qi Jianfeng, Hu Kan-Nian, Karnik Rahul, Growney Joseph D, Sharma Kirti, Schalm Stefanie S, Gollerkeri Ashwin M, Mainolfi Nello, Williams Juliet A, Weiss Matthew M

机构信息

Kymera Therapeutics, Inc., 500 North Beacon Street, Watertown, Massachusetts.

出版信息

Mol Cancer Ther. 2025 Apr 2;24(4):497-510. doi: 10.1158/1535-7163.MCT-24-0306.

DOI:10.1158/1535-7163.MCT-24-0306
PMID:39648478
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11962396/
Abstract

Murine double minute 2 (MDM2) is an E3 ligase that inhibits the tumor suppressor protein p53. 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.

摘要

小鼠双微体2(MDM2)是一种E3泛素连接酶,可抑制肿瘤抑制蛋白p53。采用小分子MDM2/p53相互作用抑制剂的临床试验显示活性有限,这突出表明需要一种更好的靶向MDM2的方法。KT-253是一种高效且选择性的异双功能降解剂,它克服了小分子MDM2/p53相互作用抑制剂所出现的MDM2反馈回路,并在一系列血液学和实体瘤细胞系中诱导细胞凋亡。在p53野生型急性髓系白血病和急性淋巴细胞白血病异种移植模型中,单次静脉注射KT-253可引发快速细胞凋亡并持续使肿瘤消退。此外,在急性髓系白血病异种移植模型中,单次静脉注射KT-253与标准治疗药物维奈克拉联合使用可克服维奈克拉耐药性。本文数据确定了KT-253的治疗潜力,并支持其在一系列血液学和实体p53野生型恶性肿瘤中作为单一疗法以及与标准治疗药物联合使用的临床开发。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5015/11962396/493adf2166ef/mct-24-0306_f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5015/11962396/1090cf76ecdd/mct-24-0306_ga.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5015/11962396/d6bdd95b1ef6/mct-24-0306_f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5015/11962396/f2b4014e06e2/mct-24-0306_f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5015/11962396/b1d05784c312/mct-24-0306_f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5015/11962396/6b863b7aab81/mct-24-0306_f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5015/11962396/493adf2166ef/mct-24-0306_f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5015/11962396/1090cf76ecdd/mct-24-0306_ga.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5015/11962396/9c95fd68c356/mct-24-0306_f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5015/11962396/d6bdd95b1ef6/mct-24-0306_f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5015/11962396/f2b4014e06e2/mct-24-0306_f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5015/11962396/b1d05784c312/mct-24-0306_f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5015/11962396/6b863b7aab81/mct-24-0306_f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5015/11962396/493adf2166ef/mct-24-0306_f6.jpg

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本文引用的文献

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