Author
Listed:
- David S. Rogawski
(University of Michigan)
- Jing Deng
(University of Michigan)
- Hao Li
(University of Michigan)
- Hongzhi Miao
(University of Michigan)
- Dmitry Borkin
(University of Michigan)
- Trupta Purohit
(University of Michigan)
- Jiho Song
(University of Michigan)
- Jennifer Chase
(University of Michigan)
- Shuangjiang Li
(University of Michigan)
- Juliano Ndoj
(University of Michigan)
- Szymon Klossowski
(University of Michigan)
- EunGi Kim
(University of Michigan)
- Fengbiao Mao
(University of Michigan)
- Bo Zhou
(University of Michigan)
- James Ropa
(University of Michigan
Indiana University School of Medicine)
- Marta Z. Krotoska
(University of Michigan)
- Zhuang Jin
(University of Michigan)
- Patricia Ernst
(University of Colorado Denver, Anschutz Medical Campus)
- Xiaomin Feng
(Cincinnati Children’s Hospital)
- Gang Huang
(Cincinnati Children’s Hospital)
- Kenichi Nishioka
(Enoki 1-1-5, Musashimurayama)
- Samantha Kelly
(University of Pennsylvania)
- Miao He
(University of Michigan)
- Bo Wen
(University of Michigan)
- Duxin Sun
(University of Michigan)
- Andrew Muntean
(University of Michigan)
- Yali Dou
(University of Michigan)
- Ivan Maillard
(University of Michigan
University of Pennsylvania)
- Tomasz Cierpicki
(University of Michigan)
- Jolanta Grembecka
(University of Michigan)
Abstract
ASH1L histone methyltransferase plays a crucial role in the pathogenesis of different diseases, including acute leukemia. While ASH1L represents an attractive drug target, developing ASH1L inhibitors is challenging, as the catalytic SET domain adapts an inactive conformation with autoinhibitory loop blocking the access to the active site. Here, by applying fragment-based screening followed by medicinal chemistry and a structure-based design, we developed first-in-class small molecule inhibitors of the ASH1L SET domain. The crystal structures of ASH1L-inhibitor complexes reveal compound binding to the autoinhibitory loop region in the SET domain. When tested in MLL leukemia models, our lead compound, AS-99, blocks cell proliferation, induces apoptosis and differentiation, downregulates MLL fusion target genes, and reduces the leukemia burden in vivo. This work validates the ASH1L SET domain as a druggable target and provides a chemical probe to further study the biological functions of ASH1L as well as to develop therapeutic agents.
Suggested Citation
David S. Rogawski & Jing Deng & Hao Li & Hongzhi Miao & Dmitry Borkin & Trupta Purohit & Jiho Song & Jennifer Chase & Shuangjiang Li & Juliano Ndoj & Szymon Klossowski & EunGi Kim & Fengbiao Mao & Bo , 2021.
"Discovery of first-in-class inhibitors of ASH1L histone methyltransferase with anti-leukemic activity,"
Nature Communications, Nature, vol. 12(1), pages 1-14, December.
Handle:
RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-23152-6
DOI: 10.1038/s41467-021-23152-6
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