Mechanism of A New DOT1L Inhibitor EPZ-5676 and Its Research Progress -Review.
10.7534/j.issn.1009-2137.2016.06.055
- Author:
Li-Hong LI
1
;
Jing WANG
1
;
Xiao-Yan KE
2
,
3
Author Information
1. Department of Hematology,Peking University Third Hospital, Beijing 100191,China.
2. Department of Hematology,Peking University Third Hospital, Beijing 100191,China. E-mail: xykbysy@
3. com.
- Publication Type:Journal Article
- From:
Journal of Experimental Hematology
2016;24(6):1909-1912
- CountryChina
- Language:Chinese
-
Abstract:
Leukemia carring translocation at the 11q23 locus is referred to MLL-rearranged (MLL-r) leukemia, and the occurrence of this genetic lesion is associated with a poor prognosis. The most common translocation chromosomes are chromosomes 4,9 and 10. Recently MLL protein was found to interact with DOT1L (DOT1-like) protein, which can promote leukemogenesis. A new DOT1L inhibitor EPZ-5676 can selectively inhibit proliferation, promote apoptosis and differentiation, which was also found to act synergistically with anti-AML (acute myeloid leukemia) and anti-ALL (acute lymphoblastic leukemia) drugs. EPZ-5676 can also induce sustained regression in a rat xenograft model of MLL-rearranged leukemia. Now the novel drug is in phase I of clinical trail. The results suggest that the EPZ-5676 is promising. In this article, the mechanism of EPZ-5676 and its research progress are reviwed.
