CWI1-2 is a selective inhibitor of the m6A reader protein IGF2BP2, disrupting the interaction between IGF2BP2 and m6A-modified target transcripts [1] [2]. The IC50 at the cellular level ranges from 203.1 to 781.6 nM[1] . This inhibitor is primarily used for research in acute myelocytic leukemia (AML) due to its promising anti-leukemic properties [1].
CWI1-2 exerts anti-leukemic effects by targeting IGF2BP2, inducing apoptosis and differentiation in leukemia cells. The IC50 at the cellular level ranges from 203.1 to 781.6 nM [1]. In AML cell lines, CWI1-2 at concentrations of 0.1 to1 μM over 48h inhibits cell growth and induces apoptosis [3].
CWI1-2 (5 mg/kg, intravenous injection, daily for 7-10 days) significantly reduced leukemia progression and prolonged survival in BMT recipient mice. Treatment results in a marked reduction in leukemia cell burden without significant changes in body weight [3].
References:
[1]. Zhu TY, Hong LL, Ling ZQ. Oncofetal protein IGF2BPs in human cancer: functions, mechanisms and therapeutic potential. Biomark Res. 2023 Jun 6;11(1):62. doi: 10.1186/s40364-023-00499-0.
[2]. Wang M, Chao M, Han H, et al. Hinokiflavone resists HFD-induced obesity by promoting apoptosis in an IGF2BP2-mediated Bim m6A modification dependent manner. J Biol Chem. 2024 Sep;300(9):107721. doi: 10.1016/j.jbc.2024.107721. Epub 2024 Aug 29. PMID: 39214307; PMCID: PMC11465056.
[3]. Weng H, Huang F, Yu Z, et al. The m6A reader IGF2BP2 regulates glutamine metabolism and represents a therapeutic target in acute myeloid leukemia. Cancer Cell. 2022 Dec 12;40(12):1566-1582.e10. doi: 10.1016/j.ccell.2022.10.004.
















