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.
CWI1-2是一种选择性抑制m6A识别蛋白IGF2BP2的抑制剂，能够破坏IGF2BP2与m6A修饰的目标转录本之间的相互作用 [1][2]。该抑制剂在细胞水平的IC50范围为203.1至781.6 nM [1]。由于其显著的抗白血病特性，CWI1-2主要用于急性髓性白血病（AML）的研究[1]。
CWI1-2通过靶向IGF2BP2发挥抗白血病作用，诱导白血病细胞的凋亡和分化。在细胞水平上的IC50范围为203.1至781.6 nM [1] 。在AML细胞系中，CWI1-2在0.1至1 μM浓度范围内作用48小时，可抑制细胞生长并诱导凋亡 [3] 。
CWI1-2（5 mg/kg，静脉注射，每日一次，连续7-10天）显著减缓了BMT受体小鼠白血病的进展，并延长了生存期。治疗结果显示，BMT受体小鼠白血病细胞负荷显著减少，且体重无明显变化 [3] 。