CWI1-2
目录号 : GC68916CWI1-2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。
Cas No.:2408590-36-1
Sample solution is provided at 25 µL, 10mM.
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- Purity: >98.00%
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Cell experiment [1]: | |
Cell lines | THP1 |
Preparation Method | Cells were treated with CWI1-2 (0.1-1 μM) for 48 h, cell viability was then evaluated by MTT assay. The medium was then changed with MTT solution (0.5mg/ml) in DMEM or RPMI without phenol red and FBS; cells were incubated at 37°C for 30 min and violet precipitate was dissolved with isopropanol. Absorbance at 550nm was measured through an EnSpire Multimode Plate reader. |
Reaction Conditions | 0.1 to1 μM, 48 hours |
Applications | Treatment of THP1cells with CWI1-2 induced dramatic cell differentiation and apoptosis in a concentration-dependent manner |
Animal experiment [2]: | |
Animal models | B6.SJL (CD45.1) mice |
Preparation Method | B6.SJL (CD45.1) mice were performed bone marrow transplants (BMTs) using blast cells from MAP-induced leukemia mice or C1498 murine AML cells. Following the transplantation, CWI1-2 is administered at a dosage of 5 mg/kg daily via intravenous injection for a period of 7 to 10 days. Peripheral blood (PB) samples are then collected, and flow cytometric analysis is conducted to assess leukemia engraftment. |
Dosage form | 5 mg/kg/d, 7-10 days, i.v. |
Applications | CWI1-2 treatment significantly delayed leukemia onset and prolonged the survival of BMT recipient mice |
References: [1]. 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 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] 。
Cas No. | 2408590-36-1 | SDF | Download SDF |
分子式 | C22H17Cl3N6O3 | 分子量 | 519.77 |
溶解度 | DMSO : 100 mg/mL (192.39 mM; Need ultrasonic) | 储存条件 | Store at -20°C |
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1 mg | 5 mg | 10 mg | |
1 mM | 1.9239 mL | 9.6196 mL | 19.2393 mL |
5 mM | 0.3848 mL | 1.9239 mL | 3.8479 mL |
10 mM | 0.1924 mL | 0.962 mL | 1.9239 mL |
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