State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China Medical School, Sichuan University, Sichuan 610041, China.
J Med Chem. 2013 Feb 28;56(4):1641-55. doi: 10.1021/jm301537p. Epub 2013 Feb 19.
We describe the structural optimization of a hit compound, 1-(4-(1H-pyrazolo[3,4-d]pyrimidin-4-ylamino)phenyl)-3-(3-methoxyphenyl)urea (1), which exhibits inhibitory activity but low potency against FLT3 and VEGFR2. A series of pyrazolo[3,4-d]pyrimidine derivatives were synthesized, and structure-activity relationship analysis using cell- and transgenic-zebrafish-based assays led to the discovery of a number of compounds that exhibited both high potency against FLT3-driven human acute myeloid leukemia (AML) MV4-11 cells and a considerable antiangiogenic effect in transgenic-zebrafish-based assays. The compound 1-(4-(1H-pyrazolo[3,4-d]pyrimidin-4-yloxy)phenyl)-3-(4-chloro-3-(trifluoromethyl)phenyl)urea (33), which exhibited the highest activity in preliminary in vivo anti-AML assays, was chosen for further anti-AML studies. The results demonstrated that compound 33 is a multikinase inhibitor that potently inhibits FLT3 and VEGFR2. In an MV4-11 xenograft mouse model, a once-daily dose of compound 33 at 10 mg/kg for 18 days led to complete tumor regression without obvious toxicity. Western blot and immunohistochemical analyses were performed to determine the mechanism of action of compound 33.
我们描述了一个具有抑制活性但对 FLT3 和 VEGFR2 活性低的先导化合物 1-(4-(1H-吡唑并[3,4-d]嘧啶-4-基氨基)苯基)-3-(3-甲氧基苯基)脲(1)的结构优化。我们合成了一系列吡唑并[3,4-d]嘧啶衍生物,并通过基于细胞和转(transgenic)-斑马鱼的测定进行了结构-活性关系分析,发现了一些化合物,它们不仅对 FLT3 驱动的人类急性髓系白血病(AML)MV4-11 细胞具有高活性,而且在基于转(transgenic)-斑马鱼的测定中具有相当的抗血管生成作用。在初步的体内抗 AML 试验中,活性最高的化合物 1-(4-(1H-吡唑并[3,4-d]嘧啶-4-氧基)苯基)-3-(4-氯-3-(三氟甲基)苯基)脲(33)被选为进一步的抗 AML 研究。结果表明,化合物 33 是一种多激酶抑制剂,能有效抑制 FLT3 和 VEGFR2。在 MV4-11 异种移植小鼠模型中,化合物 33 以 10mg/kg 的剂量每天一次给药 18 天,导致完全肿瘤消退,没有明显毒性。进行了 Western blot 和免疫组织化学分析以确定化合物 33 的作用机制。