FPA-124是Akt结合PH和激酶结构域的细胞渗透性抑制剂（IC 50 = 100 nM）。它抑制Colo 357 BxPC 3 BT 20和PC 3癌细胞系中的细胞增殖，IC 50值范围为7-55 nM。FPA-124抑制小鼠肿瘤生长，毒性可忽略不计。参考文献由Bioz提供支持参见Bioz的更多详细信息1）V. Barve等人，“Synthesis Molecular Characterization and Biological Activity of Novel SyntheticDerivatives of Chromen-4-one in Human Cancer Cells”J. Med. Chem. 2006 49 3800- 3808。 G. Straface等人（2009年）。“吡格列酮通过Akt依赖性VEGF介导的机制增强糖尿病小鼠缺血后肢的侧支血流量，而不管PPARgamma刺激如何。“Bavasc Diabetol 8：49.3）Brito P. M. R. L. Devillard等人（2009）。“白藜芦醇抑制平滑肌细胞中氧化LDL诱发的mTOR有丝分裂信号。“Atherosclero205（1）：126。
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FPA-124 is a cell-permeable inhibitor of Akt (IC50 = 100 nM) binding to the PH and kinase domains. It inhibits cell proliferation in Colo357 BxPC3 BT20 and PC3 cancer cell lines with IC50 values ranging from 7-55 nM. FPA-124 inhibited tumor growth in mice with negligible toxicity.References Powered by Bioz See more details on Bioz1) V. Barve et al. "Synthesis Molecular Characterization and Biological Activity of Novel SyntheticDerivatives of Chromen-4-one in Human Cancer Cells" J. Med. Chem. 2006 49 3800-3808.2) Biscetti F. G. Straface et al. (2009). "Pioglitazone enhances collateral blood flow in ischemic hindlimb of diabetic mice through an Akt-dependent VEGF-mediated mechanism regardless of PPARgamma stimulation." Cardiovasc Diabetol 8: 49.3) Brito P. M. R. l. Devillard et al. (2009). "Resveratrol inhibits the mTOR mitogenic signaling evoked by oxidized LDL in smooth muscle cells." Atherosclerosis 205(1): 126.
