PD-166866 is a selective FGFR tyrosine kinase inhibitor.

FGFR1:52.4 nM

PD166866显著导致线粒体缺陷和氧化应激[1]。PD 166866以52.4 ± 0.1 nM的IC50值抑制人源全长FGFR-1酪氨酸激酶，但对c-Src、血小板衍生生长因子受体β、表皮生长因子受体或胰岛素受体酪氨酸激酶、丝裂原活化蛋白激酶、蛋白激酶C和CDK4在高达50 μM的浓度下无效。PD 166866强效抑制在NIH 3T3细胞中表达内源性FGFR-1和在L6细胞过表达人FGFR-1酪氨酸激酶的基础成纤维生长因子（bFGF）介导的受体自磷酸化。PD 166866不抑制在血管平滑肌、A431或NIHIR细胞中由血小板衍生生长因子、表皮生长因子或胰岛素刺激的受体自磷酸化，进一步支持其对FGFR-1的特异性。此外，PD 166866是一种强效的抑制人胎盘培养动脉碎片中的微血管生长（血管生成）的抑制剂。在L6细胞中，被PD 166866抑制的磷酸化44-和42-kDa MAPK亚型的IC50值分别为4.3和7.9 nM[2]。PD166866通过抑制Akt/mTOR信号路径诱导自噬[3]。

HeLa cells are treated with PD166866 for 24 hours, the growth medium is removed, the cells are washed with PBS and fixed for 1 hour at 25°C adding a freshly made paraformaldheyde solution (4% in PBS). Samples are washed again with PBS and the endogenous oxidases were blocked for 2 minutes in the dark. Further washes with PBS followed and blocking the unspecific sites is done for 1 hour at 25℃. PARP is evidenced by immunolocalization utilizing a polyclonal antibody, directed against the N-terminal proteolytic fragment. Immuno-reaction is revealed by a secondary anti-rabbit antibody after incubation for 16 hours at 4°C. After exhaustive washing with PBS the samples are incubated for 30 minutes in solution ABC. Eventually, DAB (3,3'-Diaminobenzidine) is added and the samples are incubated for 10 minutes in the dark. The samples are washed again the plates are sealed and ready for microscopic observation.(Only for Reference)