OTSSP167 inhibits the growth of A549 (lung), T47D (breast), DU4475 (breast), 22Rv1 (prostate) and HT1197 (bladder) cancer cells with IC50 values of 6.7, 4.3, 2.3, 6.0 and 97 nM, respectively[1]. OTSSP167 effectively interferes with the mitotic checkpoint and disrupts MCC and MCC-APC/C interactions in MCF7 cells, also causing GFP-MELK localization to the cell cortex in prometaphase cells[2]. As a selective MELK inhibitor, OTSSP167 exhibits a strong in vitro activity with an IC50 of 0.41 nM[3].
体内研究
In vivo, OTSSP167 at 20 mg/kg (i.v.) achieves a tumor growth inhibition (TGI) of 73% in a xenograft mouse model; oral administrations at 1, 5, and 10 mg/kg result in TGI of 51, 91, and 108%, respectively, though a 20 mg/kg oral dose does not suppress tumor growth in PC-14 xenografts[1].
体外研究
OTSSP167 inhibits the growth of A549 (lung), T47D (breast), DU4475 (breast), 22Rv1 (prostate) and HT1197 (bladder) cancer cells with IC50 values of 6.7, 4.3, 2.3, 6.0 and 97 nM, respectively[1].
OTSSP167 effectively interferes with the mitotic checkpoint and disrupts MCC and MCC-APC/C interactions in MCF7 cells, also causing GFP-MELK localization to the cell cortex in prometaphase cells[2].
As a selective MELK inhibitor, OTSSP167 exhibits a strong in vitro activity with an IC50 of 0.41 nM[3].
作用机制
OTSSP167 optimally occupies the active site of MELK, especially the hydrophobic back pocket, mainly through van der Waals interactions.[2]
搜索
