产品
编 号：F641680
分子式：C28H35Cl2N5O4S
分子量：608.58
分子式：C28H35Cl2N5O4S
分子量：608.58
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CAS No: 1883548-93-3
产品详情
生物活性：
Mps1-IN-1 dihydrochloride is a potent and ATP-competitive Mps1 kinase inhibitor with an IC50 of 367 nM. Mps1-IN-1 dihydrochloride inhibit Mps1 mitotic kinase activity and abrogates spindle assembly checkpoint (SAC) function. Mps1-IN-1 dihydrochloride decreases the viability of both cancer and ‘normal’ cells.
体外研究：
Mps1-IN-1 dihydrochloride (2-10 μM; 96 hours) inhibits the proliferative capacity of HCT116 cells to 33% that of DMSO control. Mps1-IN-1 dihydrochloride (0.3-10 μM; 4 hours) induces bypass of a checkpoint-mediated mitotic arrest in a dose-dependent manner. Mps1-IN-1 dihydrochloride (10 μM) administration results in a dose-dependent decrease in the time spent in mitosis with nearly 100% U2OS cells initiating anaphase within 20 minutes.Mps1-IN-1 dihydrochloride (0.5, 2, 10 μM) causes a dose-dependent reduction in hyper-phosphorylated Mps1 as demonstrated by a decrease in phosphorylation-induced mobility shift in UTRM10 LAP-Mps1 WT cells. Mps1-IN-1 (5, 10 μM) arrested in mitosis using Nocodazole, results in a dose-dependent accumulation of 4c pHistone H3 negative cells in U2OS cells. Acceleration of mitosis kinetics in Mps1-IN-1-treated cells had direct consequences on genomic stability with cells exhibiting significant signs of chromosome mis-alignment and chromosome mis-segregation. Mps1-IN-1 dihydrochloride demonstrates greater than 1000-fold selectivity relative to the 352 member kinase panel with the major exceptions of Alk and Ltk.
Mps1-IN-1 dihydrochloride is a potent and ATP-competitive Mps1 kinase inhibitor with an IC50 of 367 nM. Mps1-IN-1 dihydrochloride inhibit Mps1 mitotic kinase activity and abrogates spindle assembly checkpoint (SAC) function. Mps1-IN-1 dihydrochloride decreases the viability of both cancer and ‘normal’ cells.
体外研究：
Mps1-IN-1 dihydrochloride (2-10 μM; 96 hours) inhibits the proliferative capacity of HCT116 cells to 33% that of DMSO control. Mps1-IN-1 dihydrochloride (0.3-10 μM; 4 hours) induces bypass of a checkpoint-mediated mitotic arrest in a dose-dependent manner. Mps1-IN-1 dihydrochloride (10 μM) administration results in a dose-dependent decrease in the time spent in mitosis with nearly 100% U2OS cells initiating anaphase within 20 minutes.Mps1-IN-1 dihydrochloride (0.5, 2, 10 μM) causes a dose-dependent reduction in hyper-phosphorylated Mps1 as demonstrated by a decrease in phosphorylation-induced mobility shift in UTRM10 LAP-Mps1 WT cells. Mps1-IN-1 (5, 10 μM) arrested in mitosis using Nocodazole, results in a dose-dependent accumulation of 4c pHistone H3 negative cells in U2OS cells. Acceleration of mitosis kinetics in Mps1-IN-1-treated cells had direct consequences on genomic stability with cells exhibiting significant signs of chromosome mis-alignment and chromosome mis-segregation. Mps1-IN-1 dihydrochloride demonstrates greater than 1000-fold selectivity relative to the 352 member kinase panel with the major exceptions of Alk and Ltk.
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