MY-875 is a competitive microtubulin polymerization inhibitor with an IC50 value of 0.92 μM. MY-875 inhibits microtubulin polymerization by targeting colchicine binding sites and activates the Hippo pathway. MY-875 induces apoptosis and has anticancer activity[1].
MY-875 (0-80 μM, 48 h) has significant anti-proliferative activity against cancer cells[1].
MY-875 (1-10 μM) can inhibit microtubule protein polymerization with an IC50 value of 0.92 μM while inhibiting alkylation of β-tubulin and the formation of EBI-β-tubulin adduct bands in a dose-dependent manner[1].
MY-875 (0-45 nM, 48 h) can induce the phosphorylation state of MST (Ste20-like kinases) and LATS (large tumor suppressor kinases), leading to YAP (Yes-associated protein) degradation in a dose-dependent manner[1].
MY-875 (0-45 nM, 24 h) significantly inhibits cell colony-forming ability, arrests cells in the G2/M phase and induces cell apoptosis in a dose-dependent manner[1].
Cell Proliferation Assay[1]
| Cell Line: | MGC-803, HCT-116, KYSE450, HGC-27, SGC-7901cell lines |
| Concentration: | 0-80 μM |
| Incubation Time: | 48 hours |
| Result: | Inhibited the proliferation of MGC-803, HCT-116, KYSE450, HGC-27 and SGC-7901 cells with the IC50 values of 0.027, 0.055, 0.067, 0.033 and 0.025 μM, respectively. Showed strong inhibitory effect on other tumor cell lines with the IC50 values less than 0.1 μM, such as DU145, A549, MCF-7, etc. |
Cell Cycle Analysis[1]
| Cell Line: | MGC-803, SGC-7901 cell lines |
| Concentration: | 0-45 nM |
| Incubation Time: | 24 hours |
| Result: | Increased the percentage of cells in G2/M phase from 19.38% to 76.97% in MGC-803 cells and from 7.04% to 80.89% in SGC-7901 cells, respectively at 45 nM. |
Apoptosis Analysis[1]
| Cell Line: | MGC-803, SGC-7901 cell lines |
| Concentration: | 0-45 nM |
| Incubation Time: | 48 hours |
| Result: | Induced apoptotic cells from 21.96% to 76.08% in MGC-803 cells and from 9.28% to 63.51% in SGC-7901 cells, respectively at 45 nM. Reduced expression of anti-apoptotic proteins c-IAP1, Bcl-xL and Mcl-1. |