MKI-2

MKI-2 potently inhibits recombinant MASTL kinase activity with an IC₅₀ of 37.44 nM^[1].
MKI-2 (14 h) inhibits cellular MASTL activity in MCF7 breast cancer cells with an IC₅₀ of 142.7 nM, as measured by reduced phospho-ENSA levels^[1].
MKI-2 (100 nM) is selective for MASTL, as it does not inhibit recombinant ROCK1, PKACα, or p70S6K kinases and only slightly inhibits AKT1 at a concentration of 100 nM^[1].
MKI-2 (250 nM; 12-24 h) modulates the MASTL-PP2A-c-Myc axis in MCF7, BT549, and MDA-MB-468 breast cancer cells by increasing PP2A activity, reducing phospho-ENSA and total, phospho-c-Myc levels^[1].
MKI-2 (250 nM; 24 h) induces mitotic catastrophe in MCF7 breast cancer cells at 250 nM for 24 h, as evidenced by mitotic arrest, altered apoptotic and increased DNA damage marker (γ-H2AX) levels, and increased aberrant nuclear cells^[1].
MKI-2 (15.63-1000 nM; 72 h) inhibits the proliferation of MCF7, BT549, MDA-MB-468, and 4T1 breast cancer cells with IC₅₀ values ranging from 56.53 nM to 124.6 nM after 72 h of treatment^[1].
MKI-2 (6.25-25 nM) inhibits colony, 3D spheroid, and mammosphere formation of MCF7 breast cancer cells^[1].
MKI-2 (250 nM; 24 h) inhibits the migration and invasion of BT549 breast cancer cells at 250 nM for 24 h^[1].
MKI-2 (250 nM-2 μM; 12-48 h) reduces the percentage of GVBD and has no significant effects on mouse oocytes viability^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.