MKI-3 is a selective microtubule-associated serine/threonine kinase-like ( MASTL ) inhibitor with an IC50 of 5.72 nM and a K d of 1.89 nM. MKI-3 disrupts the MASTL-ENSA-Aurora A signaling axis. MKI-3 induces chromosomal instability, mitotic catastrophe and apoptosis ( apoptosis ) in cancer cells. MKI-3 is applicable to research related to triple-negative breast cancer [1].
In Vivo, MKI-3 (8 mg/kg; i.p.; daily; 2 weeks) significantly reduces tumor growth in a 4T1 triple-negative breast cancer mouse model, induces mitotic cell death, and suppresses the MASTL−ENSA−Aurora A signaling pathway[1].
In Vitro, MKI-3 inhibits cellular MASTL activity with an IC50 of 114.9 nM[1]. MKI-3 (72 h) inhibits proliferation of breast cancer cell lines 4T1, MCF7, MDA-MB-231, and BT549 with IC50 values of 42.01 nM, 93.61 nM, 91.44 nM, and 160.9 nM, respectively[1]. MKI-3 (250 nM; 12 h) suppresses the MASTL-ENSA-Aurora A signaling axis, inducing apoptotic markers, in BT549 and 4T1 breast cancer cells[1]. MKI-3 (250 nM; 24 h) activates PP2A in BT549 breast cancer cells[1]. MKI-3 (250 nM; 24 h) induces mitotic defects including aberrant nuclear morphology, multipolar spindles, and centrosome abnormalities in BT549 breast cancer cells[1]. MKI-3 (250 nM; 48 h) antiproliferative activity in BT549 breast cancer cells is mediated in part by PP2A activation, as co-treatment with 20 nM okadaic acid rescues cell viability[1].
References:
[1]. Kim JI, et al. Development of MKI-3: A Potent and Selective MASTL Inhibitor with Improved Efficacy for Cancer Treatment. J Med Chem. Published online March 19, 2026.
In Vivo, MKI-3 (8 mg/kg; i.p.; daily; 2 weeks) significantly reduces tumor growth in a 4T1 triple-negative breast cancer mouse model, induces mitotic cell death, and suppresses the MASTL−ENSA−Aurora A signaling pathway[1].
In Vitro, MKI-3 inhibits cellular MASTL activity with an IC50 of 114.9 nM[1]. MKI-3 (72 h) inhibits proliferation of breast cancer cell lines 4T1, MCF7, MDA-MB-231, and BT549 with IC50 values of 42.01 nM, 93.61 nM, 91.44 nM, and 160.9 nM, respectively[1]. MKI-3 (250 nM; 12 h) suppresses the MASTL-ENSA-Aurora A signaling axis, inducing apoptotic markers, in BT549 and 4T1 breast cancer cells[1]. MKI-3 (250 nM; 24 h) activates PP2A in BT549 breast cancer cells[1]. MKI-3 (250 nM; 24 h) induces mitotic defects including aberrant nuclear morphology, multipolar spindles, and centrosome abnormalities in BT549 breast cancer cells[1]. MKI-3 (250 nM; 48 h) antiproliferative activity in BT549 breast cancer cells is mediated in part by PP2A activation, as co-treatment with 20 nM okadaic acid rescues cell viability[1].
References:
[1]. Kim JI, et al. Development of MKI-3: A Potent and Selective MASTL Inhibitor with Improved Efficacy for Cancer Treatment. J Med Chem. Published online March 19, 2026.