ATC12 is a Aurora-A kinase inhibitor. ATC12 binds to Aurora-A and competes with TPX2 for binding to disrupt the Aurora-A / TPX2 interaction. ATC12 inhibits cancer cell proliferation, induces apoptosis and cellular senescence. ATC12 can be used in the research of breast cancer [1].
In Vitro, ATC12 (1.56-100 μM; 10 min) disrupts the interaction between purified Aurora-AKDCM and the TPX21-43 peptide in vitro, with an IC50 of 25.6 μM[1]. ATC12 (10 μM; 24 h) reduces the formation of the Aurora-A/TPX2 complex on the mitotic spindle and the level of pT288 Aurora-A at spindle poles in U2OS osteosarcoma cells[1]. ATC12 (10 μM; 24 h) disrupts the formation of Aurora-A/TPX2 complexes in mitotic and interphase nuclei of MCF7 and MDA-MB-231 breast cancer cells, and reduces the nuclear level of Aurora-A[1]. ATC12 (30-50 μM; 0-48 h) inhibits the proliferation of MCF7 breast cancer cells, prolongs the mitotic process, reduces the cell growth rate, and induces apoptotic cell death[1]. ATC12 (30-50 μM; 0-72 h) inhibits the proliferation of MDA-MB-231 breast cancer cells, prolongs mitotic duration, reduces cell growth rate and induces cellular senescence without triggering cell death[1]. ATC12 (10-100 μM; 5 days) reduces the viability of patient-derived organoids BCO-21, BCO-46 and BCO-61 from triple-negative breast cancer (TNBC) in a dose-dependent manner[1].
References:
[1]. Boi D, et al. The ATC12 small molecule inhibits the Aurora-A/TPX2 interaction and impairs the proliferation of breast cancer cells. Cell Death Dis. 2026;17(1):356. Published 2026 Mar 24.
In Vitro, ATC12 (1.56-100 μM; 10 min) disrupts the interaction between purified Aurora-AKDCM and the TPX21-43 peptide in vitro, with an IC50 of 25.6 μM[1]. ATC12 (10 μM; 24 h) reduces the formation of the Aurora-A/TPX2 complex on the mitotic spindle and the level of pT288 Aurora-A at spindle poles in U2OS osteosarcoma cells[1]. ATC12 (10 μM; 24 h) disrupts the formation of Aurora-A/TPX2 complexes in mitotic and interphase nuclei of MCF7 and MDA-MB-231 breast cancer cells, and reduces the nuclear level of Aurora-A[1]. ATC12 (30-50 μM; 0-48 h) inhibits the proliferation of MCF7 breast cancer cells, prolongs the mitotic process, reduces the cell growth rate, and induces apoptotic cell death[1]. ATC12 (30-50 μM; 0-72 h) inhibits the proliferation of MDA-MB-231 breast cancer cells, prolongs mitotic duration, reduces cell growth rate and induces cellular senescence without triggering cell death[1]. ATC12 (10-100 μM; 5 days) reduces the viability of patient-derived organoids BCO-21, BCO-46 and BCO-61 from triple-negative breast cancer (TNBC) in a dose-dependent manner[1].
References:
[1]. Boi D, et al. The ATC12 small molecule inhibits the Aurora-A/TPX2 interaction and impairs the proliferation of breast cancer cells. Cell Death Dis. 2026;17(1):356. Published 2026 Mar 24.