MIC1 Inhibitors

Chemical inhibitors of MIC1 target various aspects of the cell cycle, particularly the functions of Aurora kinases, which are critical for mitotic processes. Alisertib, an Aurora A kinase inhibitor, can inhibit MIC1 by preventing the kinase's role in mitotic entry and spindle assembly, leading to a halt in the progression of the cell cycle and potentially inhibiting MIC1's associated functions. Similarly, GSK1070916, another selective inhibitor of Aurora B/C kinase, disrupts cytokinesis, which could indirectly inhibit MIC1. ZM447439, a broad-spectrum Aurora kinase inhibitor, can impede chromosome alignment and segregation, processes that might be crucial for MIC1's proper function during cell division. MLN8054 and its analog, MLN8237 (Alisertib), are selective inhibitors of Aurora A kinase, which can cause mitotic arrest and consequently inhibit MIC1 functions related to mitotic spindle formation.

Furthermore, VX-680 (Tozasertib) inhibits Aurora kinases A, B, and C, which can lead to an interruption in MIC1 activity by interfering with chromosomal alignment and spindle checkpoint function. Hesperadin, by inhibiting Aurora B kinase, can disrupt the correction of kinetochore-microtubule attachments and the spindle assembly checkpoint, potentially inhibiting MIC1's function in chromosome segregation. Barasertib's selective inhibition of Aurora B kinase could lead to the functional inhibition of MIC1 by disrupting processes critical for cell division in which MIC1 might be involved. AT9283, as a multi-targeted kinase inhibitor, affects Aurora kinases and other kinases related to the cell cycle, which can lead to indirect inhibition of MIC1 by stymieing cell cycle progression. CCT137690, another Aurora kinase inhibitor, can inhibit MIC1 by preventing necessary phosphorylation events during mitotic spindle assembly. Danusertib, targeting Aurora kinases, can lead to mitotic arrest, which would inhibit MIC1's function. Lastly, ENMD-2076, which also targets Aurora kinases, can inhibit MIC1 by potentially disrupting spindle assembly checkpoint control or cytokinesis, further illustrating the intricate relationship between cell cycle regulation and MIC1 activity.