hCAP-H Inhibitors

Chemicals classified as hCAP-H inhibitors encompass a range of compounds that interfere with mitotic functions and chromosomal architecture indirectly. These inhibitors do not target hCAP-H directly; rather, they impact the protein's function by altering the cellular processes and signaling pathways that facilitate proper chromosome condensation and segregation during mitosis. Compounds such as Paclitaxel and Vinblastine act on the microtubule network, which is essential for the mitotic spindle assembly. By stabilizing or destabilizing microtubules, these compounds can disrupt the proper function of the spindle apparatus, thereby indirectly affecting the role of hCAP-H in chromosome condensation and stabilization.

Nocodazole and Monastrol exert similar effects by targeting microtubule dynamics and kinesin motors, respectively, which are critical for spindle formation and function. BI 2536 and S-trityl-L-cysteine focus their action on key mitotic kinases like Plk1 and the motor protein Eg5, respectively. Their inhibition leads to defects in spindle assembly and function, which can indirectly inhibit the function of hCAP-H. Aurora kinases are another important target for hCAP-H inhibitors. Compounds such as ZM447439, VX-680, and Alisertib inhibit Aurora kinase activity, which is pivotal for chromosome alignment and segregation. By disrupting these processes, the compounds indirectly affect hCAP-H function, which is crucial for maintaining chromosome architecture during mitosis. Mitoxantrone and Amsacrine target topoisomerase II, which is involved in DNA replication and decatenation, processes that are fundamental for proper chromosome condensation and segregation.