SERTAD4 Inhibitors

Chemical inhibitors of SERTAD4 encompass a range of compounds known for their ability to disrupt the cell cycle by targeting cyclin-dependent kinases (CDKs), enzymes which are integral for the progression and regulation of the cell cycle. Palbociclib and Ribociclib, for instance, are selective inhibitors of CDK4/6. By inhibiting these kinases, they induce a G1 phase arrest, effectively preventing the progression to the S phase where SERTAD4 is most active. This inhibition obstructs SERTAD4's functional engagement in cell cycle regulation at a critical juncture, thereby curtailing its activity. Similarly, Abemaciclib targets the same kinases, resulting in a comparable functional inhibition of SERTAD4 by halting the cell cycle before SERTAD4's phase of activity.

Other inhibitors, such as Olomoucine, Roscovitine (Seliciclib), and Purvalanol A, take a slightly broader approach by affecting CDK1, CDK2, and CDK3, kinases that are also involved in cell cycle regulation but at different checkpoints. Olomoucine, specifically, targets early stages of cell division, leading to an arrest that precludes SERTAD4 from acting during the G1/S transition. Roscovitine and Purvalanol A extend this inhibition to other phases, encompassing CDK7 and CDK9 as well, further ensuring that SERTAD4 is unable to contribute to cell cycle progression at multiple points. Milciclib, while also affecting CDKs, extends its reach to tropomyosin receptor kinases (TRKs), adding another layer of regulation that could intersect with SERTAD4's role. The compounds Flavopiridol, Dinaciclib, and AT7519 exert their inhibitory effects on a range of CDKs that are critical for the cell cycle, thereby disrupting the cycle at multiple points and ensuring that SERTAD4 does not find a conducive environment for its activity. AZD5438 also targets CDK1, CDK2, and CDK9, which by their inhibition, arrest the cell cycle at various stages, consequently inhibiting the functional role of SERTAD4 throughout cell cycle progression.