BET5 Inhibitors

BET5 inhibitors primarily focus on the disruption or modulation of vesicular transport pathways, especially between the endoplasmic reticulum (ER) and the Golgi apparatus, given that BET5 plays a crucial role within this cellular process. The intent behind targeting these pathways is to influence the activity or functionality of BET5 indirectly. Brefeldin A and Monensin, for example, are instrumental in this regard. Brefeldin A collapses the Golgi structure and hampers transport from the ER, thereby impacting BET5's functionality, while Monensin disrupts vesicular transport, thereby potentially impacting BET5's transport role.

Microtubules and actin filaments, being structural components essential for vesicular transport, are another focal point. Nocodazole, which depolymerizes microtubules, and Latrunculin A, an actin filament disruptor, are indicative of the strategy to hinder these structural components and, by extension, the transport processes BET5 is involved in. Additionally, compounds like Thapsigargin and Tunicamycin induce ER stress, offering a different angle to modulate BET5's role.