Date published: 2025-9-12

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Rab 16 Inhibitors

The term 'Rab16 inhibitors' broadly refers to compounds that indirectly modulate the activity of Rab16, a member of the Rab family of small GTPases. Rab GTPases, including Rab16, play crucial roles in regulating vesicle trafficking, a fundamental process in cellular logistics. Since Rab16 and other Rab proteins do not typically interact directly with small molecule ligands, the inhibitors listed target associated signaling pathways or cellular processes that indirectly influence Rab16 function. The primary strategy for modulating Rab16 activity involves targeting signaling pathways and molecules that interact with or regulate Rab GTPases. Compounds like NSC23766, ML141, 2-(Benzoylcarbamothioylamino)-5,5-dimethyl-4,7-dihydrothieno[2,3-c]pyran-3-carboxylic Acid, and ZCL278 inhibit other GTPases (like Rac1, Cdc42, Rho family) or their regulators, potentially altering the cellular context in which Rab16 operates. By modulating the activity of these related GTPases, these inhibitors can indirectly affect the signaling pathways that intersect with Rab16 function.

Additionally, chemicals that disrupt vesicle trafficking or cytoskeletal dynamics can also influence Rab16 activity. Brefeldin A, for example, disrupts Golgi apparatus function, indirectly affecting vesicular transport routes involving Rab16. Similarly, inhibitors of key enzymes in vesicle formation and transport, such as Dynamin Inhibitor I, Dynasore and (S)-(-)-Blebbistatin (inhibiting myosin II), can indirectly impact Rab16-mediated vesicular trafficking. PI3K inhibitors like Wortmannin and LY 294002 are also significant, as PI3K signaling is intricately linked with membrane trafficking and cytoskeletal dynamics, processes in which Rab16 is potentially involved. In conclusion, while direct chemical inhibitors of Rab16 are not well-defined, a range of compounds that affect related GTPases, vesicle trafficking, and cytoskeletal dynamics can serve as indirect modulators. These compounds primarily exert their influence by altering signaling pathways and cellular processes that are crucial for Rab16's role in vesicle trafficking. This approach to inhibition highlights the complex network of interactions and regulatory mechanisms in which Rab GTPases are involved, offering a broader perspective on modulating their function.

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