ML-141

Cdc42 is a member of the Rho GTPase subfamily that has roles in cytoskeleton organization, cell cycle progression, signal transduction, and vesicle trafficking. It cycles between a GTP-bound active state and a GDP-bound inactive state. ML-141 is a noncompetitive, allosteric inhibitor of Cdc42 (EC₅₀ = 2.1 µM) with no inhibitory action against Rho, Ras, Rab, or Rac.^1,2 It also inhibits the constitutively active Cdc42 Q61L mutant (EC₅₀ = 2.6 µM).¹ ML-141 blocks Cdc42-dependent filopodia formation in 3T3 cells and migration of ovarian cancer cells, prevents Cdc42-regulated virus infection, and inhibits the signaling pathway of VLA-4 integrin.¹ It is a useful tool to interrogate the role of Cdc42 intracellular signaling and cell activity.^3,4

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1. Hong, L., Kenney, S.R., Phillips, G.K., et al. Characterization of a Cdc42 protein inhibitor and its use as a molecular probe. The Journal of Biological Chemisty 288(12), 8531-8543 (2013).

2. Surviladze, Z., Waller, A., Strouse, J.J., et al. A potent and selective inhibitor of Cdc42 GTPase. (2010).

3. Kalwat, M.A., Yoder, S.M., Wang, Z., et al. A p21-activated kinase (PAK1) signaling cascade coordinately regulates F-actin remodeling and insulin granule exocytosis in pancreatic β cells. Biochem. Pharmacol. 85(6), 808-816 (2013).

4. Pinzaglia, M., Montaldo, C., Polinari, D., et al. EIF6 over-expression increases the motility and invasiveness of cancer cells by modulating the expression of a critical subset of membrane-bound proteins. BMC Cancer 15, 131-146 (2015).