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. 2021 Sep 24;13(19):4769. doi: 10.3390/cancers13194769

Figure 1.

Figure 1

Proposed KGP265 mechanism in the tumor vasculature Rapid dephosphorylation of the prodrug KGP265 in the tumor vessel endothelium yields the active agent KGP18, which binds to tubulin, inhibits tubulin polymerization and leads to the activation of RhoA kinase (ROCK). The Phosphorylation of the downstream ROCK targets results in the formation of actin stress fibers. As actin stress fibers resolve, endothelial cells become round, form blebs and detach, culminating in vascular disruption. See Figure 2 and Supplementary Figures S1 and S2.