EHT-6706 (free base)

EHT-6706 free base is a tubulin inhibitor with an IC₅₀ value of 1 μM against porcine tubulin. EHT-6706 free base binds to the colchicine-binding site on tubulin to inhibit tubulin polymerization and disrupt the cellular microtubule network. EHT-6706 free base acts as an antiproliferative, vascular-disrupting, permeability-modulating, migration-inhibiting and antiangiogenic agent. EHT-6706 free base exhibits inhibitory activity against human tumor cells. EHT-6706 free base can be used in cancer and angiogenesis research^[1]. In Vitro:EHT-6706 (4 h) free base binds to the Colchicine (HY-16569)-binding site on porcine tubulin with an IC₅₀ of 0.17 μM^[1].
EHT-6706 (10 nM-50 nM; 24 h) free base disrupts the intracellular microtubule network of HCT116 cells in a concentration-dependent manner^[1].
EHT-6706 (0.0003 μM-10 μM; 72 h) free base potently inhibits the proliferation of 60 human tumor cell lines (e.g., T47D, HT-29, A498, A549), with an IC₅₀ range of 0.3 nM to 11.6 nM after 72 hours of treatment^[1].
EHT-6706 (10 nM-100 nM; 18 h) free base inhibits capillary lumen formation by HUVEC on Matrigel, with an IC₅₀ of 22 nM calculated by total lumen length and an IC₅₀ of 15 nM calculated by the number of branching points^[1].
EHT-6706 (1 nM-100 nM; overnight) free base disrupts the pre-established capillary tube structures formed by HUVEC on Matrigel^[1].
EHT-6706 (10 nM-100 nM; 15 min) free base increases the permeability of confluent HUVEC monolayers in a dose-dependent manner^[1].
EHT-6706 (10 nM-1 μM; 1 h) free base alters the morphology of HUVEC and disrupts the stability of the F-actin cytoskeleton, with prominent vesicular protrusions observable^[1].
EHT-6706 (10 nM-100 nM; 22 h) free base inhibits FGF-2- and VEGF-induced HUVEC migration in a concentration-dependent manner, with the maximum inhibitory effect achieved after treatment with 100 nM for 22 hours^[1].
EHT-6706 (40 nM; 18 h) free base causes abnormal regulation of expression levels in 3364 genes by ≥2-fold, most of which are upregulated anti-angiogenic genes, with a subset being downregulated pro-angiogenic genes, while also increasing the level of TLL-1 protein in cell supernatants^[1].