hVEGF-IN-1

hVEGF-IN-1, a quinazoline derivative, could specifically bind to the G-rich sequence in the internal ribosome entry site A (IRES-A) and destabilize the G-quadruplex structure. hVEGF-IN-1 binds to the IRES-A (WT) with a K_d of 0.928 μM in SPR experiments. hVEGF-IN-1 could hinder tumor cells migration and repress tumor growth by decreasing VEGF-A protein expression^[1]. IC50 & Target: VEGFR^[1] In Vitro: hVEGF-IN-1 (compound 1) (1 nM-100 μM; 5 min) binds to IRES-A (WT) and IRES-A mutant RNA oligomer (IRES-MU1) with K_ds of 1.29 and 13.4 μM by microscale thermophoresis (MST) measurements, respectively^[1].
hVEGF-IN-1 (0.375-3 μM; 0-24 h) reduces MDA-MB-231 cell migration approximately 25% at the concentration of 3 μM^[1].
hVEGF-IN-1 (0.1875-3 μM; 48 h) reduces the level of VEGF-A protein in MCF-7 cells^[1].
hVEGF-IN-1 (0.375-3 μM; 48 h) decreases the relative wound closure of migrated MCF-7 cells by ∼35% at the concentration of 3 μM^[1].
hVEGF-IN-1 (1.25-10 μM) reduces the stability of the IRES-A G-Quadruplex in a dose-dependent manner^[1]. In Vivo: hVEGF-IN-1 (compound 1) (7.5 mg/kg; i.p. once daily for 20 d) inhibits tumor growth in a human breast tumor xenograft^[1].