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 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 d s of 1.29 and 13.4 μM by microscale thermophoresis (MST) measurements, respectively. hVEGF-IN-1 (0.375-3 μM; 0-24 h) reduces MDA-MB-231 cell migration approximately 25% at the concentration of 3 μM. hVEGF-IN-1 (0.1875-3 μM; 48 h) reduces the level of VEGF-A protein in MCF-7 cells. 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. hVEGF-IN-1 (1.25-10 μM) reduces the stability of the IRES-A G-Quadruplex in a dose-dependent manner. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Western Blot AnalysisCell Line: MCF-7 cells Concentration: 0.1875, 0.375, 0.75, 1.5, 3 μM Incubation Time: 48 hours Result: Down-regulated h VEGF -A expression. 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 . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: BALB/c female nude mice were implanted MCF-7 cells Dosage: 7.5 mg/kg Administration: I.p. once daily for 20 days Result: Reduced the tumor volume to Form:Solid IC50& Target:VEGFR