VEGFR2 AUTOTAC-1

VEGFR2 AUTOTAC-1 potently inhibits the proliferation of MDA-MB-468 cells with an IC₅₀ of 0.74 μM, and this activity is mainly dependent on the degradation of VEGFR2^[1].
VEGFR2 AUTOTAC-1 (0.5-5 μM for 8-24 h, and 2.5 μM for 0, 16, 24, 48 h) promotes VEGFR2 protein degradation in a concentration- and time-dependent manner without altering the transcription level of VEGFR2 mRNA in MDA-MB-468 cells^[1].

VEGFR2 AUTOTAC-1 (5.0 μM; 48 h) exerts VEGFR2-dependent antiproliferative effects in VEGFR2-knockdown MDA-MB-468 cells, and significantly inhibits cell proliferation in wild-type MDA-MB-468 (IC50 = 0.74 μM) cells^[1].

VEGFR2 AUTOTAC-1 (1-5 μM; 6-24 h) concentration-dependently degrades VEGFR2 protein, inhibits VEGF165-induced endothelial tube formation and cell migration, upregulates the epithelial marker E-cadherin, and downregulates the mesenchymal marker MMP2^[1] in HUVEC cells.

VEGFR2 AUTOTAC-1 (Compound 11bg) (2.5 μM; 24 h) significantly activates autophagy in MDA-MB-231, MDA-MB-468 and MDA-MB-436 cells^[1].
VEGFR2 AUTOTAC-1 (1-2.5 μM; 12-48 h) promotes the accumulation of p62 and LC3-II in MDA-MB-468 cells^[1].
VEGFR2 AUTOTAC-1 (2.5 μM; 3 min) increases the thermal stability of VEGFR2 and p62 proteins in MDA-MB-468 cells^[1].
VEGFR2 AUTOTAC-1 (0.5-5 μM; 48 h) concentration-dependently inhibits colony formation, induces G1-phase cell cycle arrest and apoptosis, upregulates pro-apoptotic proteins and downregulates anti-apoptotic proteins, and suppresses cell migration in MDA-MB-468 cells^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.