GZD-552 is a potent orally active FAK inhibitor with a human FAK IC50 of 5.8 nM. GZD-552 suppresses FAK phosphorylation activation and downstream ERK signaling. GZD-552 induces apoptosis and G 2 /M cell cycle arrest, and exhibits antiproliferative activities in glioblastoma multiforme cells. GZD-552 exhibits antitumor efficacy in mice xenograft model. GZD-552 can be used for the research of glioblastoma multiforme [1].
In Vivo, GZD-552 (compound 16c) (10 and 20 mg/kg/day; i.g.; daily; 18 days) inhibits tumor growth in mouse U87-MG xenograft model without detectable systemic toxicity[1].
In Vitro, GZD-552 (compound 16c) potently and selectively inhibits the proliferation of U87-MG and U118-MG glioblastoma cells with IC50 values of 6.6 nM and 4.3 nM, respectively, and shows limited activity against NCI-H1975 (IC50 = 0.16 μM), MDA-MB-231 (IC50 = 0.28 μM), and LO2 cells (IC50 = 0.74 μM)[1]. GZD-552 strongly and stably binds to FAK protein in U87-MG cells[1]. GZD-552 (0.002-0.08 μM) suppresses FAK protein expression and activation, and downregulates downstream ERK phosphorylation in U87-MG cells in a concentration-dependent manner[1]. GZD-552 (0.004-0.12 μM; 24 h) induces dose-dependent apoptosis and G2/M cell cycle arrest in U87-MG cells[1].
References:
[1]. Xu Y, et al. Design, synthesis, and anti-glioblastoma multiforme evaluation of novel multikinase inhibitors via a cyclization strategy with potent FAK inhibition. Eur J Med Chem. 2026;312:118877.
In Vivo, GZD-552 (compound 16c) (10 and 20 mg/kg/day; i.g.; daily; 18 days) inhibits tumor growth in mouse U87-MG xenograft model without detectable systemic toxicity[1].
In Vitro, GZD-552 (compound 16c) potently and selectively inhibits the proliferation of U87-MG and U118-MG glioblastoma cells with IC50 values of 6.6 nM and 4.3 nM, respectively, and shows limited activity against NCI-H1975 (IC50 = 0.16 μM), MDA-MB-231 (IC50 = 0.28 μM), and LO2 cells (IC50 = 0.74 μM)[1]. GZD-552 strongly and stably binds to FAK protein in U87-MG cells[1]. GZD-552 (0.002-0.08 μM) suppresses FAK protein expression and activation, and downregulates downstream ERK phosphorylation in U87-MG cells in a concentration-dependent manner[1]. GZD-552 (0.004-0.12 μM; 24 h) induces dose-dependent apoptosis and G2/M cell cycle arrest in U87-MG cells[1].
References:
[1]. Xu Y, et al. Design, synthesis, and anti-glioblastoma multiforme evaluation of novel multikinase inhibitors via a cyclization strategy with potent FAK inhibition. Eur J Med Chem. 2026;312:118877.