Anticancer agent 337

Anticancer agent 337 (compound 5n) (48 h) potently inhibits the proliferation of A549, HepG2, and HeLa cancer cells with IC₅₀ values of 5.22 μM, 6.28 μM, and 3.62 μM, respectively, while exhibiting minimal toxicity to normal LO-2 hepatocytes^[1].
Anticancer agent 337 (10-100 μM; 30 min) inhibits human Topo I activity in a concentration-dependent manner, blocking supercoiled DNA relaxation at concentrations ranging from 10.0 μM to 100.0 μM^[1].
Anticancer agent 337 (100 μM; 30 min) acts as a Topo I poison at 100.0 μM, stabilizing the Topo I-DNA cleavage complex to induce DNA strand breaks, consistent with the mechanism of CPT (HY-16560)^[1].
Anticancer agent 337 (1.25-5 μM; 48 h treatment followed by 14-day culture) suppresses the long-term proliferation of A549 cells in a concentration-dependent manner, with stronger inhibition at 5.0 μM than the positive control CPT^[1].
Anticancer agent 337 (1.25-5 μM; 24 h, 48 h) inhibits the migration of A549 cells in a concentration-dependent manner over 24 h and 48 h, demonstrating anti-metastatic potential^[1].

Anticancer agent 337 (1.25-5 μM; 24 h) potently induces apoptosis in A549 cells in vitro in a concentration-dependent manner, with an 84.0% total apoptosis rate at 5.0 μM, which is significantly higher than that of the positive control CPT^[1].

Anticancer agent 337 (1.25-5 μM; 24 h) induces dose-dependent G1/G0 phase cell cycle arrest in A549 cells, with 74.36% of cells accumulating in G1 phase at a concentration of 5.0 μM^[1].

Anticancer agent 337 (1.25-5 μM; 48 h) induces concentration-dependent DNA double-strand breaks in A549 cells, with γ-H2AX foci levels at 5.0 μM comparable to those induced by the positive control CPT^[1].

Anticancer agent 337 (1.25-5 μM; 24 h) induces concentration-dependent mitochondrial dysfunction in A549 cells, reducing mitochondrial membrane potential at concentrations of 1.25 μM, 2.5 μM, and 5.0 μM^[1].

Anticancer agent 337 (1.25-5 μM; 12 h) induces concentration-dependent oxidative stress in A549 cells, significantly increasing intracellular ROS levels at concentrations of 1.25 μM, 2.5 μM, and 5.0 μM^[1].