ABT-751

ABT-751 (E7010) is a novel, highly orally bioavailable sulfonamides antimitotic compound and tubulin binder. It prevents tubulin aggregation by binding to the colchicine site on β-tubulin, leading to cell cycle arrest in G2/M phase and inducing apoptosis, thus effectively preventing cell division. ABT-751 induces autophagy by inhibiting the AKT/MTOR signaling pathway. ABT-751 showed significant inhibition against various types of cancer cells, including lung, gastric, colon, and breast cancer^{[1][2][3][4][5][6][7][8]}. In Vitro:ABT-751 (2 μM; 4, 8, 24h) can disrupt mitosis, disrupt mitochondrial membrane potential, induce ROS generation and DNA damage in hepatocellular carcinoma-derived Hep-3B cells ^[6].
ABT-751 (2 μM; 4, 8, 24h) can cause DNA damage in Hep-3B cells, inhibit cell proliferation and induce G2/M cell cycle arrest ^[6].
ABT-751 (2 μM; 4, 8, 24h) induces autophagy in TP53-deficient Hep-3B cells by inhibiting the AKT/MTOR signaling pathway, and induces apoptosis through Caspase-dependent, exogenous, and endogenous pathways. Exogenous expression of TP53 gene further increased the autophagy and apoptosis of these cells induced by ABT-751 [6].
In Vivo:ABT-751 (100 mg/kg/day, Oral gavage (p.o.), 5 days on, 5 days off x2, 21 days) has a significant inhibitory effect in neuroblastoma models and can induce significant reduction or regression of tumor volume in rhabdomyosarcoma and nephroblastoma models. ABT-751 has synergistic effect on Vincristine and Paclitaxel (HY-B0015)^[7].
ABT-751 (100 mg/kg/day, Oral gavage (p.o.), 5 days on, 5 days off x2) has a synergistic effect on Docetaxel (HY-B0011) in prostate, NSCLC, and breast tumor xenografts in mice. Improve the inhibitory effect on tumor^[8].