Tubulin-IN-55 is a tubulin inhibitor that disrupts the PI3K/Akt signaling pathway in cancer cells. It exhibits broad-spectrum antiproliferative activity against various tumor cell lines (HeLa, HCT116, 4T1, A549, H1299, MDA-MB231). Tubulin-IN-55 induces G2/M phase arrest and apoptosis (apoptosis) while inhibiting cancer cell migration and invasion. It demonstrates significant antitumor efficacy in an in situ autologous mouse model and is applicable in cancer research.

Tubulin-IN-55 (Compound 89) exhibits potent antiproliferative effects on HeLa, HCT116, and 4T1 cells at concentrations of 0.1-10 μM over 24 hours, with IC50 values of 1.20 μM, 4.91 μM, 1.13 μM, and 0.65 μM, respectively. At 0.3-0.9 μM for 12-24 hours, it demonstrates anti-migration and anti-invasion properties in the same cell lines. Tubulin-IN-55 also induces apoptosis and G2/M phase arrest in HeLa, HCT116, and 4T1 cells within the 0.3-1.2 μM range over 24 hours. It inhibits tubulin polymerization in vitro in a dose-dependent manner at concentrations of 6.25-100 μM over 60 minutes. Additionally, Tubulin-IN-55 downregulates the phosphorylation levels of PI3K and Akt in HeLa, HCT116, and 4T1 cells without affecting total PI3K and Akt levels when used in concentrations of 0.3-0.9 μM for 24 hours. Furthermore, Tubulin-IN-55 shows antitumor activity in breast cancer organoids (BC-PDO1, BC-PDO2, and BC-PDO10), reducing organoid viability with IC50 values of 1.07 μM, 0.81 μM, and 0.42 μM, respectively.

Tubulin-IN-55 (Compound 89), administered intraperitoneally at a dose of 10 mg/kg every other day for four weeks, demonstrates significant antitumor activity in an orthotopic autograft model using BALB/c mice.