ILK-IN-2

ILK-IN-2 (OSU-T315 analog) is an oral PDK2 inhibitor and also an ILK inhibitor, with an IC₅₀ of 0.6 μM. ILK-IN-2 induces cell autophagy and apoptosis, showing anti-tumor activity. ILK-IN-2 directly abolishes AKT activation by preventing AKT from translocating to lipid rafts, triggering Caspase-dependent apoptosis in chronic lymphocytic leukemia (CLL) and extending the lifespan in TCL1 mouse models^[1][2]. In Vitro:ILK-IN-2 (0-10 μM, 24 h) shows dose-dependent selective cytotoxicity on CLL-derived cell lines and primary CLL cells, but has minimal impact on normal lymphocytes^[1].
ILK-IN-2 (4 μM, 16 h) reduces levels of Mcl-1 and Bcl-xl in CLL cells, triggering caspase activation within those cells^[1].
ILK-IN-2 (1-4 μM, 15 min) does not affect proximal membrane signaling of AKT in Mec-1 and OSU-CLL cells^[1].
ILK-IN-2 (0-5 μM, 24 h) inhibits the proliferation of prostate and breast cancer cell lines, with IC₅₀ values for LNCaP, PC-3, MDA-MB-231, MDA-MB-468, SKBR3, and MCF-7 being 1.6, 2, 1, 1.5, 1.8, and 2.5 μM respectively, while having no effect on normal epithelial cells^[2].
ILK-IN-2 (0-4 μM, 24 h) inhibits PDK2 in PC3 and MDA-MB-231 by suppressing the phosphorylation of Akt at the Ser-473 site^[2].
ILK-IN-2 (0-4 μM, 24 h) induces cell death in PC-3 cells through autophagy and apoptosis^[2]. In Vivo:ILK-IN-2 (25-50 mg/kg, oral or intraperitoneal injection, once daily, 2-4 weeks) delays leukemia progression in mice and significantly improves the overall survival rate of mice harboring TCL1 leukemia cells^{[ 1 ]}.
ILK-IN-2 (25-50 mg/kg, orally, daily, for 35 days) inhibits the growth of PC-3 xenograft tumors in nude mice^[2].