EC359 is a potent and selective inhibitor of leukemia inhibitory factor receptor (LIFR), a potent inhibitor with anticancer activity, blocks LIF/LIFR interaction, and can be used in the study of leukemia and endometrial cancer.

LIFR:10.2 nM (Kd)

EC359 treatment (0-100 nM) for 3 days in BT-549, SUM-159, MDA-MB-231, MDA-MB-468, and HCC1806 cells leads to a dose-dependent reduction in cell viability[1].
In MDA-MB-231 and BT-549 cells, treatment with EC359 at concentrations of 20 nM and 25 nM for 72 hours significantly increases caspase-3/7 activity and the proportion of Annexin V-positive cells. EC359 exhibits noteworthy inhibitory activity on invasion and promotes apoptosis in triple-negative breast cancer (TNBC) cells[1].Treatment with EC359 at 100 nM for 12 hours in BT549 cells significantly decreases the expression of several known STAT3 target genes, including STAT1, TGFB1, JUNB, MCL-1, etc[1].In MDA-MB-231 and BT-549 cells, EC359 treatment at 100 nM for 1 hour substantially reduces STAT3 activation induced by LIF, OSM, and CNTF. Additionally, EC359 treatment leads to a significant decrease in the phosphorylation of AKT, mTOR, S6, and ERK1/2. Furthermore, EC359 treatment enhances the phosphorylation of proapoptotic p38MAPK in BT549 cells[1].

Subcutaneous injection of EC359 at a dose of 5 mg/kg, administered three days per week for 25 days in female athymic nude mice, significantly reduces tumor progression. Importantly, the body weights of mice in the EC359-treated groups remain unchanged, confirming the low toxicity of EC359[1].