MO-I-1100, an inhibitor of ASPH (Aspartyl-(Asparaginyl)-β-hydroxylase) enzymatic activity, effectively suppresses HCC cell migration, invasion, and anchorage-independent growth. It exhibits antitumor properties by inhibiting the Notch signaling cascade in HCC.

MO-I-1100 does not impact the viability of NIH3T3 cells deficient in cell surface ASPH. At concentrations of 1-10 μM, MO-I-1100 inhibits the viability of FOCUS cells, which exhibit high levels of ASPH expression.

MO-I-100 administered at a dose of 50 mg/kg via intraperitoneal injection, on a schedule of five consecutive days per week for two weeks, followed by administration every other day, effectively reduced tumor growth in an orthotopic HCC model in the liver. Similarly, MO-I-1100, given at 50 mg/kg/day through intraperitoneal injection continuously for five days, decreased the expression of activated Notch 1 (cleavage fragment) along with the downstream genes HES1 and HEY1.