In SKOV3 cell line, Alofanib induces mainly apoptosis with cleavage of caspase 3, PARP and Bcl-2. It has a low cytotoxic effect on ovarian cancer cells [1]. Alofanib inhibits phosphorylation of FRS2α with the IC50 values of 7 and 9 nmol/l in cancer cells expressing different FGFR2 isoforms. In a panel of four cell lines representing several tumor types (triple-negative breast cancer, melanoma, and ovarian cancer), alofanib inhibits FGF-mediated proliferation with 50% growth inhibition (GI50) values of 16-370 nmol/l. Alofanib dose-dependently inhibits the proliferation and migration of human and mouse endothelial cells (GI50: 11-58 nmol/l) compared with brivanib and bevacizumab [2].

Alofanib (i.v.) significantly in a dose-dependent manner potentiated the efficiency of the combination of paclitaxel and carboplatin. Alofanib suppresses angiogenesis in the ovarian cancer mouse model[1]. In an FGFR-driven human tumor xenograft model, oral administration of alofanib is well tolerated and results in potent antitumor activity[2].