Lucitanib (E-3810) dihydrochloride is a dual inhibitor of VEGFR and FGFR, efficiently and selectively inhibiting VEGFR1, VEGFR2, VEGFR3, FGFR1, and FGFR2, with respective IC50 values of 7 nM, 25 nM, 10 nM, 17.5 nM, and 82.5 nM.

FGFR1:17.5 nM, FGFR2:82.5 nM, VEGFR3:10 nM, VEGFR2:25 nM, VEGFR1:7 nM

Lucitanib (E-3810) dihydrochloride demonstrates strong inhibitory effects on VEGFR and FGFR auto-phosphorylation, effectively suppressing VEGF and bFGF-induced HUVEC proliferation with IC 50 values of 40 and 50 nM, respectively. Additionally, it inhibits CSF-1R with an IC 50 of 5 nM. Lucitanib exhibits potent inhibition of FGFR2 activity (K i <0.05 μM), followed by PDGFRα (K i =0.11 μM). The K i values for DDR2, LYN, CARDIAK, CSBP (2), EPHA2, and YES are found to range between 0.26 and 8 μM.

Administered orally at a dosage of 20 mg/kg for seven straight days, Lucitanib (E-3810) wholly suppresses (P<0.01) the bFGF-induced angiogenic response in comparison to vehicle-treated mice. Lucitanib demonstrates extensive efficacy across various xenograft models including HT29 colon carcinoma, A2780 ovarian carcinoma, and A498, SN12K1, and RXF393 renal carcinomas, exhibiting a dose-dependent decrease in tumor growth. While the compound significantly curtails tumor expansion during administration, growth resumes upon cessation of treatment, with tumor regression noted in select instances. Furthermore, Lucitanib (E-3810)'s effect was evaluated at a dosage of 15 mg/kg on MDA-MB-231 advanced stage breast cancer with subcutaneous tumors weighing 350 to 400 mg, where it effectively stabilized tumor growth for the duration of the 30-day treatment. Post-treatment, however, tumors began to grow again at rates comparable to the control group.