Preclinical Development of U3-1784, a Novel FGFR4 Antibody Against Cancer, and Avoidance of Its On-target Toxicity

FGF19型 癌症 成纤维细胞生长因子受体4 抗体 肝癌 胆汁酸 癌症研究 毒性 体内 MAPK/ERK通路 成纤维细胞生长因子 肝细胞癌 结直肠癌 药理学 医学 受体 信号转导 生物 生物化学 内科学 免疫学 成纤维细胞生长因子受体 生物技术
作者
René Bartz,Kenji Fukuchi,Toshiaki Ohtsuka,Tanja Lange,Katrin Grüner,Ichirô Watanabe,Shigeru Hayashi,Yoko Oda,Reimi Kawaida,Hironobu Komori,Yoshinori Kashimoto,Peter Wirtz,Jan-Peter A. Mayer,Mauricio Redondo-Müller,Shuntaro Saito,Mizuki Takahashi,Hiroyuki Hanzawa,Emi Imai,Alberto Martínez,Masaharu Hanai,Dieter Häussinger,Roger W. Chapman,Toshinori Agatsuma,Johannes Bange,Reimar Abraham
出处
期刊:Molecular Cancer Therapeutics [American Association for Cancer Research]
卷期号:18 (10): 1832-1843 被引量:16
标识
DOI:10.1158/1535-7163.mct-18-0048
摘要

The FGFR4/FGF19 signaling axis is overactivated in 20% of liver tumors and currently represents a promising targetable signaling mechanism in this cancer type. However, blocking FGFR4 or FGF19 has proven challenging due to its physiological role in suppressing bile acid synthesis which leads to increased toxic bile acid plasma levels upon FGFR4 inhibition. An FGFR4-targeting antibody, U3-1784, was generated in order to investigate its suitability as a cancer treatment without major side effects.U3-1784 is a high-affinity fully human antibody that was obtained by phage display technology and specifically binds to FGFR4. The antibody inhibits cell signaling by competing with various FGFs for their FGFR4 binding site thereby inhibiting receptor activation and downstream signaling via FRS2 and Erk. The inhibitory effect on tumor growth was investigated in 10 different liver cancer models in vivo The antibody specifically slowed tumor growth of models overexpressing FGF19 by up to 90% whereas tumor growth of models not expressing FGF19 was unaffected. In cynomolgus monkeys, intravenous injection of U3-1784 caused elevated serum bile acid and liver enzyme levels indicating potential liver damage. These effects could be completely prevented by the concomitant oral treatment with the bile acid sequestrant colestyramine, which binds and eliminates bile acids in the gut. These results offer a new biomarker-driven treatment modality in liver cancer without toxicity and they suggest a general strategy for avoiding adverse events with FGFR4 inhibitors.
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