Aberrant activation in fibroblast growth factor signaling has been implicated in 
the development of various cancers, including squamous cell lung cancer, 
squamous cell head and neck carcinoma, colorectal and bladder cancer. Thus, 
fibroblast growth factor receptors (FGFRs) present promising targets for novel 
cancer therapeutics. Here, we evaluated the activity of a novel pan-FGFR 
inhibitor, rogaratinib, in biochemical, cellular and in vivo efficacy studies in 
a variety of preclinical cancer models. In vitro kinase activity assays 
demonstrate that rogaratinib potently and selectively inhibits the activity of 
FGFRs 1, 2, 3 and 4. In line with this, rogaratinib reduced proliferation in 
FGFR-addicted cancer cell lines of various cancer types including lung, breast, 
colon and bladder cancer. FGFR and ERK phosphorylation interruption by 
rogaratinib treatment in several FGFR-amplified cell lines suggests that the 
anti-proliferative effects are mediated by FGFR/ERK pathway inhibition. 
Furthermore, rogaratinib exhibited strong in vivo efficacy in several cell line- 
and patient-derived xenograft models characterized by FGFR overexpression. The 
observed efficacy of rogaratinib strongly correlated with FGFR mRNA expression 
levels. These promising results warrant further development of rogaratinib and 
clinical trials are currently ongoing (ClinicalTrials.gov Identifiers: 
NCT01976741, NCT03410693, NCT03473756).