ArticleCell death & disease2026
Nintedanib inhibits the VEGFR-ERK signaling pathway in human KRAS-mutated cancer cells.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors.
Funding
Abstract
KRAS mutations are significant drivers in various cancers, and existing drug discovery attempts targeting these mutations have largely been unsuccessful, emphasizing the need for more effective therapies. In this study, the screening library, which contains 1,374 chemical compounds, identified nintedanib, a VEGFR inhibitor, as exerting a potent and selective antiproliferative effect against KRAS-mutant cells, surpassing other VEGFR inhibitors. Nintedanib effectively suppressed tumor growth in xenografted mice with KRAS mutations and significantly inhibited phosphorylated VEGFR2 levels and its downstream signaling molecules pAKT and pERK in KRAS-mutant cells, suggesting that VEGFR2 inhibition affects the oncogenic AKT/ERK pathway. Moreover, in VEGFR2-knockout cells, inhibition of SOS1 protein reduced KRAS-GTP activity, which decreased the phosphorylation of ERK, AKT, and DRP1, thereby inducing apoptosis. Remarkably, KRAS
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.