ReviewRSC advances2025
Recent advances in focal adhesion kinase (FAK)-targeting antitumor agents.
Review in RSC advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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
7 citing papers in PubMed.
- Anoikis in cancer: molecular mechanisms, resistance, and therapeutic strategies.Apoptosis : an international journal on programmed cell death · 2026Review
- Strategic selection of MDM2 inhibitors enhances the efficacy of FAK inhibition in mesothelioma based on TP53 genotype.PloS one · 2026Article
- A Comprehensive Review of Designing and Synthetic Aspects of Pyrazolopyrimidine Derivatives as Anticancer Agents.Mini reviews in medicinal chemistry · 2026Review
- Multi-omics investigation reveals molecular determinants of cancer cell evolution on soft extracellular matrix.bioRxiv : the preprint server for biology · 2025Article
- Medicinal chemistry perspectives on anticancer drug design based on clinical applications (2015-2025).RSC advances · 2025Review
- Novel FAK inhibitors suppress tumor growth and reverse EGFR-TKI resistance in non-small cell lung cancer.Cancer drug resistance (Alhambra, Calif.) · 2025Article
- Molecular docking analysis with ICBioinformation · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Focal adhesion kinase (FAK) is a non-receptor intracellular tyrosine kinase that plays an important role in cell adhesion, survival, proliferation, and other processes. Research studies have shown that overexpression of FAK can promote the proliferation and migration of tumor cells. Therefore, FAK has become a promising target for small molecular anticancer drugs with great clinical potential. In recent years, research studies on small molecular FAK inhibitors have been increasing. With the rise of proteolysis-targeting chimera (PROTAC) technology, FAK PROTACs have also been developed to induce FAK degradation. This article reviews the design and biological activity of FAK-targeting antitumor agents, with a focus on their chemical structures, antitumor effects, and clinical progress.
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.