ReviewACS pharmacology & translational science2025
Molecular Pharmacology of Dasatinib Provides Unique Insights into the Mechanistic Basis of Success and Failure of Targeted Cancer Therapy.
Review in ACS pharmacology & translational science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Dasatinib Cube-O-Needle hybrid system for effective and safe site-specific treatment for triple-negative breast cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- OPTIMIS: Optimizing Personalized Therapies through Integrated Multiscale Intelligent Simulation.bioRxiv : the preprint server for biology · 2026Article
- Unlocking the potential of EphA2 with precision-guided cancer therapy: bicycle drug conjugates.Journal of translational medicine · 2026Review
- Inhibition of SRC prevents bone metastasis of breast cancer by blocking metastatic cell motility and bone directionality.Theranostics · 2026Article
- Dasatinib Pharmacokinetics and Advanced Nanocarrier Strategies: from Systemic Limitations to Targeted Success.AAPS PharmSciTech · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite the enthusiasm for targeted cancer therapies in preclinical studies and the success of a select few drugs, many promising drug candidates fail in clinical trials. The gap between preclinical promise and clinical outcomes underscores the need to investigate factors influencing the success or failure of targeted therapies. Dasatinib, an inhibitor of Abl and Src protein tyrosine kinases, is highly effective toward chronic myeloid leukemia (CML) by targeting BCR-Abl, but it is ineffective against solid tumors when targeting Src kinases. A review reveals cytotoxic inhibition is a key attribute predictive of dasatinib's clinical efficacy toward CML, and cytostatic inhibition by targeting Src kinases is the underlying reason for the preclinical promise and clinical inefficacy toward solid tumors. The analysis reveals that preclinical cytotoxic inhibition is highly predictive of clinical efficacy and shows that cancer regression can only be achieved when the drug-target is an essential oncogenic driver in a monodriver cancer. The analysis highlights dasatinib's potential in achieving stable disease in solid tumors, supporting its use in combination therapies.
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.