ReviewDeutsches Arzteblatt international2025
The Pharmacologic Inhibition of KRAS Mutants as a Treatment for Cancer: Therapeutic Principles and Clinical Results.
Review in Deutsches Arzteblatt international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- A case of T-prolymphocytic leukemia harboring RAS mutation.Annals of hematology · 2026Article
- Colorectal cancer pathogenesis, oncogenic signaling networks and targeted therapeutic advances.Molecular biomedicine · 2026Review
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
backgroundMutations of the KRAS oncogene are found in up to 20% of all cancers, and particularly in non-small-cell lung cancer (NSCLC) (20-40%) and colorectal cancer (CRC) (30-50%). Inhibitors of specific KRAS mutants have recently become available and are now a part of routine care.
methodsThis review is based on articles published in the past 5 years that were retrieved by a selective search in PubMed for clinical trials of the pharmacological inhibition of KRAS.
resultsSotorasib and adagrasib have already been approved, on the basis of two randomized phase III trials, as specific inhibitors of the KRASG12C mutant for palliative second-line treatment. Compared to standard chemotherapy with docetaxel, both drugs significantly prolonged progression-free survival (PFS): 5.6 months (95% confidence interval [4.3; 7.8]) for sotorasib versus 4.5 [3.0; 5.7] for docetaxel, and 5.5 months [4.5; 6.7] for adagrasib versus 3.8 [2.7; 4.7] for docetaxel. Sotorasib was also found to cause fewer severe adverse drug events (33%, versus 40% with docetaxel). The most common ones were diarrhea and elevated liver enzymes. For already treated CRC, sotorasib combined with the anti-epidermal growth factor receptor (anti-EGFR) antibody panitumumab was found, in a randomized phase III trial, to prolong progression-free survival significantly compared to standard therapy with triflurdin/tipiracil or regorafenib (5.6 months [4.2; 6.3] versus 2.2 months [1.9; 3.9]), while also improving patients' quality of life. Approval by the European Medicines Agency is pending. Further KRAS and pan-RAS inhibitors are now in early clinical development.
conclusionPharmacological KRAS inhibition is a promising new approach to the treatment of many kinds of cancer.
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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.