ReviewCancer2025
Proteolysis-targeting chimeras in cancer therapy: Targeted protein degradation for next-generation treatment.
Review in Cancer, 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.
- Proteolysis Targeting Chimeric-Based Technology in Myeloma and Lymphoma.Molecular cancer therapeutics · 2026Review
- Ubiquitin family as novel protein partners for molecular glues.npj drug discovery · 2026Review
- Review
- The evolution of cancer therapeutics: from "undruggable" to "drugged".Translational cancer research · 2026Article
- Histone modifications across cancers: mechanisms, therapy and clinical translation.Molecular cancer · 2026Review
- Key Considerations for TargetingDrug design, development and therapy · 2026Review
- Proteolysis-targeting chimeras in cancer therapy: Targeted protein degradation for next-generation treatment.Cancer · 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
8 authors.
Funding
Abstract
Proteolysis-targeting chimeras (PROTACs) have the potential to revolutionize cancer treatment by specifically targeting and degrading oncogenic proteins. Using the ubiquitin-proteasome system, PROTACs allow the selective degradation of disease-causing proteins, including those traditionally deemed "undruggable" by conventional small-molecule inhibitors. By catalytically eliminating rather than inhibiting proteins, PROTACs provide sustained target suppression with lower doses and reduced toxicity. Their bifunctional design linking a protein of interest to an E3 ligase drives targeted ubiquitination and subsequent proteasomal degradation. Recent progress demonstrates promise in treating solid and hematologic malignancies, with several candidates advancing to clinical trials. This review provides a comprehensive overview of developing PROTACs, from understanding their mechanism to clinical applications, and highlights their emerging role in overcoming drug resistance and advancing the limits of cancer treatment. In addition, the authors discuss the challenges of optimizing PROTACs, including issues related to pharmacokinetics, E3 ligase compatibility, and the delivery of PROTACs to tumors. With their modularity, adaptability, and precision, PROTACs represent a next-generation platform for personalized cancer therapy across various patient groups.
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.