ReviewCurrent medicinal chemistry2026
Targeted Protein Degradation in Lung Cancer: The Emerging Role of PROTAC Technology and E3 Ligases.
Review in Current medicinal chemistry, 2026. 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
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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.
- Review
- Post-Covid Alzheimer and Its Remediation via PROTACs Therapy: A Comprehensive Review.Health science reports · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung cancer remains one of the most prevalent and lethal malignancies, with poor drug response and high mortality rates. Proteolysis-targeting chimeras (PROTACs) are emerging as a novel therapeutic strategy, leveraging E3 ligases to degrade oncogenic proteins selectively via the ubiquitin-proteasome pathway. These degraders offer higher selectivity and bioavailability compared to traditional inhibitors. This review explores how PROTACs eliminate oncogenic proteins in lung cancer and examines the role of E3 ligases in this process. Commonly utilized ligases include Cereblon (CRBN) and Von Hippel-Lindau (VHL), while newer ones, such as MDM2 and Kelch-like ECH-associated protein 1 (KEAP1), are being investigated for therapeutic potential. We discuss key factors in PROTAC design, including ligand selection, linker optimization, and pharmacokinetic properties, which influence tumor specificity and efficacy while minimizing off- target effects. Additionally, we highlight targetable oncogenic drivers in lung cancer, such as KRAS, EGFR, and ALK fusion proteins, and evaluate preclinical and clinical studies that demonstrate PROTACs' potential for overcoming drug resistance. The challenges associated with clinical translation, tumor microenvironment interactions, and E3 ligase selection are also discussed. Finally, we present future perspectives, including expanding the range of E3 ligases, developing multitargeting strategies, and integrating next-generation molecular glue degraders. By offering a comparative analysis of E3 ligase- specific PROTACs, this review underscores the potential of PROTAC technology to advance precision oncology in lung cancer.
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Identifiers
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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.