ReviewFrontiers in immunology2025
STING-targeting PROTACs: emerging therapeutic tools for enhanced immunotherapy in inflammatory diseases.
Review in Frontiers in immunology, 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
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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
5 citing papers in PubMed.
- Discovery of a novel STING-binding peptide associated with reduced cGAMP-induced inflammatory gene expression.Journal of enzyme inhibition and medicinal chemistry · 2026Article
- The cGAS-STING pathway: mechanistic basis, dual biological functions and translational therapeutic advances.Apoptosis : an international journal on programmed cell death · 2026Review
- STING: An Attractive Target for Autoimmune and Inflammatory Diseases.Medicinal research reviews · 2026Review
- The Role and Therapeutic Potential of the STING Signaling Pathway in the Pathogenesis of Diabetic Nephropathy.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Viral Mimicry of Alzheimer's Disease: Innate Sensing of Self-Nucleic Acids as a Driver of Glial Senescence.Journal of molecular neuroscience : MN · 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The stimulator of interferon genes (STING) pathway is a central regulator of innate immunity, mediating host defense against pathogens but driving chronic inflammation when dysregulated-underpinning autoimmune diseases, fibrosis, and cancer. Traditional therapies targeting STING (e.g., small-molecule inhibitors, monoclonal antibodies) face limitations including incomplete pathway suppression, off-target effects, and reliance on continuous dosing. Proteolysis-targeting chimeras (PROTACs) offer a transformative approach by enabling selective degradation of STING, achieving sustained suppression of pathological signaling. However, critical gaps remain in understanding their selectivity for pathological vs. homeostatic STING activity, risks of immune suppression, and translational challenges. This review critically evaluates the rationale for STING degradation, with a comparative analysis of recent PROTAC designs (including warhead, E3 ligase, and linker optimization) and their pharmacokinetic/pharmacodynamic trade-offs. We address compensatory innate immune pathways, biomarker development hurdles, and safety risks, highlighting strategies to enhance specificity and clinical utility. STING-targeting PROTACs hold promise for inflammatory diseases, but their success depends on overcoming these challenges.
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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.