ArticleClinical & translational immunology2026
cGAS inhibitor IMSB301 modifies interferon signalling in peripheral mononuclear cells of
Article in Clinical & translational immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Therapeutic targeting of the cGAS-STING pathway in human disease.The Journal of clinical investigation · 2026Review
- Spotlight on cGAS-STING: role in disease pathogenesis and therapeutic potential.Molecular biomedicine · 2026Review
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: Aicardi-Goutières syndrome (AGS) is a rare genetic interferonopathy because of aberrant DNA or RNA metabolism that lacks effective disease modifying therapies. Methods: Single-cell RNA sequencing was performed on peripheral blood mononuclear cells (PBMCs) obtained from a patient with AGS because of pathogenic biallelic Results: In PBMCs from the patient with Conclusion: The cGAS inhibitor IMSB301 resulted in specific reduction in interferon signalling
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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.