ArticleiScience2026
Identification of ADAR1i-124: The first effective A-to-I RNA editing inhibitor with promising cancer therapeutic potential.
Article in iScience, 2026. 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
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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
7 citing papers in PubMed.
- The role of RNA modifications in cancer translational control.RNA biology · 2026Review
- Tumour-associated dsRNA accumulation and innate immune activation: mechanistic basis and therapeutic strategies.EBioMedicine · 2026Review
- Targeting ADAR1 in Cancer: Biology, Therapeutic Strategies, Challenges, and Limitations.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Immune response to DNA and RNA: structural insights, molecular mechanisms, and therapeutic targeting.Molecular biomedicine · 2026Review
- ADAR-mediated RNA editing in CNS disorders: from pathogenic mechanisms to therapeutic opportunities.Cellular & molecular biology letters · 2026Review
- Inducing tumor-intrinsic innate immune response to break cancer immunotherapy resistance.Frontiers in medicine · 2026Review
- Orchestrating innate immunity through RNA editing and helicase activity: ADAR1, dsRNA sensors, and tumor immune evasion.Frontiers in cell and developmental biology · 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
9 authors.
Funding
Abstract
Two ADAR1 isoforms, p150 and p110, are involved in adenosine-to-inosine RNA editing. ADAR1p150-mediated hyper-editing of endogenous dsRNAs prevents their activation of type I interferon signaling-mediated via Melanoma Differentiation-Associated Protein 5 (MDA5), which enables cancer resistance to immune checkpoint blockade. ADAR1p150 also inhibits Z-RNA-mediated activation of Z-DNA Binding Protein 1 (ZBP1) and induction of necroptosis. ADAR1p110 suppresses the formation of telomeric repeat R-loops, which would otherwise induce apoptosis in telomerase-reactivated cancer cells. Together, ADAR1 inhibitors could serve as novel cancer therapeutics. Here, we identified, ADAR1i-124, which inhibits the catalytic activities of both ADAR1p150 and ADAR1p110. ADAR1i-124 activated MDA5 and ZBP1 pathways and dose-dependently inhibited viability across different types of cancer cell lines. Some cancer cell lines, unresponsive to ADAR1i-124 alone, became responsive when co-treated with 5-Aza-CdR. The DNA methylase inhibitor reactivated endogenous retroviruses, leading to the formation of retrovirus dsRNAs and the emergence of a new ADAR1 dependency. Our study establishes the potential of ADAR1i-124 as a future cancer therapeutic.
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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.