ArticleMolecular therapy. Nucleic acids2025
SNA-modified antisense oligonucleotides: A new pathway for renal targeting?
Article in Molecular therapy. Nucleic acids, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antisense oligonucleotides (ASOs) have emerged as a powerful class of therapeutics capable of suppressing gene expression with remarkable specificity. However, the clinical applications of ASOs have been limited by delivery challenges and toxicities, particularly when repeated or high dosing is required. In the study by Tsuboi et al., the authors present serinol nucleic acid (SNA)-modified gapmer ASOs that target the sodium-glucose cotransporter 2 (SGLT2) in mouse kidneys. With promising results, these SNA-modified ASOs display dose-dependent efficacy, prolonged knockdown, and importantly, a more favorable safety profile in both the kidney and liver compared with the 2'-MOE-modified counterpart. While some caveats remain-particularly around high-dose toxicity-these findings open the door to an approach that couples potency with improved tolerability, thereby highlighting SNA-modified ASOs as a potential next-generation platform for renal diseases.
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 Socratic graph.