ArticleACS medicinal chemistry letters2026
Selective 7‑Azaindole Modulators Targeting Fyn and GSK-3β for Dual-Target Neuromodulation.
Article in ACS medicinal chemistry letters, 2026. 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.
- Fyn kinase: a key mechanistic regulator and therapeutic target in tauopathy and neurodegenerative diseases.Translational neurodegeneration · 2026Review
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Authors and funding
3 authors.
Funding
Abstract
Fyn proto-oncogene kinase (Fyn) and glycogen synthase kinase-3β (GSK-3β) belong to distinct branches of the protein kinase (PK) superfamily. Fyn is a member of the Src family of tyrosine kinases, whereas GSK-3β is classified within the CMGC group of serine/threonine kinases. Both play critical roles in neurodegenerative processes, and their dysregulation has been implicated in disease progression. The development of Fyn and GSK-3β inhibitors has attracted increasing research attention. The design of multitarget inhibitors represents a promising, though underexplored, therapeutic strategy. A recent study reported a series of dual selective nanomolar inhibitors based on structure-activity relationship (SAR) optimization. In-depth profiling of the lead compound's neuroprotective and modulatory properties establishes a foundation for the development of next-generation neuroregenerative therapeutics.
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Registered trials
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