ArticleInternational journal of molecular sciences2025
The Identification of Gyrophoric Acid, a Phytochemical Derived from Lichen, as a Potent Inhibitor for Aggregation of Amyloid Beta Peptide: In Silico and Biochemical Evaluation.
Article in International journal of molecular sciences, 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.
- Integrated In Silico Prioritization of Antidiabetic Phytochemicals fromMolecules (Basel, Switzerland) · 2026Article
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Authors and funding
9 authors.
Funding
Abstract
Alzheimer's disease (AD) is characterized by amyloid-beta (Aβ) plaque accumulation and neurodegeneration. This study identified gyrophoric acid, a lichen-derived phenolic metabolite, as a dual-action Aβ42 inhibitor preventing aggregation and disassembling of mature Aβ42 fibrils. Integrated in silico studies revealed that gyrophoric acid was a strong thermodynamic stabilizer of Aβ42 (MM-GBSA: -27.3 kcal/mol) via entropically driven hydrophobic interactions and disruption of aggregation-prone conformations (100 ns MD simulations). Through biochemical analysis of the fluorescent dye thioflavin T (ThT), gyrophoric acid induced rapid Aβ42 fibril disassembly within 5 h, with time-lapse confocal microscopy quantitatively confirming the near-complete dissolution of large aggregates by 24 h. ADMET profiling revealed favorable pharmacokinetics (moderate oral absorption: 48.5-57.3%; low toxicity) and Lipinski's rule compliance. These results establish gyrophoric acid as a promising natural bioactive compound for anti-AD therapeutics with a unique hydrophobic-stabilization mechanism.
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Registered trials
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