ArticleInternational journal of molecular sciences2025
From Phytochemistry to Metabolic Regulation: The Insulin-Promoting Effects of Loureirin B Analogous to an Agonist of GLP-1 Receptor.
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 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Pharmaceutical therapies for pyroptosis in lung injury.Inflammopharmacology · 2026Review
- Interpreting the Black Box: Interpretable Machine Learning and Systems Pharmacology in Small-Molecule Therapeutics.Pharmaceutics · 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
6 authors.
Funding
Abstract
This study aimed to develop a potent, safe, and cost-effective small-molecule hypoglycemic agent derived from Loureirin B, with preliminary evaluation of its efficacy and mechanistic underpinnings. Thirty structural analogs of Loureirin B were synthesized. Molecular docking identified LB-A as the lead compound targeting GLP-1R. Its hypoglycemic activity was initially assessed in a murine model. Molecular dynamics simulations, surface plasmon resonance (SPR), and circular dichroism (CD) were employed to characterize LB-A-GLP-1R interactions. The involvement of the GLP-1R/cAMP/PKA pathway and downstream mediators was examined using cellular assays, gene knockout, and Western blotting, with emphasis on FOXO1. LB-A exhibited the strongest binding affinity for GLP-1R among the analogs and significantly reduced blood glucose levels in mice. It formed hydrogen bonds and hydrophobic interactions with key residues (e.g., LYS197) and induced conformational changes in GLP-1R. LB-A activation of GLP-1R upregulated cAMP, PKA, and pCREB, suppressed PTEN/FOXO1 signaling, and subsequently stimulated insulin secretion. LB-A represents a novel small molecule agonist that ameliorates hyperglycemia in diabetic mice through specific activation of the GLP-1R/cAMP/PKA/pCREB/PTEN/FOXO1 pathway.
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What Socratic 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 Socratic graph.