A THERAPEUTIC COMPOSITION BASED ON THE CO-TRANSPORT OF ROYAL JELLY-DERIVED EXTRACELLULAR VESICS WITH MIR-1906 AND GALANGIN, SIMULTANEOUSLY SUPPRESSING CUPROPTOS, FERROPTOS, AND PYROPTOS IN ALZHEIMER'S DISEASE, AND THE METHOD OF ITS PREPARATION.

TR202617696A2Pending Publication Date: 2026-10-21SELCUK OZDEMIR +1
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Patent Information

Application Number
TR202617696
Authority / Receiving Office
TR · TR
Patent Type
Applications
Current Assignee / Owner
Filing Date
2026-10-12
Publication Date
2026-10-21

AI Technical Summary

Technical Problem

Current treatments for Alzheimer's disease do not adequately suppress the concurrent pathways of cuproptosis, ferroptosis, and pyroptosis, which contribute to neuronal loss and amyloid-beta accumulation, and lack a biocompatible carrier system for delivering miR-1906 and galangin to target these pathways effectively.

Method used

A therapeutic compound is developed using royal jelly-derived extracellular vesicles (RJ-HDV) loaded with hsa-miR-1906 mimics and galangin, which synergistically suppresses cuproptosis, ferroptosis, and pyroptosis pathways, maintaining cell viability and reducing amyloid-beta accumulation.

Benefits of technology

The compound achieves a synergistic suppression of all three pathways, with a recovery rate exceeding 80% and maintaining cell viability above 87%, significantly outperforming individual components, and is produced using scalable laboratory methods.

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Abstract

The invention relates to a therapeutic compound obtained by co-loading hsa-miR-1906 mimic and galangin into extracellular vesicles (RJ-HDV) isolated from royal jelly, and to the method of preparing this compound. The median diameter of the vesicles in the compound is 89.1 nm, and the zeta potential is ≥32.1 mV; they contain CD63 and sintenin-1 but not calnexin. The compound reduces hsa_circ_0007556 (circAPP) levels by 75% and increases miR-1906 levels in the APPswe-SH-SY5Y Alzheimer's cell model; it eliminates 88% of the difference between diseased and healthy cells by simultaneously suppressing the coupeptosis, ferroptosis, and pyroptosis pathways. The effect obtained is 20 points above the expected value from the independent effects of the components. The compound maintains cell viability at 88% at the application dose.
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