Pharmaceutical compositions for treating or preventing diseases caused by a decrease or deficiency of τm5U modification.

JP7873865B2Inactive Publication Date: 2026-06-15THE UNIV OF TOKYO
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Patent Information

Authority / Receiving Office
JP · JP
Patent Type
Patents
Current Assignee / Owner
THE UNIV OF TOKYO
Filing Date
2022-07-06
Publication Date
2026-06-15
Estimated Expiration
Not applicable · inactive patent

AI Technical Summary

⚠Technical Problem

Mitochondrial diseases such as MELAS are caused by reduced or absent 5-taurinomethyluridine (τm5U) modifications in mitochondrial tRNA, leading to impaired mitochondrial function and structural instability of mutant tRNA, which current detection methods like the primer extension method are cumbersome and require specific conditions.

⚗Method used

Overexpressing MTO1, a component of U-modifying enzymes, in patients to restore τm5U modifications, and using water-soluble carbodiimides to facilitate reverse transcription reactions for easy detection and improvement of U-modification rates.

🎯Benefits of technology

Enhances τm5U modification rates, potentially activating mitochondrial function and providing a straightforward method to detect τm5U modifications, thereby treating or preventing diseases caused by τm5U deficiencies.

✦ Generated by Eureka AI based on patent content.

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Abstract

The present invention provides a pharmaceutical composition for treating or preventing a disease associated with the reduction or defect of the modification of 5-taurinomethyluridine (τm5U) in mitochondrial tRNA, the pharmaceutical composition containing MTO1 (mitochondrial tRNA translation optimization 1) or a nucleic acid encoding MTO1, and being configured such that an excessive amount of MTO1 is administered or MTO1 is over-expressed in a patient to whom the nucleic acid has been administered.
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