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Study · Animal study (in vivo) · rat · 2026

3 results

Beta-nicotinamide mononucleotide attenuates creatine kinase release in Duchenne muscular dystrophy model rats.

Nakamura K, Kanou M, Ito S, Jimbo T, Kouzaki K, Nakazato K, Nakamjima R, Yamanouchi K, Ueda H, Yamana K

The Journal of veterinary medical science2 Dec 2025

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: CC BY-NC-ND. Results still quote short attributed sentences.

Results from this study3

3 results from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In DMD rats, NMN did not improve muscle function.

    In plain wordsIn rats with muscular dystrophy, NMN did not improve muscle function.

    Outcome
    No significant changeMuscle function
    Study

    ratn: not reported in source

    Duchenne muscular dystrophy rats
    Outcome group
    Exercise and physical function · Musculoskeletal
    Studied dose
    Dose not stated · 2 monthsAs given in this study (rat).

    Source sentences

    Summary
    Although NMN administration did not improve muscle function in DMD rats, it did reduce the release of creatine kinase in their blood.
    1 context sentence
    Summary · context
    In this study, we explored the therapeutic potential of NMN as an NAD+ booster for muscular dystrophy by administering NMN to DMD rats, which exhibit severe phenotypes comparable to those of human DMD patients, for 2 months.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In DMD rats, NMN reduced creatine kinase release into blood.

    In plain wordsIn rats with muscular dystrophy, NMN reduced creatine kinase release into blood.

    Outcome
    DecreaseBlood creatine kinase release
    Study

    ratn: not reported in source

    Duchenne muscular dystrophy rats
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated · 2 monthsAs given in this study (rat).

    Source sentences

    Summary
    Although NMN administration did not improve muscle function in DMD rats, it did reduce the release of creatine kinase in their blood.
    1 context sentence
    Summary · context
    In this study, we explored the therapeutic potential of NMN as an NAD+ booster for muscular dystrophy by administering NMN to DMD rats, which exhibit severe phenotypes comparable to those of human DMD patients, for 2 months.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In DMD rats, NMN could reverse disease-related gene expression changes associated with skeletal muscle homeostasis.

    In plain wordsIn rats with muscular dystrophy, NMN could reverse disease-related changes in muscle gene expression.

    Outcome
    MixedSkeletal muscle homeostasis gene expression
    Study

    ratn: not reported in source

    Duchenne muscular dystrophy rats
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated · 2 monthsAs given in this study (rat).

    Source sentences

    Summary
    RNA-seq analysis revealed that NMN administration could reverse DMD-related gene expression changes associated with skeletal muscle homeostasis.
    1 context sentence
    Summary · context
    In this study, we explored the therapeutic potential of NMN as an NAD+ booster for muscular dystrophy by administering NMN to DMD rats, which exhibit severe phenotypes comparable to those of human DMD patients, for 2 months.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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