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Mitolbnox

Mitolbnox has been studied in 2 papers since 2023: 1 observational study in people, 1 in cells. The newest paper, Aug 15, 2023: “Complex I deficiency in m.3243A>G fibroblasts is alleviated by reducing NADH accumulation”.

Intervention

2 papers study it4 findingsUpdated

See all 2 papers on mitolbnox

At a glance

The findings reach cells, none yet in people. 2 independent labs in 2 countries.

None of its findings points the other way.

Cells: a single group. Worms or flies, mice and humans: nothing yet.

C, W, M, H: cells, worms or flies, mice, humans. Dark: independent labs found the same change there. Light: one lab or one study. Outline: nothing yet.

Labs are independent when their papers share no last author and no institution.

  • 2 independent labs in 2 countries
  • Funders: Beijing Municipal Science and Technology Commission and others
  • Humans1
  • Cells1

What did studies of mitolbnox find?

4

Studies of mitolbnox measured 4 outcomes, among them HIF1α stabilization, NAD/NADH ratio and NADH.

HIF1α stabilization

downin cells1

1 study

  1. Mitolbnox decreases HIF1α stabilization in cells (reversal of ethanol-induced changes).

    “MitoLbNOX treatment reversed redox imbalance, HIF1α stabilization, global acetylation and myostatin expression (p < 0.05).”

    Cellsreversal of ethanol-induced changesmitochondrial-targeted

    Integrated Multiomics Analyses of the Molecular Landscape of Sarcopenia in Alcohol-Related Liver Disease

    Journal of cachexia, sarcopenia and muscle

More on HIF1α stabilization

NAD/NADH ratio

upin human cells1

1 study

  1. Mitolbnox increases NAD/NADH ratio in human cells (m.3243 A>G fibroblasts, more pronounced than NR treatment) (more pronounced than NR).

    “after treatment with mitoLbNOX, the NAD+/NADH ratio, complex I-independent OCR, and ATP levels increased more pronouncedly compared with the NR treatment group”

    Cellsm.3243 A>G fibroblasts, more pronounced than NR treatmentmitochondria-targeted H2O-forming NADH oxidasefibroblast

    Complex I deficiency in m.3243A>G fibroblasts is alleviated by reducing NADH accumulation

    Frontiers in physiology

More on NAD/NADH ratio

NADH

downin human cells1

1 study

  1. Mitolbnox decreases NADH in human cells (m.3243 A>G fibroblasts, compared with NR treatment) (significantly reduced).

    “after treatment with mitoLbNOX, the NAD+/NADH ratio, complex I-independent OCR, and ATP levels increased more pronouncedly compared with the NR treatment group, accompanied by significantly reduced NADH levels.”

    Cellsm.3243 A>G fibroblasts, compared with NR treatmentmitochondria-targeted H2O-forming NADH oxidasefibroblast

    Complex I deficiency in m.3243A>G fibroblasts is alleviated by reducing NADH accumulation

    Frontiers in physiology

More on NADH

Oxidative stress and ROS signaling

downin cells1

1 study

  1. Mitolbnox decreases oxidative stress and ROS signaling in ammonia-treated myotubes.

    “Mitochondrial-targeted Lactobacillus brevis NADH oxidase (MitoLbNOX), but not NAD+ precursor nicotinamide riboside, reversed ammonia-induced oxidative dysfunction”

    Cellsin ammonia-treated myotubesmitochondrial-targeted

    Dysregulated cellular redox status during hyperammonemia causes mitochondrial dysfunction and senescence by inhibiting sirtuin-mediated deacetylation

    Aging cell

More on Oxidative stress and ROS signaling

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