MitoQ (mitoquinone mesylate) is a derivative of CoQ10 believed to play a role in mitochondrial function, but without much supporting evidence.

Our evidence-based analysis features 9 unique references to scientific papers.

Research analysis by and verified by the Research Team. Last updated on Jul 19, 2018.

Scientific Research

1Sources and Structure

1.1. Sources

MitoQ is a term used to refer to mitoquinone mesylate ( with {10-(4,5-dimethoxy-2-methyl-3,6-dioxo-1,4-cycloheexadienlyl) decyl triphenylphosphonium methanesulfonate}) as the prolonged chemical name), which is a derivative of CoQ10 where said molecule is covalently bonded to a triphenylphosphonium cation.

The CoQ10 moiety is delivered to the matrix side of the inner mitochondrial matrix,[1] which is the site of most mitochondrial oxidative stress.[2] Despite accumulation in the mitrochondria, however, MitoQ is a poor substrate for the electron transport chain (at complex I) and is not thought to contribute much to bioenergetics.[3][4]

1.2. Biological Significance

Oral administration of MitoQ in otherwise healthy wild type mice over 28 weeks fails to significantly alter mitochondrial function or gene expression, and no overall influence on systemic energy metabolism.[5]


2.1. Dementia

Alzheimer's is known to be associated with mitochondrial abnormalities in neurons associated with oxidative stress[6][7]

Beta-amyloid toxicity has been noted to be reduced in N2a cells with MitoQ incubation[8] and at 1-100nM mostly abolished cell death from amyloid proteins (no dose dependence noted).[9]

100μM of MitoQ daily to a mouse model of Alzheimer's has been noted to improve spatial memory and cognitive performance associated with a reduction in lipid peroxidation.[9]

Scientific Support & Reference Citations


  1. Murphy MP, Smith RA. Targeting antioxidants to mitochondria by conjugation to lipophilic cations . Annu Rev Pharmacol Toxicol. (2007)
  2. Free Radicals in Biology and Medicine .
  3. Interactions of Mitochondria-targeted and Untargeted Ubiquinones with the Mitochondrial Respiratory Chain and Reactive Oxygen Species .
  4. James AM, et al. Interactions of mitochondria-targeted and untargeted ubiquinones with the mitochondrial respiratory chain and reactive oxygen species. Implications for the use of exogenous ubiquinones as therapies and experimental tools . J Biol Chem. (2005)
  5. Rodriguez-Cuenca S, et al. Consequences of long-term oral administration of the mitochondria-targeted antioxidant MitoQ to wild-type mice . Free Radic Biol Med. (2010)
  6. Hoyer S. Oxidative metabolism deficiencies in brains of patients with Alzheimer's disease . Acta Neurol Scand Suppl. (1996)
  7. Hirai K, et al. Mitochondrial abnormalities in Alzheimer's disease . J Neurosci. (2001)
  8. Manczak M, et al. Mitochondria-targeted antioxidants protect against amyloid-beta toxicity in Alzheimer's disease neurons . J Alzheimers Dis. (2010)
  9. McManus MJ, Murphy MP, Franklin JL. The mitochondria-targeted antioxidant MitoQ prevents loss of spatial memory retention and early neuropathology in a transgenic mouse model of Alzheimer's disease . J Neurosci. (2011)

Cite this page

"MitoQ,", published on 4 July 2013, last updated on 19 July 2018,