Mitoquinone mesylate (Mitoquinone methanesulfonate)

Mitoquinone mesylate (Mitoquinone methanesulfonate) is among the widely used antioxidants that target the mitochondria. It was developed to readily penetrate the BBB and neuronal membranes, where it is concentrated into several hundred-folds within the mitochondria where it mediates the local anti-oxidative capacity ^[1]. Within the ETC, complex II, also known as succinate dehydrogenase, reduces Mitoquinone mesylate ubiquinone moiety to the active antioxidant ubiquinol which scavenges excess ROS ^[2].

Mitoquinone mesylate (50 nM) reduced 6-OHDA-induced mitochondrial fragmentation, when used in SH-SY5Y cell line. It inhibited mitochondrial fission protein and the translocation of pro-apoptotic protein (Bax) in the mitochondria ^[3].

Mitoquinone mesylate treatment inhibited the loss of dopaminergic neurons and enhanced behavioral performance, showed neuroprotective effects in mouse models of PD ^[4]. Mitoquinone mesylate treatment enhanced the fine motor control and reduced markers of oxidative damage in muscles in a Huntington's disease (HD) mouse model ^[5]. Mitoquinone mesylate reduced white matter injury, improved neurological performance, and decreased motor-evoked potential latency in intracerebral hemorrhagic (ICH) mice ^[6].

References:
[1]. Murphy M P, Smith R A J. Targeting antioxidants to mitochondria by conjugation to lipophilic cations[J]. Annu. Rev. Pharmacol. Toxicol., 2007, 47: 629-656.
[2]. James A M, CochemÉ H M, Smith R A J, 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]. Journal of Biological Chemistry, 2005, 280(22): 21295-21312.
[3]. Solesio M E, Prime T A, Logan A, et al. The mitochondria-targeted anti-oxidant MitoQ reduces aspects of mitochondrial fission in the 6-OHDA cell model of Parkinson's disease[J]. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease, 2013, 1832(1): 174-182.
[4]. Pinho B R, Duarte A I, Canas P M, et al. The interplay between redox signalling and proteostasis in neurodegeneration: In vivo effects of a mitochondria-targeted antioxidant in Huntington's disease mice[J]. Free Radical Biology and Medicine, 2020, 146: 372-382.
[5]. Pinho B R, Duarte A I, Canas P M, et al. The interplay between redox signalling and proteostasis in neurodegeneration: In vivo effects of a mitochondria-targeted antioxidant in Huntington's disease mice[J]. Free Radical Biology and Medicine, 2020, 146: 372-382.
[6]. Chen W, Guo C, Jia Z, et al. Inhibition of mitochondrial ROS by MitoQ alleviates white matter injury and improves outcomes after intracerebral haemorrhage in mice[J]. Oxidative medicine and cellular longevity, 2020, 2020.