Metatrin is a biologically active supplement which contains 100 mg of CoQ10.
Coenzyme Q (CoQ) is an essential component of the mitochondrial electron transport chain and an antioxidant in plasma membranes and lipoproteins. It is endogenously produced in all cells by a highly regulated pathway that involves a mitochondrial multiprotein complex. Defects in either the structural and/or regulatory components of CoQ complex or in non-CoQ biosynthetic mitochondrial proteins can result in a decrease in CoQ concentration and/or an increase in oxidative stress. Besides CoQ10 deficiency syndrome and aging, there are chronic diseases in which lower levels of CoQ10 are detected in tissues and organs providing the hypothesis that CoQ10 supplementation could alleviate aging symptoms and/or retard the onset of these diseases. [1]
CoQ provides antioxidant protection to cell membranes and plasma lipoproteins. By lowering lipid peroxidation of low-density lipoprotein (LDL) particles that contributes to atherosclerosis, CoQ treatment confers health benefits against cardiovascular diseases.The anti-oxidant function of CoQ is especially important in the plasma membrane by reducing vitamins C and E, and in preventing ceramide-mediated apoptosis, an important regulator of lifespan in the context of normal aging. The pharmacokinetics variability of the different compositions of CoQ10 may result in fairly different plasma concentration-time profiles after CoQ10 administration. Indeed, the major amount of orally supplemented CoQ10 is eliminated via feces, with only a fraction of ingested CoQ10 reaching the blood and ultimately the various tissues and organs. [2,3] 
Primary CoQ10 deficiency is characterized by highly heterogeneous clinical signs, with the severity and symptoms varying greatly as is the age of onset, which can be from birth to the seventh decade, and beyond. Current clinical manifestations that may indicate primary CoQ10 deficiency are: [4]

1. Steroid-resistant nephrotic syndrome without mutations in NPHS1 and/or NPHS2 genes particularly when associated with deafness, retinopathy, and other neurological defects;
2. Mitochondrial encephalopathy including hypotonia, strokes, cerebellar ataxia, spasticity, peripheral neuropathy, and intellectual disability. These patients may also be presenting symptoms of myopathy, retinopathy, optic atrophy, sensorineural hearing loss, and hypertrophic cardiomyopathy; 
3. Unexplained ataxia particularly when family history suggests a recessive autosomal heritage; 
4. Exercise intolerance appearing from 6 to 33 years of age, with muscular weakness and high serum creatine kinase.

In individuals with primary CoQ10 deficiency, early treatment with high-dose oral CoQ10 supplementation improves the pathological phenotype, limits the progression of encephalopathy, and helps recover kidney damage. [5]
CoQ10 has been used in the treatment of a number of human pathologies and disorders. Clinical trials, systematic reviews, and meta-analyses have examined the safety and efficacy of CoQ10 in treating human diseases. With regards to safety, the highest dose for CoQ10 supplementation is 1200 mg daily according to well-designed randomized, controlled human trials, although doses as high as 3000 mg/day have been used in shorter clinical trials. [6] CoQ is generally safe and well-tolerated in treating patients suffering from early-stage Huntington disease with 2400 mg/day of CoQ10. [7]
Statins reduce cholesterol production by inhibiting the mevalonate pathway, which also produces compounds needed for normal mitochondrial function, including ubiquinone or CoQ10. Studies in animals and humans have demonstrated statin-induced reduction of CoQ10 in blood and tissues such as the heart and liver. Since CoQ10 is fundamentally important to mitochondrial function and cellular energy production (ATP), the depletion of CoQ10 and resultant mitochondrial dysfunction is hypothesized as the primary pathophysiologic cause of statin-associated muscle symptoms (SAMS). Therein lies the rational for using exogenous supplementation of CoQ10 to ameliorate SAMS. [8]
As a supplement CoQ10 is available in different doses. Although there is no established minimum or maximum effective dose, the average dose necessary to attain a therapeutic blood level of > 2.5 mcg/mL is 200 mg taken twice daily with a meal. In cardiac-related trials, daily doses of 100 to 400 mg have been used, while in neurodegenerative diseases (Huntington's disease, Parkinson's disease, and amyotrophic lateral sclerosis), doses of 600 to 3,000 mg have been used. [9] 

References
[1] Hernández-Camacho JD, Bernier M, López-Lluch G, Navas P. Coenzyme Q10 Supplementation in Aging and Disease. Front Physiol. 2018 Feb 5;9:44. doi: 10.3389/fphys.2018.00044. PMID: 29459830; PMCID: PMC5807419.
[2] De Cabo R., Cabello R., Rios M., López-Lluch G., Ingram D. K., Lane M. A., et al.. (2004). Calorie restriction attenuates age-related alterations in the plasma membrane antioxidant system in rat liver. Exp. Gerontol. 39, 297–304. 10.1016/j.exger.2003.12.003
[3] Alehagen U., Alexander J., Aaseth J. (2016). Supplementation with selenium and coenzyme Q10 reduces cardiovascular mortality in elderly with low selenium status. A secondary analysis of a randomised clinical trial. PLoS ONE 11:e0157541. 10.1371/journal.pone.0157541
[4] Salviati L., Trevisson E., Doimo M., Navas P. (2017). Primary Coenzyme Q10 Deficiency, in GeneReviews(R), eds Pagon R. A., Adam M. P., Ardinger H. H., Wallace S. E., Amemiya A., Bean L. J. H., et al. (Seattle, WA: University of Washington; ).
[5] Montini G., Malaventura C., Salviati L. (2008). Early coenzyme Q10 supplementation in primary coenzyme Q10 deficiency. N. Engl. J. Med. 358, 2849–2850. 10.1056/NEJMc0800582
[6] Hathcock J. N., Shao A. (2006). Risk assessment for coenzyme Q10 (Ubiquinone). Regul. Toxicol. Pharmacol. 45, 282–288. 10.1016/j.yrtph.2006.05.006
[7] McGarry A., McDermott M., Kieburtz K., De Blieck E. A., Beal F., Marder K., et al.. (2017). A randomized, double-blind, placebo-controlled trial of coenzyme Q10 in Huntington disease. Neurology 88, 152–159. 10.1212/WNL.0000000000003478
[8] Taylor BA. Does Coenzyme Q10 Supplementation Mitigate Statin-Associated Muscle Symptoms? Pharmacological and Methodological Considerations. Am J Cardiovasc Drugs. 2018 Apr;18(2):75–82.
[9] Langsjoen PH, Langsjoen AM. Comparison study of plasma Coenzyme Q10 levels in healthy subjects supplemented with ubiquinol versus ubiquinone. Clin Pharmacol Drug Dev. 2014 Jan;3(1):13–7.