Coenzyme Q₁₀

Territorial Availability: Available through Bertin Technologies only in France

• Synonyms
  • 2-[(2E,6E,10E,14E,18E,22E,26E,30E,34E)-3,7,11,15,19,23,27,31,35,39-decamethyl-2,6,10,14,18,22,26,30,34,38-tetracontadecaen-1-yl]-5,6-dimethoxy-3-methyl-2,5-cyclohexadiene-1,4-dione
• Correlated keywords
  • quinones mitochondria mitochondrial disorders electron transport chains redox ATP ROS antioxidants cells membranes hearts lungs livers kidneys spleens pancreas adrenals glands hypertension Parkinson’s diseases 13448-14-1 55127-92-9 55870-43-4 aqua Q 10L10 bio-quinone Q10 cosmesome Q 10 Li-Q-sorb liquid-Q neuquinon puresorb Q 40 Q 10AA Q-Gel; Q-gel 100; Q-absorb ubidecarenone ubiquinone 10 ubiquinone 50 ubiquinone Q10 unispheres Q 10 aqua Q10 kudesan cudesan neuquinone adelir ensorb kaneka Q10 vitamin Q ferroptosis
• Product Overview:
  Coenzyme Q10 (CoQ10) is a quinone that is found throughout the human body in cell membranes, primarily in mitochondrial membranes, with the highest levels in the heart, lungs, liver, kidneys, spleen, pancreas, and adrenal glands.{20672} It exists in three redox states: fully oxidized (CoQ10/ubiquinone), partially reduced (semiquinone or ubisemiquinone), and fully reduced (ubiquinol; Item No. 19677).{63365} CoQ10 acts as an electron shuttle in the electron transport chain via its reduction to ubiquinol between mitochondrial complexes I and II, also known as NADH dehydrogenase and succinate dehydrogenase, respectively, and mitochondrial complex III, also known as cytochrome bc1 complex.{20670,63366} CoQ10 is also reduced to ubiquinol by ferroptosis suppressor protein 1 (FSP1) with NADPH as a cofactor, and ubiquinol traps lipid peroxyl radicals and inhibits lipid peroxidation helping to prevent ferroptosis.{50700} Mutations in genes encoding enzymes involved in CoQ10 biosynthesis lead to primary CoQ10 deficiency, which is characterized by encephalopathy, cerebellar ataxia, infantile multisystemic form, nephropathy, and isolated myopathy.{62500} Secondary CoQ10 deficiency, induced by non-genetic impaired CoQ10 biosynthesis, insufficient CoQ10 intake, or excessive CoQ10 utilization, has been observed in a variety of conditions, including ataxia-oculomotor-apraxia 1 (AOA1), mitochondrial diseases, and hypercholesteremia with statin therapy.{20671,62501} Formulations containing CoQ10 have been used in the treatment of CoQ10 deficiency.