Coenzyme Q10

Antioxidant CAS# 303-98-0

Coenzyme Q10

Catalog No. BCN5954----Order now to get a substantial discount!

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Quality Control of Coenzyme Q10

Number of papers citing our products

Chemical structure

Coenzyme Q10

3D structure

Chemical Properties of Coenzyme Q10

Cas No. 303-98-0 SDF Download SDF
PubChem ID 5281915 Appearance Yellow cryst.
Formula C59H90O4 M.Wt 863.36
Type of Compound Quinones Storage Desiccate at -20°C
Solubility DMF : 7.14 mg/mL (8.27 mM; Need ultrasonic)
DMSO : < 1 mg/mL (insoluble or slightly soluble)
Chemical Name 2-[(2E,6E,10E,14E,18E,22E,26E,30E,34E)-3,7,11,15,19,23,27,31,35,39-decamethyltetraconta-2,6,10,14,18,22,26,30,34,38-decaenyl]-5,6-dimethoxy-3-methylcyclohexa-2,5-diene-1,4-dione
SMILES CC1=C(C(=O)C(=C(C1=O)OC)OC)CC=C(C)CCC=C(C)CCC=C(C)CCC=C(C)CCC=C(C)CCC=C(C)CCC=C(C)CCC=C(C)CCC=C(C)CCC=C(C)C
Standard InChIKey ACTIUHUUMQJHFO-UPTCCGCDSA-N
Standard InChI InChI=1S/C59H90O4/c1-44(2)24-15-25-45(3)26-16-27-46(4)28-17-29-47(5)30-18-31-48(6)32-19-33-49(7)34-20-35-50(8)36-21-37-51(9)38-22-39-52(10)40-23-41-53(11)42-43-55-54(12)56(60)58(62-13)59(63-14)57(55)61/h24,26,28,30,32,34,36,38,40,42H,15-23,25,27,29,31,33,35,37,39,41,43H2,1-14H3/b45-26+,46-28+,47-30+,48-32+,49-34+,50-36+,51-38+,52-40+,53-42+
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Coenzyme Q10

This product is produced with Gibberella fujikuroi

Biological Activity of Coenzyme Q10

DescriptionCoenzyme Q10, an essential cofactor of the electron transport chain, has neuroprotective effect in the cerebral ischemia via as a potent antioxidant and oxygen derived free radicals scavenger. Treatment with coenzyme Q10 in patients with myocardial infarction (MI) may be beneficial in patients with high risk of atherothrombosis. The coenzyme Q10 and alpha-lipoic acid supplementation can improve bladder function after outlet obstruction. The combination of Coenzyme Q10 and creatine may be useful in the treatment of neurodegenerative diseases such as Parkinson's disease and Huntington's Diseases. Coenzyme Q10 supplementation improves endothelial function of conduit arteries of the peripheral circulation in dyslipidaemic patients with Type II diabetes, the mechanism could involve increased endothelial release and/or activity of nitric oxide due to improvement in vascular oxidative stress.
TargetsAkt | mTOR | PGE | TNF-α | IL Receptor | ATP
In vitro

Coenzyme Q10 Inhibits the Aging of Mesenchymal Stem Cells Induced by D-Galactose through Akt/mTOR Signaling.[Pubmed: 25789082]

Oxid Med Cell Longev. 2015;2015:867293.

Increasing evidences indicate that reactive oxygen species are the main factor promoting stem cell aging. Recent studies have demonstrated that Coenzyme Q10 (CoQ10) plays a positive role in organ and cellular aging. However, the potential for CoQ10 to protect stem cell aging has not been fully evaluated, and the mechanisms of cell senescence inhibited by CoQ10 are still poorly understood. Our previous study had indicated that D-galactose (D-gal) can remarkably induce mesenchymal stem cell (MSC) aging through promoting intracellular ROS generation.
METHODS AND RESULTS:
In this study, we showed that CoQ10 could significantly inhibit MSC aging induced by D-gal. Moreover, in the CoQ10 group, the expression of p-Akt and p-mTOR was clearly reduced compared with that in the D-gal group. However, after Akt activating by CA-Akt plasmid, the senescence-cell number in the CoQ10 group was significantly higher than that in the control group.
CONCLUSIONS:
These results indicated that CoQ10 could inhibit D-gal-induced MSC aging through the Akt/mTOR signaling.

In vivo

Coenzyme q10 administration in community-acquired pneumonia in the elderly.[Pubmed: 25763241]

Iran Red Crescent Med J. 2014 Dec 1;16(12):e18852.

Community-acquired pneumonia (CAP) is generally considered a major cause of morbidity and mortality in the elderly. This study aimed to assess the efficacy of adjunctive Coenzyme Q10 (CoQ10) in the treatment of elderly CAP.
METHODS AND RESULTS:
Hospitalized elderly patients with CAP (diagnosed by using defined clinical and radiological criteria) were randomized to receive oral CoQ10 (200 mg/d) or placebo for 14 days, along with antibiotics. Primary and secondary outcomes on days 3, 7, and 14 were measured. Disease severity was scored using CURB-65 index. Statistical analysis was performed using SPSS and P value < 0.05 was considered significant. We enrolled 150 patients for this research. Then, 141 patients, including 70 patients in the trial group and 71 patients in the control group were analyzed. Mean age of the trial and control groups were 67.6 ± 7.2 years and 68.7 ± 7.9 years, respectively. Clinical cure at days 3 and 7 were 24 (34.3%) and 62 (88.6%) in the trial group (P value = 0.6745) and 22 (31%) and 52 (73.2%) in the placebo group (P value = 0.0209). Patients on CoQ10 had faster defervescence (P value = 0.0206) and shorter hospital stay (P value = 0.0144) compared with the placebo group. The subgroup analysis of the patients with severe pneumonia showed differences in clinical cure at day 14. Treatment failure was less in CoQ10 group than in the placebo group (10% versus 22.5% and P value = 0.0440). Adverse events in two groups were few and similar.
CONCLUSIONS:
CoQ10 administration has no serious side effects and can improve outcome in hospitalized elderly CAP; therefore, we recommend it as an adjunctive treatment in elderly patients.

Coenzyme Q(10) improves endothelial dysfunction of the brachial artery in Type II diabetes mellitus.[Pubmed: 11914748 ]

Diabetologia. 2002 Mar;45(3):420-6.

We assessed whether dietary supplementation with coenzyme Q(10) improves endothelial function of the brachial artery in patients with Type II (non-insulin-dependent) diabetes mellitus and dyslipidaemia.
METHODS AND RESULTS:
A total of 40 patients with Type II diabetes and dyslipidaemia were randomized to receive 200 mg of coenzyme Q(10) or placebo orally for 12 weeks. Endothelium-dependent and independent function of the brachial artery was measured as flow-mediated dilatation and glyceryl-trinitrate-mediated dilatation, respectively. A computerized system was used to quantitate vessel diameter changes before and after intervention. Arterial function was compared with 18 non-diabetic subjects. Oxidative stress was assessed by measuring plasma F(2)-isoprostane concentrations, and plasma antioxidant status by oxygen radical absorbance capacity. The diabetic patients had impaired flow-mediated dilation [3.8 % (SEM 0.5) vs 6.4 % (SEM 1.0), p = 0.016], but preserved glyceryl-trinitrate-mediated dilation, of the brachial artery compared with non-diabetic subjects. Flow-mediated dilation of the brachial artery increased by 1.6 % (SEM 0.3) with coenzyme Q(10) and decreased by -0.4 % (SEM 0.5) with placebo (p = 0.005); there were no group differences in the changes in pre-stimulatory arterial diameter, post-ischaemic hyperaemia or glyceryl-trinitrate-mediated dilation response. Coenzyme Q(10) treatment resulted in a threefold increase in plasma coenzyme Q(10) (p < 0.001) but did not alter plasma F(2)-isoprostanes, oxygen radical absorbance capacity, lipid concentrations, glycaemic control or blood pressure.
CONCLUSIONS:
Coenzyme Q(10) supplementation improves endothelial function of conduit arteries of the peripheral circulation in dyslipidaemic patients with Type II diabetes. The mechanism could involve increased endothelial release and/or activity of nitric oxide due to improvement in vascular oxidative stress, an effect that might not be reflected by changes in plasma F(2)-isoprostane concentrations.

Protocol of Coenzyme Q10

Animal Research

The beneficial effect of coenzyme Q10 and lipoic acid on obstructive bladder dysfunction in the rabbit.[Pubmed: 18804800 ]

Attenuating effects of coenzyme Q10 and amlodipine in ulcerative colitis model in rats.[Pubmed: 25753843]

Immunopharmacol Immunotoxicol. 2015 Mar 10:1-8.

Ulcerative colitis is a chronic inflammatory bowel disease. Recent studies reported a pivotal role of elevated intracellular calcium in this disorder. Coenzyme Q10 (CoQ10) and amlodipine are known to maintain cellular energy, decrease intracellular calcium concentration in addition to their antioxidant and anti-inflammatory properties. The aim of this study was to evaluate the possible protective effects of CoQ10, amlodipine and their combination on ulcerative colitis.
METHODS AND RESULTS:
Colitis was induced in rats by intracolonic injection of 3% acetic acid. CoQ10 (10 mg/kg), amlodipine (3 mg/kg) and their combination were administered for 8 consecutive days before induction of colitis. Our results showed that administration of CoQ10, amlodipine and their combination decreased colon tissue malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), prostaglandin E2 (PGE2), myeloperoxidase (MPO) and heat shock protein (HSP70) levels induced by intracolonic injection of acetic acid and restored many of the colon structure in histological examination. On the other hand, they increased superoxide dismutase (SOD) activity, adenosine-5'-triphosphate (ATP) and interleukin-10 (IL-10) colonic contents.
CONCLUSIONS:
Administration of either CoQ10 or amlodipine was found to protect against acetic acid-induced colitis. Moreover, their combination was more effective than individual administration of either of them. The protective effect of CoQ10 and amlodipine may be in part via their antioxidant, anti-inflammatory and energy restoration properties.

J Urol. 2008 Nov;180(5):2234-40.

Recent evidence indicates that ischemia and reperfusion are major etiological factors in the bladder dysfunction that occurs after partial bladder outlet obstruction. Coenzyme Q10 and alpha-lipoic acid are found naturally in mitochondria and act as potent antioxidants. We investigated the beneficial effects of Coenzyme Q10 plus alpha-lipoic acid in a rabbit model of bladder outlet obstruction.
METHODS AND RESULTS:
Twenty male rabbits were divided into 5 groups. Group 1 served as control and group 2 received three weeks of Coenzyme Q10 plus alpha-lipoic acid supplementation. Rabbits in group 3 underwent surgical partial bladder outlet obstruction for duration of four weeks and groups 4 and 5 were obstructed for seven weeks. In group 5, Coenzyme Q10 plus alpha-lipoic acid supplementation was given following 4 weeks obstruction and continued till the end of the seven weeks. The contractile responses to various agents were determined. The protein nitration and carbonylation levels were studied by immunoblotting. Nerve function was determined by choline acetyltransferase activity and nerve density. The contractile responses to different forms of stimulations, including field stimulation, ATP, carbachol and KCl all showed decreases following 4 and 7 weeks obstruction. Treatment with Coenzyme Q10 plus alpha-lipoic acid significantly restored contractile responses to all forms of stimulation. Treatment also had mitochondrial and neuronal effects and reduced protein nitration and carbonylation. Histologically there was less detrusor muscle hypertrophy.
CONCLUSIONS:
The current study clearly demonstrates that Coenzyme Q10 and alpha-lipoic acid supplementation can improve bladder function after outlet obstruction.

Coenzyme Q10 Dilution Calculator

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Preparing Stock Solutions of Coenzyme Q10

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.1583 mL 5.7913 mL 11.5827 mL 23.1653 mL 28.9566 mL
5 mM 0.2317 mL 1.1583 mL 2.3165 mL 4.6331 mL 5.7913 mL
10 mM 0.1158 mL 0.5791 mL 1.1583 mL 2.3165 mL 2.8957 mL
50 mM 0.0232 mL 0.1158 mL 0.2317 mL 0.4633 mL 0.5791 mL
100 mM 0.0116 mL 0.0579 mL 0.1158 mL 0.2317 mL 0.2896 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on Coenzyme Q10

Coenzyme Q(10) improves endothelial dysfunction of the brachial artery in Type II diabetes mellitus.[Pubmed:11914748]

Diabetologia. 2002 Mar;45(3):420-6.

AIM/HYPOTHESIS: We assessed whether dietary supplementation with coenzyme Q(10) improves endothelial function of the brachial artery in patients with Type II (non-insulin-dependent) diabetes mellitus and dyslipidaemia. METHODS: A total of 40 patients with Type II diabetes and dyslipidaemia were randomized to receive 200 mg of coenzyme Q(10) or placebo orally for 12 weeks. Endothelium-dependent and independent function of the brachial artery was measured as flow-mediated dilatation and glyceryl-trinitrate-mediated dilatation, respectively. A computerized system was used to quantitate vessel diameter changes before and after intervention. Arterial function was compared with 18 non-diabetic subjects. Oxidative stress was assessed by measuring plasma F(2)-isoprostane concentrations, and plasma antioxidant status by oxygen radical absorbance capacity. RESULTS: The diabetic patients had impaired flow-mediated dilation [3.8 % (SEM 0.5) vs 6.4 % (SEM 1.0), p = 0.016], but preserved glyceryl-trinitrate-mediated dilation, of the brachial artery compared with non-diabetic subjects. Flow-mediated dilation of the brachial artery increased by 1.6 % (SEM 0.3) with coenzyme Q(10) and decreased by -0.4 % (SEM 0.5) with placebo (p = 0.005); there were no group differences in the changes in pre-stimulatory arterial diameter, post-ischaemic hyperaemia or glyceryl-trinitrate-mediated dilation response. Coenzyme Q(10) treatment resulted in a threefold increase in plasma coenzyme Q(10) (p < 0.001) but did not alter plasma F(2)-isoprostanes, oxygen radical absorbance capacity, lipid concentrations, glycaemic control or blood pressure. CONCLUSION/INTERPRETATION: Coenzyme Q(10) supplementation improves endothelial function of conduit arteries of the peripheral circulation in dyslipidaemic patients with Type II diabetes. The mechanism could involve increased endothelial release and/or activity of nitric oxide due to improvement in vascular oxidative stress, an effect that might not be reflected by changes in plasma F(2)-isoprostane concentrations.

Coenzyme Q10 inhibits the aging of mesenchymal stem cells induced by D-galactose through Akt/mTOR signaling.[Pubmed:25789082]

Oxid Med Cell Longev. 2015;2015:867293.

Increasing evidences indicate that reactive oxygen species are the main factor promoting stem cell aging. Recent studies have demonstrated that Coenzyme Q10 (CoQ10) plays a positive role in organ and cellular aging. However, the potential for CoQ10 to protect stem cell aging has not been fully evaluated, and the mechanisms of cell senescence inhibited by CoQ10 are still poorly understood. Our previous study had indicated that D-galactose (D-gal) can remarkably induce mesenchymal stem cell (MSC) aging through promoting intracellular ROS generation. In this study, we showed that CoQ10 could significantly inhibit MSC aging induced by D-gal. Moreover, in the CoQ10 group, the expression of p-Akt and p-mTOR was clearly reduced compared with that in the D-gal group. However, after Akt activating by CA-Akt plasmid, the senescence-cell number in the CoQ10 group was significantly higher than that in the control group. These results indicated that CoQ10 could inhibit D-gal-induced MSC aging through the Akt/mTOR signaling.

The beneficial effect of coenzyme Q10 and lipoic acid on obstructive bladder dysfunction in the rabbit.[Pubmed:18804800]

J Urol. 2008 Nov;180(5):2234-40.

PURPOSE: Recent evidence indicates that ischemia and reperfusion are major etiological factors in the bladder dysfunction that occurs after partial bladder outlet obstruction. Coenzyme Q10 and alpha-lipoic acid are found naturally in mitochondria and act as potent antioxidants. We investigated the beneficial effects of Coenzyme Q10 plus alpha-lipoic acid in a rabbit model of bladder outlet obstruction. MATERIALS AND METHODS: Twenty male rabbits were divided into 5 groups. Group 1 served as control and group 2 received three weeks of Coenzyme Q10 plus alpha-lipoic acid supplementation. Rabbits in group 3 underwent surgical partial bladder outlet obstruction for duration of four weeks and groups 4 and 5 were obstructed for seven weeks. In group 5, Coenzyme Q10 plus alpha-lipoic acid supplementation was given following 4 weeks obstruction and continued till the end of the seven weeks. The contractile responses to various agents were determined. The protein nitration and carbonylation levels were studied by immunoblotting. Nerve function was determined by choline acetyltransferase activity and nerve density. RESULTS: The contractile responses to different forms of stimulations, including field stimulation, ATP, carbachol and KCl all showed decreases following 4 and 7 weeks obstruction. Treatment with Coenzyme Q10 plus alpha-lipoic acid significantly restored contractile responses to all forms of stimulation. Treatment also had mitochondrial and neuronal effects and reduced protein nitration and carbonylation. Histologically there was less detrusor muscle hypertrophy. CONCLUSIONS: The current study clearly demonstrates that Coenzyme Q10 and alpha-lipoic acid supplementation can improve bladder function after outlet obstruction.

Coenzyme q10 administration in community-acquired pneumonia in the elderly.[Pubmed:25763241]

Iran Red Crescent Med J. 2014 Dec 1;16(12):e18852.

BACKGROUND: Community-acquired pneumonia (CAP) is generally considered a major cause of morbidity and mortality in the elderly. OBJECTIVES: This study aimed to assess the efficacy of adjunctive Coenzyme Q10 (CoQ10) in the treatment of elderly CAP. PATIENTS AND METHODS: Hospitalized elderly patients with CAP (diagnosed by using defined clinical and radiological criteria) were randomized to receive oral CoQ10 (200 mg/d) or placebo for 14 days, along with antibiotics. Primary and secondary outcomes on days 3, 7, and 14 were measured. Disease severity was scored using CURB-65 index. Statistical analysis was performed using SPSS and P value < 0.05 was considered significant. RESULTS: We enrolled 150 patients for this research. Then, 141 patients, including 70 patients in the trial group and 71 patients in the control group were analyzed. Mean age of the trial and control groups were 67.6 +/- 7.2 years and 68.7 +/- 7.9 years, respectively. Clinical cure at days 3 and 7 were 24 (34.3%) and 62 (88.6%) in the trial group (P value = 0.6745) and 22 (31%) and 52 (73.2%) in the placebo group (P value = 0.0209). Patients on CoQ10 had faster defervescence (P value = 0.0206) and shorter hospital stay (P value = 0.0144) compared with the placebo group. The subgroup analysis of the patients with severe pneumonia showed differences in clinical cure at day 14. Treatment failure was less in CoQ10 group than in the placebo group (10% versus 22.5% and P value = 0.0440). Adverse events in two groups were few and similar. CONCLUSIONS: CoQ10 administration has no serious side effects and can improve outcome in hospitalized elderly CAP; therefore, we recommend it as an adjunctive treatment in elderly patients.

Attenuating effects of coenzyme Q10 and amlodipine in ulcerative colitis model in rats.[Pubmed:25753843]

Immunopharmacol Immunotoxicol. 2015 Jun;37(3):244-51.

CONTEXT: Ulcerative colitis is a chronic inflammatory bowel disease. Recent studies reported a pivotal role of elevated intracellular calcium in this disorder. Coenzyme Q10 (CoQ10) and amlodipine are known to maintain cellular energy, decrease intracellular calcium concentration in addition to their antioxidant and anti-inflammatory properties. OBJECTIVE: The aim of this study was to evaluate the possible protective effects of CoQ10, amlodipine and their combination on ulcerative colitis. MATERIALS AND METHODS: Colitis was induced in rats by intracolonic injection of 3% acetic acid. CoQ10 (10 mg/kg), amlodipine (3 mg/kg) and their combination were administered for 8 consecutive days before induction of colitis. RESULTS: Our results showed that administration of CoQ10, amlodipine and their combination decreased colon tissue malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), prostaglandin E2 (PGE2), myeloperoxidase (MPO) and heat shock protein (HSP70) levels induced by intracolonic injection of acetic acid and restored many of the colon structure in histological examination. On the other hand, they increased superoxide dismutase (SOD) activity, adenosine-5'-triphosphate (ATP) and interleukin-10 (IL-10) colonic contents. DISCUSSION AND CONCLUSION: Administration of either CoQ10 or amlodipine was found to protect against acetic acid-induced colitis. Moreover, their combination was more effective than individual administration of either of them. The protective effect of CoQ10 and amlodipine may be in part via their antioxidant, anti-inflammatory and energy restoration properties.

Coenzyme Q10: a review of its promise as a neuroprotectant.[Pubmed:17192765]

CNS Spectr. 2007 Jan;12(1):62-8.

Coenzyme Q10 (CoQ10) is a powerful antioxidant that buffers the potential adverse consequences of free radicals produced during oxidative phosphorylation in the inner mitochondrial membrane. Oxidative stress, resulting in glutathione loss and oxidative DNA and protein damage, has been implicated in many neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, and Huntington's disease. Experimental studies in animal models suggest that CoQ10 may protect against neuronal damage that is produced by ischemia, atherosclerosis and toxic injury. Though most have tended to be pilot studies, there are published preliminary clinical trials showing that CoQ10 may offer promise in many brain disorders. For example, a 16-month randomized, placebo-controlled pilot trial in 80 subjects with mild Parkinson's disease found significant benefits for oral CoQ10 1,200 mg/day to slow functional deterioration. However, to date, there are no published clinical trials of CoQ10 in Alzheimer's disease. Available data suggests that oral CoQ10 seems to be relatively safe and tolerated across the range of 300-2,400 mg/day. Randomized controlled trials are warranted to confirm CoQ10's safety and promise as a clinically effective neuroprotectant.

Coenzyme Q10 in neurodegenerative diseases.[Pubmed:12871093]

Curr Med Chem. 2003 Oct;10(19):1917-21.

Coenzyme Q(10) (ubiquinone), which serves as the electron acceptor for complexes I and II of the mitochondrial electron transport chain and also acts as an antioxidant, has the potential to be a beneficial agent in neurodegenerative diseases in which there is impaired mitochondrial function and/or excessive oxidative damage. Substantial data have accumulated to implicate these processes in the pathogenesis in certain neurodegenerative disorders, including Parkinson's disease, Huntington's disease and Friedreich's ataxia. Although no study to date has unequivocally demonstrated that coenzyme Q(10) can slow the progression of a neurodegenerative disease, recent clinical trials in these three disorders suggest that supplemental coenzyme Q(10) can slow the functional decline in these disorders, particularly Parkinson's disease.

Description

Coenzyme Q10 is an essential cofactor of the electron transport chain and a potent antioxidant agent.

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