Ubidecarenone 120mg capsules
Ubidecarenone, also called coenzyme Q10, is a 1,4-benzoquinone.
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Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 14 · Randomised trials: 1 · Trials: 9 · 1988–2026
Showing the 50 most relevant studies, sorted by most relevant.
Ahmad K, Manongi NJ, Rajapandian R, et al.
2024
Statins are among the most widely prescribed drugs for treating dyslipidemia and reducing the incidence of heart disease and stroke. However, they come with a wide range of side effects, from myopathy to necrotizing rhabdomyolysis, as well as diabetes, hepatotoxicity, and sleep problems. The most common side effect of statins is statin-induced myopathy, often leading to discontinuation of statin therapy and noncompliance in many patients. This study aims to assess the effectiveness of coenzyme Q10 (CoQ10) supplementation as a treatment for patients with statin-induced myopathy. This systematic review was conducted by following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 statement. Relevant studies were identified through searches of Medline, PMC, PubMed, Science Direct, and Google Scholar. Only randomized control trials and meta-analyses of oral CoQ10 supplementation versus placebo in adults with statin-associated myalgia were included. The risk of bias was assessed using the Cochrane Risk of Bias tool (The Cochrane Collaboration, London, England, UK) and the measurement tool for the "assessment of multiple systematic reviews" (AMSTAR tool). Out of 5,000 records identified, only five were selected for this review: one meta-analysis and four randomized controlled trials. All of these studies were conducted between 2010 and 2023, involving a total of 800 patients. All randomized controlled trials showed improvement in statin-associated myopathy with CoQ10 supplementation, along with or without a reduced dosage of statins, without any notable side effects of CoQ10. Therefore, it can be deduced that CoQ10 supplementation significantly ameliorates statin-induced musculoskeletal symptoms.
Abstract licence: CC BY
Lee HY, Pyun JH, Shim SR, et al.
2024
PurposeTo investigate the efficacy of medical treatment options for Peyronie's disease (PD) including oral drugs, intralesional treatment and mechanical treatment compared with placebo treatment using network meta-analysis (NMA).Materials and methodsWe searched the randomized controlled trials (RCTs) of PD in PubMed, Cochrane library, and EMBASE up to October 2022. RCTs included medical treatment options: oral drugs, intralesional treatment and mechanical treatment. Studies reporting at least one of the outcome measures of interest including curvature degree, plaque size, and structured questionnaires (International Index of Erectile Function, IIEF) were included.ResultsFinally, 24 studies including 1,643 participants met our selection criteria for NMA. There was no statistically significant treatment compared to placebo of the curvature degree, plaque size, IIEF in Bayesian analysis. The SUCRA values of ranking probabilities for each treatment performance, which indicated that hyperthermia device ranked first in NMA. However, in frequentist analysis, 7 of mono treatments (coenzyme Q10 [CoQ10] 300 mg, hyperthermia device, interferon alpha 2b, pentoxifylline 400 mg, propionyl-L-carnitine 1 g, penile traction therapy [PTT], vitamin E 300 mg) and 2 of combination treatments ("PTT-extracorporeal shockwave treatment", "vitamin E 300 mg-propionyl-L-carnitine 1 g") were statistically significant for improvement of curvature degree, and 9 of mono treatments (CoQ10 300 mg, hyaluronic acid 16 mg, hyperthermia device, interferon alpha 2b, pentoxifylline 400 mg, propionyl-L-carnitine 1 g, verapamil 10 mg, vitamin E 300 mg, vitamin E 400 U) and 3 of combination treatments ("interferon alpha 2b-vitamin E 400 U", "verapamil 10 mg-antioxidants", "vitamin E 300 mg-propionyl-L-carnitine 1 g") were statistically significant in the improvement of plaque size.ConclusionsAt present, there is no clinical treatment alternatives that have been demonstrated to be effective compared to placebo. Nonetheless, as the frequentist approach has shown that a number of agents are efficacious, further research is expected to develop more effective treatment options.
Abstract licence: CC BY-NC
Karimi M, Pirzad S, Hooshmand F, et al.
2025
Background and objectiveCoenzyme Q10 is a naturally occurring antioxidant that has been suggested to improve cardiovascular health. Studies examining the effects of Q10 on blood pressure (BP) and heart rate (HR) have found inconsistent results. This meta-analysis aims to clarify the effects of Q10 administration on BP and HR in adults.MethodsA comprehensive search of online databases was conducted until February 2025 to identify relevant randomized controlled trials (RCTs). Following screening, relevant data were extracted from the eligible studies. Statistical analyses were conducted using weighted mean differences (WMD) with 95 % confidence intervals (CI). Data analysis was performed using the "meta" package in R.ResultsThe pooled analysis of 45 RCTs (48 effect sizes) showed that Q10 administration significantly reduced systolic BP (WMD: -3.44 mmHg; 95 %CI: [-5.13 to -1.55], p p = 0.23) and HR (WMD: -0.10 bpm; 95 %CI: [-2.09 - 1.89], p = 0.44). Subgroup analysis indicated that lower doses (8 weeks) resulted in greater systolic BP reductions.ConclusionThis meta-analysis indicates that CoQ10 supplementation may be an effective adjunctive therapy for reducing systolic blood pressure, especially at doses below 200 mg/day and with longer treatment durations. However, its impact on diastolic blood pressure and heart rate appears minimal. Given its favorable safety profile, CoQ10 could be considered as a supportive option in the management of hypertension, particularly for patients seeking non-pharmacological interventions or those with mild elevations in systolic BP.
Abstract licence: CC BY-NC-ND
Abe Y, Nishiwaki H, Suzuki T, et al.
2024
- Ubiquinone
- Vitamins
- Dietary Supplements
IntroductionCoenzyme Q10 (CoQ10) is a fat-soluble vitamin-like quinone. The plasma levels of CoQ10 are reduced in patients with chronic kidney disease (CKD). CoQ10 supplementation can improve mitochondrial function and decrease oxidative stress in these patients. This systematic review will assess the renoprotective effects of CoQ10 supplementation in patients with CKD.Methods and analysisWe will include the following studies: (1) randomised-controlled trials, (2) participants with CKD and (3) participants treated with CoQ10 as an intervention. The systematic review protocol was prepared in accordance with the Preferred Reporting Items for Systematic Review and Meta-Analysis Protocols. MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials and International Clinical Trials Register databases will be searched for articles without language restrictions in December 2024. The authors will be divided into two groups. Two independent authors will screen the titles and abstracts of all reports extracted via an electronic search. After the initial screening, the authors will independently review the full-text articles and perform a directed content analysis of the extracted data. For outcomes measured using continuous scales of measurement, we will adopt standardised mean differences as the effect measures. We will pool the data using the random-effects model.Ethics and disseminationNo human participants will be involved in the study. On completion of the analysis, the manuscript will be prepared for publication in a peer-reviewed journal.Prospero registration numberCRD42021241085.
Abstract licence: CC BY-NC
L.G. Leivas, A.I. Cachafeiro Pin, L.V. Piñeiro, et al.
Neurology Perspectives, 2026
Musazadeh V, Falahatzadeh M, Mahmoudinezhad M, et al.
2026
- Diabetes Mellitus, Type 2
- Ubiquinone
- Blood Glucose
BackgroundSeveral meta-analyses suggest that Coenzyme Q10 (CoQ10) supplementation is associated with glycemic control; however, findings about fasting blood glucose (FBG) and haemoglobin A1c (HbA1c) remain inconsistent across studies. Accordingly, this study aimed to synthesise the results to present a firm conclusion in relation to the efficacy of CoQ10 on glycemic control.MethodsA systematic search was conducted to find meta-analyses of randomised controlled trials using PubMed, Scopus, Web of Science and the Cochrane Database of Systematic Reviews from inception to March 6, 2025. Also, the methodological quality of included studies was evaluated using the AMSTAR2 tool.ResultsIn total, eight meta-analyses were included in this umbrella systematic review and meta-analysis. Pooled analysis using standardized mean difference analysis demonstrated that CoQ10 is associated with decreased FBG. While it didn't exert any significant changes on the HbA1c, HOMA-IR, and insulin levels. In addition, the combined effect of CoQ10 using weighted mean difference analysis revealed that CoQ10 is able to decrease the FBG (5.04 mg/dL), HbA1c (0.17%), HOMA-IR (0.72), and insulin (1.32 μIU/mL) levels significantly.ConclusionThe present study suggests that CoQ10 supplementation may have a moderate beneficial effect on glycemic control in diabetic patients, though findings differ depending on analytic approach.
Abstract licence: CC BY
Zhang SY, Yang KL, Zeng LT, et al.
2018
ObjectiveTo evaluate the effectiveness and safety of coenzyme Q10 for patients with type 2 diabetes mellitus (T2DM).MethodsData from randomized controlled trials were obtained to assess the effects of coenzyme Q10 versus placebo or western medicine on patients with T2DM. The study's registration number is CRD42018088474. The primary outcomes included glycosylated hemoglobin, fasting blood glucose, and fasting insulin.ResultThirteen trials involving 765 patients were included. Compared with the control group, coenzyme Q10 may decrease the HbA1c (WMD -0.29; 95% CI -0.54, -0.03; P = 0.03) and the fasting blood glucose (WMD -11.21; 95% CI -18.99, -3.43; P = 0.005). For fasting insulin, there is also not strong evidence that confirms which one is better because there was no statistical difference (WMD -0.48; 95% CI -2.54, 1.57; P = 0.65).ConclusionBased on current evidence, coenzyme Q10 may assist glycemic control, decrease TG, and improve HDL-C in patients with T2DM.
Abstract licence: CC BY
G. Hajiluian, Javad Heshmati, Sahar Jafari Karegar, et al.
Complementary Medicine Research, 2021
- Diabetes Mellitus
- Ubiquinone
- Age Factors
Xu Y, Liu J, Han E, et al.
2019
- Research Design
- Systematic Reviews as Topic
- Ubiquinone
IntroductionCoenzyme Q10 (CoQ10) is a fat-soluble vitamin-like quinone that exerts antioxidative functions and is also an important factor in mitochondrial metabolism. Plasma concentrations of CoQ10 are depressed in patients with chronic kidney disease (CKD). CoQ10 supplement can reduce adverse cardiovascular events, improve mitochondrial function and decrease oxidative stress in patients with non-dialysis CKD and dialysis CKD. We performed this study as a systematic review to comprehensively assess the effect of CoQ10 supplement on patients with CKD.Methods and analysisThe present systematic review protocol is reported in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-analysis Protocols guidelines. The MEDLINE, EMBASE and Cochrane library databases will be searched without language restrictions in December 2018. Two reviewers will independently screen the references in two stages: screening of the title/abstract and then of the full-text, to identify references meeting the inclusion criteria. A descriptive overview and tabular and/or graphical summaries will be generated, and directed content analysis will be carried out on the extracted data.Ethics and disseminationThis systematic review will evaluate the efficacy and safety of CoQ10 in patients with CKD. Ethical approval is not required for this study. The results of this systematic review will be presented in relevant conferences and published in a peer-review journal.Prospero registration numberCRD42019120201.
Abstract licence: CC BY-NC
Agnès Rötig, Eeva‐Liisa Appelkvist, Vanna Géromel, et al.
The Lancet, 2000
- Antioxidants
- Biopsy
- Cells, Cultured
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
95 found
Half-life
21.7 h
Mechanism
Ubidecarenone is an essential cofactor in the mitochondrial electron transport chain.
Food interactions
1 warning
Human targets
2 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
7.9 h
Half-life
21.7 h
[A31414]
Protein binding
95%
[L1065]…
Volume of distribution
20.4 L/kg
[L1065]…
Metabolism
Elimination
60%
Clearance
1.18 ml
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L1064]
It is important to highlight that these products are not FDA approved and it is recommended to use under discretion.
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 234 interactions
[A31417]
The normal side effects reported in humans are related to the gastrointestinal tract.
[A31416]
How the body processes this drug — absorption, distribution, metabolism, and elimination
The daily dosage of ubidecarenone presents the reach of maximal serum concentration by reaching a plateau after three weeks.
[L1065]
The pharmacokinetic properties may vary between different brands but studies have reported an AUC of 11.51 mcg h/ml and a Cmax of 0.32 mcg/ml at a time of 7.9 h.
[A31414]
[A31414]
[L1065]
The plasma concentration of ubidecarenone is highly dependent on the presence of plasma lipoproteins and about 95% of the administered form is found in the reduced form.
[A31416]
[L1065]
In preclinical studies with intravenous administration of ubidecarenone, it is reported a volume of distribution of 20.4 L/kg which reflects its ability to penetrate extensively into organs and tissues.
[A31415]
AS a general rule, tissues with high-energy requirements or metabolic activity tend to presents higher amounts of ubidecarenone, these organs can be heart, kidney, liver and muscle.
[A31416]
[L1066]
After exerting its action, ubidecarenone is reduced and forms hydroquinone which is capable of recycling and regenerates other antioxidants such as tocopherol and ascorbate. The later metabolism of hydroquinone generates the formation of Q acid I and Q acid II in free and conjugated forms.
[A31416]
[L1065][A31416]
In the urine, ubidecarenone is bound to saposin B protein and represents only 8.3% of the total administered dose.
[A31416]
[A31415]
Proteins and enzymes this drug interacts with in the body
May be the terminally assembled subunit of Complex I
PMID:10746566 PMID:24781757
SDH also oxidizes malate to the non-canonical enol form of oxaloacetate, enol-oxaloacetate (By similarity). Enol-oxaloacetate, which is a potent inhibitor of the succinate dehydrogenase activity, is further isomerized into keto-oxaloacetate (By similarity). Can act as a tumor suppressor PMID:20484225
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
Proteins that carry this drug through the body
PMID:24381170 PMID:30873003
In the off-state of the pathway, forms homooligomers or heterooligomers with LRP8 .
PMID:30873003
Upon binding to ligands, homooligomers are rearranged to higher order receptor clusters that transmit the extracellular RELN signal to intracellular signaling processes by binding to DAB1 .
PMID:30873003
This interaction results in phosphorylation of DAB1 leading to the ultimate cell responses required for the correct positioning of newly generated neurons. Later, mediates a stop signal for migrating neurons, preventing them from entering the marginal zone (By similarity)
ATC C01EB09
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Ubidecarenone
Additional database identifiers
Drugs Product Database (DPD)
1357
ChemSpider
4445197
PDB
U10
ZINC
ZINC000085427689
HUGO Gene Nomenclature Committee (HGNC)
HGNC:7719
GenAtlas
NDUFV3
GeneCards
NDUFV3
GenBank Gene Database
X99726
GenBank Protein Database
6002197
UniProt Accession
NDUV3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10680
GenAtlas
SDHA
GeneCards
SDHA
GenBank Gene Database
D30648
GenBank Protein Database
506338
UniProt Accession
SDHA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5006
GenAtlas
HMGCR
GeneCards
HMGCR
GenBank Gene Database
M11058
GenBank Protein Database
306865
Guide to Pharmacology
639
UniProt Accession
HMDH_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6547
GenAtlas
LDLR
GeneCards
LDLR
GenBank Gene Database
L00352
GenBank Protein Database
307121
UniProt Accession
LDLR_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12698
GeneCards
VLDLR
GenBank Gene Database
L20470
GenBank Protein Database
409426
UniProt Accession
VLDLR_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:40
GenAtlas
ABCB1
GeneCards
ABCB1
GenBank Gene Database
M14758
GenBank Protein Database
307180
Guide to Pharmacology
768
UniProt Accession
MDR1_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
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Structured knowledge from the free knowledge base
Molecular structure

ATC classifications (Wikidata)
Linked open data from Wikidata (Q321285), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication. Molecular structure images from Wikimedia Commons.