Double Blind, Randomized, Placebo-Controlled Study of MitoQ as Adjunctive Treatment for Patients With Early-phase Schizophrenia-spectrum Disorder and Mitochondrial Dysfunction

The goal of this double-blind, placebo-controlled randomized clinical trial is to test the effect of 12 weeks of orally administered MitoQ (mitoquinol mesylate) supplementation on cognition in 50 people with early phase schizophrenia-spectrum disorders (E-SSD) who have mitochondrial dysfunction (called high risk, or HR). Cognitive impairments in SSD can cause significant disability. Yet, there are no effective treatments for cognitive impairments in SSD. It has been shown that alterations in a certain type of brain cell (parvalbumin interneurons, or PVI) underlie cognitive deficits in SSD. These PVI, which fire at a fast rate, utilize high amounts of energy from the mitochondria and are highly vulnerable to oxidative stress. MitoQ is an antioxidant. Research has shown that, in mice, MitoQ can reduce oxidative stress in the mitochondria. The main question that this clinical trial aims to answer is:
• Does MitoQ supplementation, compared to placebo, improve cognition in HR patients?
Secondary questions that this clinical trial aims to answer are the following: Does MitoQ supplementation, compared to placebo:
Improve positive and negative symptoms of SSD in HR patients?
Improve functioning in HR patients?
Improve/normalize blood markers of mitochondrial dysfunction in HR patients?
The investigators will enroll 100 individuals with E-SSD. These enrolled participants will participate in an initial screening visit to determine if they qualify for the actual clinical trial. At the screening visit, the investigators will ask about psychiatric history to determine diagnosis; ask about medical history; do a physical exam; collect blood and urine samples; do a pregnancy test; and ask participants to bring in their current medications in their original packaging so it is known what they are taking.
After the screening visit, the investigators will invite 50 HR patients (identified with a blood test) to continue with the clinical trial. Participants who qualify for the clinical trial will be asked to:
Take a supplement (MitoQ or placebo) once per day for 12 weeks in addition to their usual medications.
Come in for a study visit every 4 weeks over the 16-week study period. At these study visits, the investigators will do a physical exam; ask about symptoms and side effects; take blood and urine samples; and ask questions about general health and well-being, quality of life, mental health, emotional health, and mood. At visits 1 (baseline) and 4 (12 weeks), participants will also take a cognitive assessment.

Start Date01 Jun 2024

Sponsor / Collaborator

McLean Hospital, Inc.

[+2]

NCT06351683 / RecruitingPhase 2IIT

Mito-LUTS: A Pilot Study of the Effect of MitoQ on Lower Urinary Tract Symptoms in Older Women With Metabolic Syndrome

The goal of this clinical trial is to test the effect of a supplement called MitoQ (mitoquinol mesylate) on bladder symptoms such as urgency and frequency in women aged 50-75 years old who have the metabolic syndrome. The main questions it aims to answer are:
Is the study design feasible and acceptable to participants?
Do participants taking the study drug get any improvement to their bladder symptoms compared to participants taking a placebo (a look-alike substance that contains no drug)?
Participants will take 2 capsules of the study drug every morning for 4 months, answer many questions about their health including questions about their bladder health, perform physical and cognitive testing, give blood and urine samples, collect urine over 24 hour periods 3 times over the 4 months of the study, complete 3 day bladder diaries about how much they drink and void, undergo electrocardiograms, have their vitals and measurements (weight, height, waist circumference) taken, participate in 4 visits to the clinical research area and participate in many phone calls of varying length. Researchers will compare participants who were taking capsules containing MitoQ and participants taking capsules not containing MitoQ to see if MitoQ improves their bladder symptoms (urgency, frequency, nocturia, incontinence, etc.)

Start Date03 Apr 2024

Sponsor / Collaborator

University of Connecticut Health Center

[+1]

NCT06027554 / Not yet recruitingPhase 2IIT

The Mito-Frail Trial: Effects of MitoQ on Vasodilation, Mobility and Cognitive Performance in Frail Older Adults

The goal of this clinical trial is to test the effects of MitoQ supplementation in older adults and frail older adults with physical dysfunction and/or cognitive dysfunction. The main question[s] it aims to answer are:
To compare vascular function, oxidative stress levels, and physical and cognitive function among older adults and frail older adults with physical and cognitive dysfunction
To determine whether MitoQ supplementation has the potential to improve vascular function in central and cerebral vessels
To determine whether MitoQ supplementation can enhance physical and cognitive capabilities.

Start Date28 Feb 2024

Sponsor / Collaborator

University of Connecticut Health Center

[+2]

100 Clinical Results associated with Mitoquinone mesylate

100 Translational Medicine associated with Mitoquinone mesylate

100 Patents (Medical) associated with Mitoquinone mesylate

923

Literatures (Medical) associated with Mitoquinone mesylate

01 Dec 2024·Molecular biology reports

Evaluation of the effect of mitoquinone on functional parameters, DNA structure, and genes expression related to the apoptotic and antioxidants of human sperm after freezing–thawing

Article

Author: Mazaheri, Fahime ; Tavakolpoor Saleh, Nafiseh ; Karami, Somayeh ; Mirzaei Azandaryani, Zahra ; Shahandeh, Erfan ; Mohammadi, Hiwa ; Moradi Gardeshi, Tohid

OBJECTIVE:

Sperm freezing is considered as an effective way in assisted reproductive technology (ART) programs, it has detrimental effects on sperm function, due to the production of reactive oxygen species (ROS). This study aimed to investigate the potential of Mitoquinone (MitoQ) in inhibiting the production of mitochondrial ROS during sperm freezing.

METHODS:

A total of 20 human normozoosperm samples were collected for this study. The samples were divided into four groups, each containing different concentrations of MitoQ (0, 0.2, 2, and 20 nM), and then subjected to the freezing process. After thawing, the sperm suspensions were evaluated for parameters including motility, morphology, acrosome integrity, adenosine triphosphate (ATP) level, intracellular ROS, viability, chromatin packaging, DNA denaturation, DNA fragmentation, as well as the expression of antioxidants (GPX, SOD) and apoptotic (Bax, Bcl₂) genes.

RESULTS:

The results showed that total and progressive mobility of sperms significantly increased in the 2 nM group, while significantly decreased in the 20 nM group (p ≤ 0.05). Sperm morphology did not significantly improve across all the tested concentrations (p ≥ 0.05). Intracellular ROS levels showed a significant decrease and increase in the concentrations of 2 and 20 nM, respectively (p ≤ 0.05). Furthermore, a significant increase was observed in viability, ATP, acrosome integrity, chromatin packaging, and non-denatured and non-fragmented DNA after treatment with 2 nM of MitoQ, compared with the control group (p ≤ 0.05). Regarding gene expressions, the relative expressions of oxidative stress genes were increased in the 2 nM group and decreased in the 20 nM group (p ≤ 0.05), while no significant difference was observed in the expressions of apoptotic genes compared with the control group (p ≥ 0.05). All the comparisons were made with respect to the control group.

CONCLUSION:

Adding the optimal concentration of MitoQ (2 nM) to the sperm freezing medium not only improves sperm functional parameters and reduces DNA damages, but also stimulates the expression of antioxidant genes, leading to even greater benefits for sperm cryopreservation.

01 Mar 2024·Ecotoxicology and environmental safety

From inflammation to pyroptosis: Understanding the consequences of cadmium exposure in chicken liver cells

Article

Author: Zhang, Yu ; Ye, Ruiqi ; Li, Shenghe ; Liu, Chang ; Wang, Yan ; Li, Jing ; Jin, Erhui ; Li, Xiaojin ; Li, Wen ; Cao, Mixia ; Li, Lei ; Yang, Jingyi ; Xu, Hao ; Wu, Jiale

Hepatotoxicity is frequently observed following acute cadmium (Cd) exposure in chicken. Oxidative stress and subsequent inflammation are regarded as the main reasons for cadmium-induced liver injury. NOD-like receptor (NLR) family pyrin domain-containing 3 (NLRP3) inflammasome-induced pyroptosis is involved in various inflammatory diseases, including liver injury. Poultry are more susceptible to harmful effects of heavy metals. However, the mechanism of cadmium-induced liver injury in chicken is still elusive. In this study, the effect of cadmium on chicken liver cells and the underlying mechanisms were investigated. The results showed mitochondria was damaged and excessive reactive oxygen species (ROS) were generated in chicken liver cell line LMH after cadmium exposure. Furthermore, cadmium-induced NLRP3 inflammasome activation and the cell membrane rupture indicated LMH cells pyroptosis. The ROS scavengers, acetylcysteine (NAC) and Mito-TEMPO prevented pyroptosis in LMH cells, suggesting that ROS were responsible for the activation of the NLRP3 inflammasome induced by cadmium. Additionally, anti-oxidative transcription factor Nrf2 was inhibited after cadmium exposure, explaining the excessive ROS generation. In summary, our study showed that cadmium leads to ROS generation by inducing mitochondrial damage and inhibiting Nrf2 activity, which promotes NLRP3 inflammasome activation and eventually induces pyroptosis in LMH cells.

01 Mar 2024·Neural regeneration research

Single-neuron neurodegeneration as a degenerative model for Parkinson's disease.

Review

Author: Huenchuguala, Sandro ; Segura-Aguilar, Juan

The positive effect of levodopa in the treatment of Parkinson's disease, although it is limited in time and has severe side effects, has encouraged the scientific community to look for new drugs that can stop the neurodegenerative process or even regenerate the neuromelanin-containing dopaminergic nigrostriatal neurons. Successful preclinical studies with coenzyme Q10, mitoquinone, isradipine, nilotinib, TCH346, neurturin, zonisamide, deferiprone, prasinezumab, and cinpanemab prompted clinical trials. However, these failed and after more than 50 years levodopa continues to be the key drug in the treatment of the disease, despite its severe side effects after 4-6 years of chronic treatment. The lack of translated successful results obtained in preclinical investigations based on the use of neurotoxins that do not exist in the human body as new drugs for Parkinson's disease treatment is a big problem. In our opinion, the cause of these failures lies in the experimental animal models involving neurotoxins that do not exist in the human body, such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and 6-hydroxydopamine, that induce a very fast, massive and expansive neurodegenerative process, which contrasts with the extremely slow one of neuromelanin-containing dopaminergic neurons. The exceedingly slow progress of the neurodegenerative process of the nigrostriatal neurons in idiopathic Parkinson's patients is due to (i) a degenerative model in which the neurotoxic effect of an endogenous neurotoxin affects a single neuron, (ii) a neurotoxic event that is not expansive and (iii) the fact that the neurotoxin that triggers the neurodegenerative process is produced inside the neuromelanin-containing dopaminergic neurons. The endogenous neurotoxin that fits this degenerative model involving one single neuron at a time is aminochrome, since it (i) is generated within neuromelanin-containing dopaminergic neurons, (ii) does not cause an expansive neurotoxic effect and (iii) triggers all the mechanisms involved in the neurodegenerative process of the nigrostriatal neurons in idiopathic Parkinson's disease. In conclusion, based on the hypothesis that the neurodegenerative process of idiopathic Parkinson's disease corresponds to a single-neuron neurodegeneration model, we must search for molecules that increase the expression of the neuroprotective enzymes DT-diaphorase and glutathione transferase M2-2. It has been observed that the activation of the Kelch-like ECH-associated protein 1/nuclear factor (erythroid-derived 2)-like 2 pathway is associated with the transcriptional activation of the DT-diaphorase and glutathione transferase genes.

News (Medical) associated with Mitoquinone mesylate

13 Jun 2023

·www.businesswire.com

MitoQ Hires New CSO: Siobhan Mitchell

AUCKLAND, New Zealand & IRVINE, Calif.--( BUSINESS WIRE )-- MitoQ Ltd. , a New Zealand-based cell health company that developed a world-first sub-cellular targeted antioxidant which directly combats cell stress, announces the appointment of Siobhan Mitchell as Chief Science and Technology Officer. MitoQ is the developer of the unique, next-generation cell health molecule with the same name, that is scientifically shown to penetrate deep within the cells to reduce cell stress. By supporting the body’s primary energy source – the mitochondria -- MitoQ is able to target cell stress and improve energy, increase exercise recovery and promote healthy aging. Mitchell, who relocated from the US to New Zealand’s MitoQ HQ for her new role, is a PhD scientist with expertise in strategy, execution and launch of digital health programs and nutrition products with targeted health benefits and claims. She completed a postdoctoral fellowship at the University of Washington and is experienced in all aspects of clinical trial management, with a special focus on studies assessing behavior change, weight loss, mental health, nutrition, cognition, metabolism, and pharmacokinetics. She has spent the last 25 years researching how nutrition affects the brain, especially how it may delay brain aging. She’s worked on metabolic health, skin health, appetite, sports physiology, and cellular health. She’s also spent 15 years in functional food and medical nutrition companies and led a group working on digital health interventions for mental wellbeing and weight loss. Mitchell was most recently the Senior Director of Academic Research at NOOM Inc. where she led a team of clinical researchers investigating digital health interventions for weight loss, diabetes support, diabetes prevention, stress and anxiety management, and cancer support. Prior to that she was the Senior Principal Scientist at PepsiCo for over 4 years where she conducted studies assessing functional potential of novel ingredients or differentiated micronutrient forms and evaluated the business potential of new ingredients and health claims. Prior to that she was a Project Manager/Scientist for the Nestle Institute of Health Sciences and a Project Manager/Scientist at Unilever. “Siobhan is a fantastic addition to our team. She brings a depth of expertise and experience which will help take MitoQ to the next level. But more importantly – help everyone to understand the foundational role that cells play in their overall health and wellbeing,” says Mahara Inglis, Chief Executive Officer of MitoQ. In her role as CSO, Mitchell drives the science strategy for MitoQ, and makes sure all evidence for products is top-quality. She ensures that MitoQ is at the forefront of cellular health by spearheading partnerships with likeminded companies and universities. She’s currently working with the University of Colorado to assess how MitoQ can improve vascular health in older women as it’s been shown that exercise isn’t cardioprotective in post-menopausal women. The MitoQ team is eager to find out if they can help women keep their vasculature healthy via reducing oxidative stress. “What led me to MitoQ was the incredible science behind its patented ingredient Mitoquinol Mesylate, and the exciting future for cellular health solutions. MitoQ truly cares about gold standard science and has already shown to be hugely innovative as a supplement company,” says Siobhan Mitchell. MitoQ is a multi-patented, advanced antioxidant molecule that delivers targeted support to the cells’ mitochondria. The mitochondria provide approximately 90% of the energy the human body needs to function. As a by-product of this energy production process, the mitochondria also produce free radicals, and with age (coupled with other external and environmental stressors), the body loses its natural resistance to diffuse them. MitoQ is bio-designed to be absorbed deep inside of the cells where it can neutralize free radicals to combat cell stress, resulting in more energy, faster exercise recovery, immune support, deeper focus and overall optimized health. MitoQ Pure, the company's all-round flagship product, has been repeatedly shown to enhance energy levels and attention, with the brand having already committed over $60 million towards research supporting the varied benefits of their invention. For more information, visit www.mitoQ.com . MitoQ is available globally via the brand website ( www.mitoQ.com ) and on Amazon.com. About MitoQ MitoQ is a New Zealand cellular health company that invented an advanced molecule which is clinically proven to target cells for better health. Created at the University of Otago in the 1990s, MitoQ’s unique ingredient is available in a range of cellular products designed to empower the health and ambitions of every body. MitoQ’s potential benefits to health have been the subject of 18 clinical trials and over 750 independent published research papers by the likes of Harvard Medical School, UCLA and the University of Cambridge, and it holds 60 patents globally. For more information about the company and its products, visit www.mitoQ.com

Executive Change

24 Mar 2023

·www.sciencedaily.com

A readily available dietary supplement may reverse organ damage caused by HIV and antiretroviral therapy

MitoQ, a mitochondrial antioxidant that is available to the public as a diet supplement, was found in a mouse study to reverse the detrimental effects that HIV and antiretroviral therapy (ART) have on mitochondria in the brain, heart, aorta, lungs, kidney and liver. MitoQ, a mitochondrial antioxidant that is available to the public as a diet supplement, was found in a mouse study to reverse the detrimental effects that HIV and antiretroviral therapy (ART) have on mitochondria in the brain, heart, aorta, lungs, kidney and liver. The researchers used a molecular method to measure the ratio of human and murine mitochondrial (mtDNA) to nuclear DNA (ntDNA) ratio, a measure of mitochondrial dysfunction. Reduction in this ratio reflects mitochondrial dysfunction. Compared to uninfected mice, HIV infected mice treated with ART had mitochondrial dysfunction in the human immune cells in the brain, heart, liver, lungs, and gut. ART itself also affected mitochondrial function in mouse heart cells. When treated with MitoQ for 90 days, HIV infected mice had reduced mitochondrial dysfunction in organs compared to HIV infected mice on ART. Mitochondria are the key cell structures that are important for the smooth function of organs such as the brain, heart, liver and kidney. HIV causes a chronic state of inflammation and immune dysfunction that contribute to organ damage organs. The reasons for this are unclear, but it is known that mitochondrial dysfunction contributes to organ damage and is present in chronic HIV. There are no therapies for HIV associated diseases that affect organs such as the brain, heart and liver. The researchers used humanized mice, which have human immune cells that can be infected with HIV. They infected them with the virus, treated them with ART consisting of tenofovir disoproxil fumarate, emtricitabine, and raltegravir, then fed them MitoQ through drinking water for three months. The control mice were not given MitoQ. The researchers note that humanized mice do not exactly recreate HIV infection in humans. Also, the infected mice were exposed to both the virus and the ART and they could not dissect the exact contribution of the virus versus the ART to mitochondrial dysfunction in human cells. These preclinical findings could serve as the foundation for clinical trials in humans with HIV. "MitoQ is a diet supplement that is known to be safe in humans and is readily available for use," said senior author Dr. Theodoros Kelesidis, associate professor of medicine in the division of infectious diseases at the David Geffen School of Medicine at UCLA. "Our findings support clinical trials of MitoQ in people with HIV who take antiretrovirals to determine whether it can be a potential treatment for comorbidities associated with chronic HIV infection. Until then people with HIV should not take this diet supplement for treatment of any conditions associated with HIV infection." The study was funded by the National Institutes of Health (R01AG059501, R21AI36708, R21HL134444, R03AG059462, R03AG059462, K08AI108272), the California HIV/AIDS Research Program (OS17-LA-002), and Campbell Foundation.

Clinical Study

27 Nov 2006

·www.biospace.com

Antipodean Pharmaceuticals, Inc. Completes Phase 2 Trial Enrollment For MitoQ In Parkinson's Disease

SAN FRANCISCO, Nov. 27 /PRNewswire/ -- Antipodean Pharmaceuticals, a privately held pharmaceutical company developing treatments for disorders associated with mitochondrial dysfunction, today announced that it completed enrollment in a Phase 2 study to evaluate its lead compound, MitoQ (mitoquinone), in Parkinson's disease, a neurodegenerative disorder that affects up to four million people worldwide. "We believe that MitoQ's novel mechanism of action may yield additional therapeutic options for Parkinson's disease patients, who have limited treatments available for symptom relief, and none to halt disease progression," said Ken Taylor, CEO, Antipodean Pharmaceuticals. "MitoQ blocks the effects of oxidation, a chemical reaction that generates oxygen free radicals, which can attack and destroy cells. We achieved enrollment in this Phase 2 trial ahead of schedule, demonstrating the rapid advancement of our clinical programs." The randomized, double-blind multi-center clinical trial is evaluating 128 patients in New Zealand and Australia who have met the diagnosis criteria for Parkinson's, but have not begun any treatment. Patients were randomized into one of three treatment arms to compare treatment with MitoQ at 40 mg and 80 mg to placebo, orally administered once daily. The primary endpoint is disease progression according to the Unified Parkinson's disease Rating Scale (UPDRS). An independent data safety monitoring board is reviewing safety data periodically. "Several neurodegenerative disorders, including Parkinson's, are associated with mitochondrial dysfunction from oxidative damage," said Dr. Barry Snow, Head of Department of Neurology, Auckland Hospital, and lead investigator of the trial. "MitoQ may be able to stem the progression of these difficult-to-treat conditions." About MitoQ MitoQ is based on a novel technology, targeted lipophilic cations, that transport and concentrate antioxidants into the mitochondria -- organelles inside cells that provide energy for life processes -- where they accumulate up to a thousand fold. In 2004, a genomic study of hereditary early-onset Parkinson's disease demonstrated a direct molecular link between mitochondrial dysfunction and the pathogenesis of Parkinson's disease. Mitochondrial dysfunction also has been shown to represent an early critical event in the pathogenesis of the sporadic form of Parkinson's disease. Clinical studies by the Parkinson's Study Group show that very high doses of an antioxidant called Coenzyme Q (which MitoQ effectively targets into mitochondria) appear to slow the progression of Parkinson's disease symptoms. For more information on the trial, please visit . About Parkinson's Disease Parkinson's disease is a progressive disorder that results from nerve cell death or impairment in the part of the brain that controls movement. It can cause tremors, stiffness, and other difficulty moving. Parkinson's disease affects as many as 1.5 million people in the United States and up to four million worldwide. While most patients are over 65 years of age, up to 15% are under 50. Current medicines that treat symptoms can lose potency over time; no available treatment delays or modifies the course of the disease. About Antipodean Antipodean is a clinical-stage pharmaceutical company developing treatments for Parkinson's disease and other disorders associated with mitochondrial dysfunction. The company's lead product, MitoQ, is being investigated in Phase 2 trials in Parkinson's disease. Antipodean recently opened its corporate headquarters in San Francisco, California and maintains an operational base in Auckland, New Zealand. The company works closely with researchers and investigators in New Zealand and Australia as well as in the Bay Area and elsewhere in the United States to develop MitoQ and other therapeutics based on mitochondrial targeting. Antipodean investors include: Delphi Ventures, 5AM Ventures, GBS Venture Partners and Versant Ventures. Further information is available at . Antipodean Pharmaceuticals CONTACT: Eric Bizjak of Antipodean Pharmaceuticals, Inc., +1-415-692-0610,ebizjak@antipodeanpharma.com; or media, Katie Compa of WeissComm Partners,+1-415-946-1078, or kcompa@weisscommpartners.com, for AntipodeanPharmaceuticals, Inc. Web site:

100 Deals associated with Mitoquinone mesylate

External Link

KEGG	Wiki	ATC	Drug Bank
-	-	-	DB05063

R&D Status

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Lower Urinary Tract Symptoms	Phase 2	US	University of Connecticut Health Center	03 Apr 2024
Overactive bladder syndrome	Phase 2	US	University of Connecticut Health Center	03 Apr 2024
Hepatitis C, Chronic	Phase 2	NZ	Antipodean Pharmaceuticals, Inc.	01 Mar 2007
Parkinson Disease	Phase 2	AU	Antipodean Pharmaceuticals, Inc.	01 May 2006
Parkinson Disease	Phase 2	NZ	Antipodean Pharmaceuticals, Inc.	01 May 2006
Hepatitis C	Phase 2	-	Antipodean (UK) Ltd.	-
Liver Cirrhosis	Phase 2	NZ	Antipodean Pharmaceuticals, Inc.	-
Friedreich Ataxia	Phase 1	NZ	Antipodean Pharmaceuticals, Inc.	-
Alzheimer Disease	Preclinical	NZ	Antipodean Pharmaceuticals, Inc.	-
Chemotherapy-induced damage	Preclinical	NZ	Antipodean Pharmaceuticals, Inc.	-

Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


ASN2014	Not Applicable	Polycystic Kidney, Autosomal Dominant	-	MitoQ	izomqpcupp(jncxfyjhjh) = fulcdjjcuf pirmlzpbon (bkogzkmnnf )	Positive	11 Nov 2014
ASN2013	Not Applicable	Common Cold	-	MitoQ	iqavmuydqv(iipqhyjbut) = We also showed that adding MitoQ increased ATP after cold storage (24 hr) alone irhthjnkij (hdswyivayb ) View more	Positive	05 Nov 2013
ASN2013	Not Applicable	Common Cold	-	Cold storage + MitoQ (100 μM)		Positive	05 Nov 2013

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