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.

开始日期2024-06-01

申办/合作机构

McLean Hospital, Inc.

[+2]

NCT06351683 / Recruiting临床2期IIT

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.)

开始日期2024-04-03

申办/合作机构

American Urological Association Education & Research, Inc.

[+1]

NCT06027554 / Not yet recruiting临床2期IIT

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.

开始日期2024-02-28

申办/合作机构

University of Connecticut Health Center

[+2]

100 项与 Mitoquinone mesylate 相关的临床结果

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100 项与 Mitoquinone mesylate 相关的转化医学

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100 项与 Mitoquinone mesylate 相关的专利（医药）

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项与 Mitoquinone mesylate 相关的文献（医药）

2024-12-01·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

作者: Mazaheri, Fahime ; Tavakolpoor Saleh, Nafiseh ; Karami, Somayeh ; Shahandeh, Erfan ; Mirzaei Azandaryani, Zahra ; 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.

2024-03-01·Ecotoxicology and environmental safety

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

Article

作者: 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.

2024-03-01·Neural regeneration research

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

Review

作者: 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.

项与 Mitoquinone mesylate 相关的新闻（医药）

2023-10-09

·生物探索

改善癌症免疫疗法疗效的新策略

代谢适应性对于T细胞的活力至关重要，而这在很大程度上取决于线粒体的行为。肿瘤浸润的T细胞内线粒体行为的性质尚不清楚。2023年9月22日，中山大学韩辉，高嵩和北京大学白凡共同通讯在Science Immunology（IF=25）在线发表题为“Mitochondria-ER contact mediated by MFN2-SERCA2 interaction supports CD8+ T cell metabolic fitness and function in tumors”的研究论文，该研究展示了线粒体融合素-2（MFN2）的表达与多种癌症的预后呈正相关。在CD8+ T细胞中遗传消融Mfn2抑制了线粒体代谢和功能，促进了肿瘤的发展。在肿瘤浸润的CD8+ T细胞中，MFN2通过与内质网嵌入的Ca2+-ATP酶SERCA2相互作用，促进线粒体所需的高效线粒体Ca2+流入，增强了线粒体-内质网（ER）接触。MFN2刺激了SERCA2的ER Ca2+回收活性，从而防止过多的线粒体Ca2+积累和细胞凋亡。通过增加CD8+ T细胞中的MFN2来提高线粒体-ER接触，可以提高癌症免疫疗法的效果。因此，该研究揭示了一个调节肿瘤浸润的CD8+ T细胞代谢适应性的缓冲机制，并突显了通过增加MFN2表达以优化T细胞功能的治疗潜力。尽管在癌症免疫疗法中广泛应用了采用肿瘤反应性肿瘤浸润淋巴细胞（TILs）的移植和免疫检查点阻断（ICB），但耐久和完全的治疗反应仅在临床病例的一小部分中观察到，尤其是在固体恶性肿瘤中。T细胞在肿瘤微环境（TME）内失去效应细胞功能是T细胞免疫疗法失败的主要原因之一。新出现的证据强调了代谢适应性在编程T细胞功能和命运方面的重要性。与肿瘤细胞的营养竞争限制了TILs的代谢能力，有助于免疫逃逸。异常的线粒体表型，包括减少的总质量和活性氧（ROS）水平、增加的去极化和碎片化形态，是疲劳的CD8+ TILs的特征。在TME内低血糖条件下，通过脂肪酸氧化（FAO）驱动的氧化磷酸化（OXPHOS）对TILs的效应功能和生存至关重要。通过矫正TILs的线粒体表型来进行代谢重塑是加强T细胞免疫疗法的临床疗效的有前途的策略。线粒体融合素（MFNs）是负责线粒体融合的类似动力蛋白三磷酸酶（GTPases），这是增强OXPHOS能力的基本事件。哺乳动物有两种MFNs，MFN1和MFN2，它们在序列相似性上共享80%的相似性，并在催化线粒体外膜融合方面存在一定程度的冗余。在体外，MFN2的脂质体系结效率高于MFN1，而MFN2介导线粒体（mito）-内质网（ER）的连接，尽管其基本机制仍然存在争议。Mito-ER接触使ER到线粒体的Ca2+流动成为可能，这是激活Krebs循环的关键酶以调控线粒体腺苷5'-三磷酸（ATP）产生的必要过程。总体而言，MFN2通过控制线粒体行为而充当代谢中枢。MFN2的突变或异常表达与多种人类疾病的发病有关，包括神经肌肉疾病、心脏代谢性疾病和癌症。在肿瘤微环境内，CD8+ T细胞在被激活后表现出MFN2的上调，并与更好的效应功能、氧化磷酸化（OXPHOS）和患者生存率相关。线粒体动力学在不同激活和功能状态的CD8+ T细胞的代谢特征中起着关键作用。线粒体融合在记忆CD8+ T细胞中受到青睐，用于细胞分化和生存。在患有明显肾细胞肾癌（ccRCC）的患者的CD8+ TILs中观察到了干扰的线粒体融合。CD8+ TILs中的线粒体去极化和线粒体自噬引发了疲劳表型。平衡的线粒体动力学对肿瘤浸润的自然杀伤细胞（NK细胞）和巨噬细胞的重要性也已经得到证明。在体外模型中，强化效应T细胞中的线粒体融合会导致记忆T细胞特性，并促进抗肿瘤能力。通过磷脂酰肌醇-3-激酶δ/γ（PI3Kδ/γ）抑制剂duvelisib治疗，可以增加CD8+ 嵌合抗原受体T细胞中的MFN2表达，从而增强其细胞毒性和干细胞性。Mito-ER接触对于记忆CD8+ T细胞的快速召回反应至关重要。最近的研究表明，亚油酸通过增强mito-ER接触来增强CD8+ T细胞的代谢适应性和抗肿瘤活性。然而，关于CD8+ TILs中线粒体融合的性质知之甚少。此外，CD8+ TILs中mito-ER接触的功能和调节机制也尚未被充分了解。该研究发现MFN2介导mito-ER接触以维持线粒体Ca2+稳态，从而促进CD8+ TILs的代谢适应性和效应功能。通过增加CD8+ T细胞中的MFN2以增强mito-ER接触，可以改善癌症免疫疗法的疗效。文章来源“iNature”责编|文竞择校对|文竞择End往期精选围观历史性突破！不需卵子和精子就可以合成人类胚胎热文富豪用儿子血浆“回春”科学吗？Science：血液牛磺酸缺乏驱动衰老热文世界首例！35岁的她，通过机器人操刀移植的子宫，成功诞下宝宝热文为了避免心脏骤停，53岁的他成为“第一个”植入开创性除颤器的心脏病患者热文首次披露！175家生物制药公司的薪资数据：薪资中位数达20万美元点击“阅读原文”，了解更多~

免疫疗法细胞疗法

2023-06-13

·Business Wire

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

高管变更

2023-03-30

·生物探索

研究发现，这种“升级版”辅酶Q10能逆转HIV引起的器官损伤

MitoQ是一种抗氧化剂，可作为膳食补充剂向公众提供。它是一种特殊的辅酶Q10（CoQ10）分子，具有比普通CoQ10更强的抗氧化作用。MitoQ的全称是“Mitochondrial-targeted coenzyme Q10”，意为“线粒体定向辅酶Q10”。MitoQ由一家名为Antipodean Pharmaceuticals的公司开发，其研发背景是为了解决因氧化损伤引起的许多疾病问题。MitoQ可以穿过细胞膜，直接进入线粒体，防止线粒体内部产生自由基损伤，从而保护细胞免受氧化损伤的影响。MitoQ被认为有潜力治疗许多疾病，包括心血管疾病、神经退行性疾病、肝脏疾病、糖尿病、肿瘤等。近日，一项动物研究发现，MitoQ还可以逆转HIV 和抗逆转录病毒疗法（ antiretroviral therapy，ART）对大脑、心脏、主动脉、肺、肾脏和肝脏中线粒体的有害影响。3月24日，该研究以“Mitoquinone Mesylate and Mitochondrial DNA in End Organs in Humanized Mouse Model of Chronic Treated Human Immunodeficiency Virus Infection”为题发表于The Journal of Infectious Diseases。图1 研究成果（图源：[1]）研究人员以人源化的小鼠为研究对象，这种小鼠拥有能够感染HIV的人类免疫细胞。用病毒感染这些小鼠后，研究人员使用富马酸替诺福韦二吡呋酯、恩曲他滨和拉替拉韦组成的ART进行了治疗，然后通过饮用水给小鼠喂食3个月的MitoQ，对照组小鼠则未给予MitoQ。研究人员使用分子方法来测量人/鼠线粒体DNA（mtDNA）与核DNA（ntDNA）的比率，该比率的降低能够反映线粒体的功能障碍。结果表明，与未感染的小鼠相比，接受ART治疗的HIV感染小鼠在大脑、心脏、肝脏、肺和肠道的人体免疫细胞中存在线粒体功能障碍。这种影响不仅来自于HIV感染，也来自ART治疗。而当使用MitoQ治疗90天时，与对照组相比，小鼠的器官线粒体功能障碍有所减少。线粒体是重要的细胞器，其功能正常，对于大脑、心脏、肝脏和肾脏等器官的顺利运作至关重要。虽然尚不清楚HIV是如何通过慢性炎症和免疫功能障碍导致器官损伤的，但可以明确的是，慢性HIV会引起线粒体功能障碍。目前，还没有针对HIV相关的这些器官损伤的治疗方法。研究的资深作者、加州大学洛杉矶分校大卫格芬医学院传染病科医学副教授Theodoros Kelesidis博士表示，该研究的结果可以作为HIV感染者临床试验的基础。“MitoQ是一种已知的、对人类安全且易于使用的膳食补充剂。”“我们的研究结果支持在服用ART药物的HIV感染者身上进行MitoQ的临床试验，但在进一步证实它是否可以作为慢性HIV感染相关合并症的潜在治疗方法之前，HIV感染者不应服用MitoQ来治疗任何与HIV感染相关的疾病。”责编|风立宵校对|乔维钧End参考资料：[1]Sihyeong Song, Sandro Satta, Madhav B Sharma, et al, Mitoquinone Mesylate and Mitochondrial DNA in End Organs in Humanized Mouse Model of Chronic Treated Human Immunodeficiency Virus Infection, The Journal of Infectious Diseases (2023). DOI: 10.1093/infdis/jiad044 本文系生物探索原创，欢迎个人转发分享。其他任何媒体、网站如需转载，须在正文前注明来源生物探索。往期精选围观 ‍ADC高景气利好！东曜药业差异化CDMO战略初见成效，现金流实现首次转正热文Cell Research：阿司匹林能促进DNA双链断裂高保真修复，或可预防癌症热文罕见疾病的新突破：发现三种罕见病未知的遗传原因热文面对提上日程的单身女性冻卵，国内首个保障冻卵安全的硬件系统发布！热文发现干细胞清理蛋白质垃圾的特殊机制，或为防治老年疾病带来新希望！点击“阅读原文”，了解更多~

100 项与 Mitoquinone mesylate 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
-	-	-	DB05063

研发状态

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适应症	最高研发状态	国家/地区	公司	日期
认知功能障碍	临床3期	美国	McLean Hospital, Inc.	2024-06-01
认知功能障碍	临床3期	瑞士	McLean Hospital, Inc.	2024-06-01
线粒体细胞病变	临床3期	美国	McLean Hospital, Inc.	2024-06-01
线粒体细胞病变	临床3期	瑞士	McLean Hospital, Inc.	2024-06-01
精神分裂症	临床3期	美国	McLean Hospital, Inc.	2024-06-01
精神分裂症	临床3期	瑞士	McLean Hospital, Inc.	2024-06-01
下尿路症状	临床2期	美国	-	2024-04-03
膀胱过度活动症综合征	临床2期	美国	-	2024-04-03
慢性丙型肝炎	临床2期	新西兰	Antipodean Pharmaceuticals, Inc.	2007-03-01
丙型肝炎	临床2期	-	Antipodean (UK) Ltd.	-

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT05381454 (Pubmed)	临床1/2期	新型冠状病毒感染	-	Mito-MES 20 mg	鹹製壓鹽廠鏇顧蓋獵鬱(鹽淵製夢醖壓鬱網糧積) = 鬱艱壓淵鑰壓衊選鹽艱觸鏇廠淵廠選鑰膚範選 (獵鹽網廠範顧壓窪糧觸, -45.0%(-64.5% ~ -25.5%)) 更多	-	2024-03-07
				Mitoquinone mesylate	鹹製壓鹽廠鏇顧蓋獵鬱(鹽淵製夢醖壓鬱網糧積) = 積遞鑰膚範獵鏇觸糧簾觸鏇廠淵廠選鑰膚範選 (獵鹽網廠範顧壓窪糧觸 ) 更多
ASN2014	N/A	常染色体显性多囊肾病	-	MitoQ	鏇鹹憲糧襯選積夢簾顧(製鑰鏇襯鬱鹹鑰繭淵壓) = 構窪憲醖窪鏇網獵淵製製築淵製蓋衊觸襯網廠 (觸積廠鹹夢獵願積夢鏇 )	积极	2014-11-11
ASN2013	N/A	普通感冒	-	MitoQ	鬱鑰觸構遞憲簾構衊願(襯齋繭衊膚簾網餘淵願) = We also showed that adding MitoQ increased ATP after cold storage (24 hr) alone 鹽齋鏇遞蓋觸鹽簾選構 (繭網窪艱膚憲廠範觸淵 ) 更多	积极	2013-11-05
				Cold storage + MitoQ (100 μM)