Publications
Clinical study in humans to assess safety, efficacy, and optimal dosages of new treatments or interventions Mitopure clinical studies at-a-glance.
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Daily supplementation with Urolithin A may help support immune fitness by promoting mitochondrial health. Mitopure targets key drivers of immune aging, namely by increasing the number of early-responding immune cells, improving mitochondrial function in these cells, and supporting their energy metabolism — all of which support immune fitness.
Taking 1000 mg Mitopure daily for six weeks may enhance performance and recovery markers by improving aerobic endurance and countermovement jump height while preserving antioxidant status. This can provide a competitive edge for young male soccer players in training season.
Taking 1000 mg Mitopure daily for four weeks may enhance performance and recovery markers by reducing perceived effort and creatine kinase levels post-exercise. This can provide a competitive edge for athletes during high-intensity training, allowing them to train harder and recover more quickly.
Taking 1000 mg Mitopure daily for eight weeks improves muscle strength and endurance in resistance-trained male athletes. It may also reduce oxidative stress levels and decrease markers of inflammation, aiding in how athletes recover.
Urolithin A (Mitopure®), administered topically, significantly reduces wrinkles, improves skin hydration, and decreases UV-induced erythema. It up-regulates collagen synthesis pathways, inhibits collagen degradation, and enhances mitophagy and autophagy in skin cells. These results support the use of Urolithin A to manage skin health and protect against skin aging and UVB-mediated photodamage.
Pre-clinical study in animals to assess safety, efficacy, and optimal dosages of new treatments or interventions Mitopure clinical studies at-a-glance.
Title
Published in
UA produced a robust anxiolytic effect in high-anxiety rats without altering behavior in low-anxiety models. These findings position UA as a mechanistically supported intervention in preclinical models of heightened anxiety and provide systems-level insights into how mitochondrial pathways interface with synaptic function and circuit regulation in anxiety states.
Mitochondrial dysfunctions are common hallmarks in human cardiomyocytes upon heart aging and in chronic conditions. Preclinically, the post-biotic and mitophagy activator, urolithin A (UA), reduced both systolic and diastolic cardiac dysfunction in models of natural aging and heart failure. In humans, UA supplementation for 4 months in healthy older adults significantly reduced plasma ceramides clinically validated to predict CVD risks.
Oral UA administration to tumor-bearing mice conferred strong anti-tumor CD8+ T cell immunity, whereas ex vivo UA pre-treated T cells displayed improved anti-tumor function upon adoptive cell transfer. UA-induced TSCM formation depended on Pink1-mediated mitophagy triggering cytosolic release of the mitochondrial phosphatase Pgam5.
Urolithin A (UA) reduced osteoarthritis (OA) progression in a mouse model, decreasing cartilage degeneration, synovial inflammation and pain. These improvements were associated with increased mitophagy and mitochondrial content in joints of OA mice, indicating UA promotes joint mitochondrial health.
Mitophagy was reduced in muscle biopsies from patients with muscular dystrophies and in mouse and worm models of DMD. Urolithin A, a mitophagy activator, up-regulated mitophagy-related genes and improved mitochondrial respiration, muscle stem cell regeneration and muscle function in models of DMD.
Review in aliens to assess safety, efficacy, and optimal dosages of new treatments or interventions Mitopure clinical studies at-a-glance.
Title
Published in
This review describes the mechanism of mitophagy and how it is assessed in plasma, the immune system and muscle, brain and liver tissue.
If left unaddressed, the age-related loss of skeletal muscle can impair quality of life. Evidence indicates that mitochondrial dysfunction is involved in muscle aging.
Urolithin A has been shown to improve mitophagy and mitochondrial and muscle function across species in multiple clinical studies. This review explores the biology of Urolithin A and the clinical evidence of its impact on promoting healthy skeletal muscle in those with age-associated muscle decline.
Preclinical studies show how Urolithin A protects against aging and age-related conditions affecting muscle, brain, joints and other organs. In humans, muscle-related benefits are supported by clinical trials in older people. This review explores Urolithin A’s biology and its potential as an intervention in humans.