[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"health-studies-list:{\"conditionNormalized\":\"mitochondria\",\"overallStatus\":[\"RECRUITING\",\"AVAILABLE\",\"NOT_YET_RECRUITING\"],\"orderBy\":\"LastUpdateSubmitDate:desc\",\"size\":25,\"offset\":0}":3,"health-study-condition:mitochondria":26},{"pageToken":4,"total":5,"offset":6,"count":5,"results":7},null,3,0,[8,46,83],{"id":9,"slug":10,"hasResults":11,"nctId":12,"briefTitle":13,"officialTitle":13,"acronym":14,"eligibilityCriteria":15,"healthyVolunteers":11,"sex":16,"minAge":17,"maxAge":4,"enrollmentInfo":18,"targetDuration":4,"studyType":21,"phases":22,"briefSummary":24,"conditions":25,"keywords":28,"overallStatus":33,"whyStopped":4,"lastUpdateSubmitDate":34,"lastUpdatePostDateStruct":35,"startDateStruct":38,"completionDateStruct":40,"leadSponsor":42,"locationsCount":45},"100626480","phase-4-mitochondrial-redox-modulation-in-newly-diagnosed-type-2-diabetes-a-randomized-controlled-trial-comparing-imeglimin-vs-metformin-monotherapy-100626480",false,"NCT07436182","Mitochondrial Redox Modulation in Newly Diagnosed Type 2 Diabetes: A Randomized Controlled Trial Comparing Imeglimin vs. Metformin Monotherapy","MIRROR-DM",".1 Inclusion Criteria\n\nParticipants must meet ALL of the following criteria for enrollment:\n\n1. Age 18 or more inclusive, male or female.\n2. Confirmed diagnosis of T2DM within the preceding 12 months prior to screening, established by ADA or WHO criteria: fasting plasma glucose ≥ 126 mg\u002FdL on two separate occasions, and\u002For 2-hour OGTT plasma glucose ≥ 200 mg\u002FdL, and\u002For HbA1c ≥ 6.5%, and\u002For random plasma glucose ≥ 200 mg\u002FdL with classic hyperglycemic symptoms.\n3. HbA1c between 6.5% and 7.5 % inclusive at screening.\n4. Treatment-naive: no prior antidiabetic pharmacological treatment, or any prior antidiabetic treatment discontinued at least 3 months before screening.\n5. Estimated glomerular filtration rate (eGFR) ≥ 45 mL\u002Fmin\u002F1.73m² by CKD-EPI formula at screening.\n6. Willing and able to provide written informed consent in Arabic or English.\n7. Able to attend all scheduled study visits and comply with study procedures, dietary restrictions, and pre-analytical blood collection requirements.\n\n2 Exclusion Criteria\n\nParticipants meeting ANY of the following criteria will be excluded:\n\n1. Type 1 diabetes mellitus, Latent Autoimmune Diabetes in Adults (LADA), or other specific types of diabetes (anti-GAD antibody positivity, monogenic diabetes).\n2. HbA1c \\>7.5 gm%\n3. eGFR \\\u003C 45 mL\u002Fmin\u002F1.73m² - increase risk of drug accumulation and lactic acidosis.\n4. Hepatic impairment defined as ALT or AST \\> 2.5 times the upper limit of normal at screening. Hepatic dysfunction independently elevates plasma lactate by impairing lactate clearance and pyruvate metabolism, confounding the primary endpoint.\n5. History of or current congestive heart failure (NYHA Class III-IV) or clinically significant cardiovascular disease with hemodynamic instability major risk factor for lactic acidosis and a confound for tissue lactate metabolism.\n6. Active or recent (within 3 months) use of any antidiabetic pharmacological agent.\n7. Current use of medications known to significantly affect mitochondrial function or lactate\u002Fpyruvate metabolism: valproate, linezolid, nucleoside reverse transcriptase inhibitors (NRTIs), phenformin, zidovudine, or high-dose thiamine-depleting regimens.\n8. Pregnancy, planned pregnancy within the trial period, or active breastfeeding.\n9. Active malignancy requiring chemotherapy, radiotherapy, or immunosuppression within the preceding 6 months.\n10. Significant chronic alcohol use: \\> 21 units per week (male) or \\> 14 units per week (female). Alcohol is a major independent confound for pyruvate\u002Flactate ratio through its own effects on hepatic NAD+\u002FNADH balance.\n11. Acute illness, surgery, trauma, or hospitalization within 4 weeks of screening, acute physiological stress elevates plasma lactate independent of drug effects.\n12. Vigorous or unaccustomed physical exercise within 24 hours of any biomarker blood draw, exercise-induced lactate elevation is a major pre-analytical confound.\n13. Known hypersensitivity or contraindication to imeglimin or metformin.\n14. Participation in another interventional clinical trial within 3 months preceding screening.\n15. Any condition that, in the investigator's judgment, would render the patient unable to safely complete the trial or reliably provide valid biomarker samples.","ALL","18 Years",{"count":19,"type":20},176,"ESTIMATED","INTERVENTIONAL",[23],"PHASE4","he goal of this clinical trial is to compare the mitochondrial redox effects of imeglimin versus metformin monotherapy in adults with newly diagnosed Type 2 diabetes mellitus who are treatment-naive. The main questions it aims to answer are:\n\nDoes imeglimin improve the fasting plasma pyruvate\u002Flactate ratio (a validated surrogate of mitochondrial NAD⁺\u002FNADH redox balance) to a greater extent than metformin after 12 weeks of treatment? Does imeglimin produce more favorable changes in secondary mitochondrial and glycemic biomarkers - including fasting plasma lactate, fasting plasma pyruvate, HbA1c, HOMA-IR, and lipid profile - compared to metformin?\n\nResearchers will compare imeglimin 1000 mg twice daily to metformin up to 1000 mg twice daily to see if imeglimin produces superior improvement in mitochondrial oxidative capacity and cytoplasmic redox balance, reflected by a greater increase in the fasting plasma pyruvate\u002Flactate ratio, without compromising glycemic efficacy or safety.\n\nParticipants will:\n\nTake either imeglimin 1000 mg twice daily or metformin (titrated up to 1000 mg twice daily) orally for 12 weeks, as assigned by randomization Attend clinic visits at baseline (Week 0) and at Week 12 for fasting blood sample collection, including strict bedside deproteinization of pyruvate samples using ice-cold perchloric acid to ensure analytical accuracy Undergo measurement of fasting plasma pyruvate\u002Flactate ratio, HbA1c, HOMA-IR, fasting glucose, fasting insulin, fasting plasma lactate, fasting plasma pyruvate, and full lipid profile at both visits Be monitored for adverse events and safety parameters, including renal function (eGFR), throughout the study period",[26,27],"Mitochondria","Metformin",[29,30,27,31,32],"type 2 diabetes","Imeglimin","Pyruvate\u002FLactate ratio","Mitochondrial redox","NOT_YET_RECRUITING","2026-02-21",{"date":36,"type":37},"2026-02-27","ACTUAL",{"date":39,"type":20},"2026-03-01",{"date":41,"type":20},"2026-06-01",{"name":43,"class":44},"Mansoura University","OTHER",1,{"id":47,"slug":48,"hasResults":11,"nctId":49,"briefTitle":50,"officialTitle":51,"acronym":4,"eligibilityCriteria":52,"healthyVolunteers":11,"sex":53,"minAge":54,"maxAge":55,"enrollmentInfo":56,"targetDuration":4,"studyType":21,"phases":58,"briefSummary":60,"conditions":61,"keywords":66,"overallStatus":72,"whyStopped":4,"lastUpdateSubmitDate":73,"lastUpdatePostDateStruct":74,"startDateStruct":76,"completionDateStruct":78,"leadSponsor":80,"locationsCount":45},"100598036","adipose-stem-cell-mitochondria-supplementation-to-oocytes-ascent-100598036","NCT07066267","Adipose Stem Cell Mitochondria Supplementation to Oocytes (ASCENT)","Clinical Application of Autologous Adipose Stem Mitochondria Transplantation to Oocytes for Improving Embryo Quality in Patients With Recurrent Pregnancy Failure","Inclusion Criteria:\n\n* Having at least three previous failed IVF trial\n* Specifically consented for to collect biopsies for Preimplantation generic testing for aneuploidy (PGTA) analysis\n* Specifically consented for to have single blastocyst transfer (recommended)\n* No major uterine or ovarian abnormalities\n* Specifically consented for to have all embryos frozen\n* Specifically consented for to collect adipose tissues from subcutaneous liposuction\n* BMI level level \\\u003C26kg\u002Fm2\n\nExclusion Criteria:\n\n* Ovarian endometriosis with Chocolate cysts (American Fertility Society (AFS)) classification type 3 and 4\n* Any medical contraindication oocyte retrieval or subsequent procedures Ovarian hyperstimulation syndrome Bleeding disorders Sex hormone allergies Severe emotional defect on injections\n* Severe sperm abnormalities\n* \\\u003C5 million\u002FmL motile sperm\n* Uterine structural anomalies\n* Polycystic ovaries\n* Premature ovarian failure","FEMALE","29 Years","39 Years",{"count":57,"type":20},20,[59],"NA","The purpose of this study is to investigate the potential of autologous adipose stem cell (ASC) mitochondrial transfer (ASCENT) to oocytes along with intracytoplasmic sperm injection (ICSI)as a means of enhancing embryo development and improving the success rate of in patients with a history of multiple IVF failures. Embryo quality plays a crucial role in determining the success of assisted reproductive technologies and directly contributes to repeated pregnancy failures. Several factors, including age, physiological conditions, genetics, and environmental influences, can significantly impact embryo quality. Oocytes, the largest cells in the human body, are heavily reliant on mitochondria. Mitochondria's role in providing energy for oocytes is crucial, and insufficient energy production has been linked to poor oocyte and embryo quality. Some human studies have shown that increasing oocyte mitochondrial mass can improve embryo quality in patients who have experienced repeated IVF failures.",[62,63,26,64,65],"Female Infertility","Oocyte Competence","Recurent Implantation Failures","Advanced Age",[67,68,69,70,71],"mitochondria","mitochondria transplantation","Adipose stem cell","oocyte","Female infertility","RECRUITING","2025-07-14",{"date":75,"type":37},"2025-07-17",{"date":77,"type":37},"2025-04-25",{"date":79,"type":20},"2026-12-31",{"name":81,"class":82},"Sunkaky Medical Cooperation","INDUSTRY",{"id":84,"slug":85,"hasResults":11,"nctId":86,"briefTitle":87,"officialTitle":88,"acronym":89,"eligibilityCriteria":90,"healthyVolunteers":91,"sex":16,"minAge":17,"maxAge":92,"enrollmentInfo":93,"targetDuration":4,"studyType":21,"phases":95,"briefSummary":96,"conditions":97,"keywords":4,"overallStatus":72,"whyStopped":4,"lastUpdateSubmitDate":115,"lastUpdatePostDateStruct":116,"startDateStruct":118,"completionDateStruct":120,"leadSponsor":122,"locationsCount":45},"100462875","cancer-associated-muscle-mass---molecular-factors-and-exercise-mechanisms-100462875","NCT05307367","Cancer-associated Muscle Mass - Molecular Factors and Exercise Mechanisms","Identifying Molecular Factors Contributing to Cancer-associated Muscle Mass Loss and Providing Clinical Evidence for Exercise Mechanisms to Functionally Restore Muscle in Cancer","PANACEA","Inclusion Criteria, WP1+WP2X+WP2:\n\n* Men and women at or above the age of 18\n* Histological and radiological verified NSCLC (both squamous and adenocarcinoma) st. IIIb\u002FIV stage not eligible to concurrent chemo\u002Fradiation therapy as primary treatment\n* Referred for 1st line palliative anticancer therapy (platin based, immunotherapy, combined therapy or TKI), this goes for WP1 + WP2\n* Referred for palliative anticancer therapy (platin based, immunotherapy, combined therapy or TKI), for recurrent cancer, this goes only for WP2X.\n* Having a staging\u002Fbaseline CT within 4 weeks of initiation of treatment (PET\u002FCT are also allowed), or a baseline scan planned within the first week of treatment.\n* ECOG Performance Status 0-2\n* Having signed the informed consent form\n\nExclusion Criteria, WP1+WP2X+WP2:\n\n* Any other known malignancy requiring active treatment (prior cancer diagnosis is not some exclusion criteria if oncology-treatment is completed)\n* Local palliative radiotherapy as primary treatment\n* ECOG Performance status \\> 2\n* Physical disabilities excluding physical testing\n* Inability to understand Danish\n* Inability to understand scoring systems\u002Fpatient-reported outcome measures\n\nInclusion Criteria, WP3:\n\n* Men and women above the age of 18\n* Histological and radiological verified NSCLC (both squamous and adenocarcinoma) st. IIIb\u002FIV stage\n* ECOG Performance Status 0-2\n* Having signed the informed consent form.\n\nExclusion Criteria, WP3:\n\n* Any other known malignancy requiring active treatment (prior cancer diagnosis is not some exclusion criteria if oncology-treatment is completed)\n* ECOG Performance Status \\> 2\n* Physical disabilities excluding physical testing\n* Inability to understand Danish\n* Inability to understand scoring systems\u002Fpatient-reported outcome measures",true,"100 Years",{"count":94,"type":20},144,[59],"Muscle mass loss is a common adverse effect of cancer. Muscle mass loss occurs with or without reduction in body weight. Cancer cachexia (CC) is the involuntary loss of body weight of \\>5% within 6 months and it occurs in 50-80% of patients with metastatic cancer.\n\nIt is estimated that CC is a direct cause of up to 30% of all cancer-related deaths. No treatment currently is available to prevent CC, likely because the chemical reactions that causes of this devastating phenomenon in unknown.\n\nNo treatment currently is available to prevent muscle mass loss in patients with cancer but is urgently needed as the reduced muscle mass and function is associated with impaired physical function, reduced tolerance to anticancer therapy, poor quality of life (QoL), and reduced survival. There is evidence of an interdependence between informal caregiver (e.g. spouse) and patient QoL. Thus, identifying caregiver distress and needs can potentially benefit QoL for patients with cancer cachexia. Despite the enormous impact on disease outcomes, it is not known why the loss of muscle mass and function occurs and very few studies have investigated the underlying molecular causes in humans. In particular, there is a severe lack of studies that have obtained human skeletal muscle and adipose tissue sample material. Such reference sample materials will be invaluable to obtaining in-depth molecular information about the underlying molecular causes of the involuntary but common muscle mass and fat mass loss in cancer.\n\nAt a whole body level, cancer cachexia is associated with reduced sensitivity to the hormone insulin, high levels of lipids in the blood, and inflammation. Within the skeletal muscle, the muscle mass loss is associated with elevated protein breakdown and reduced protein build-up while emerging, yet, limited data also suggest malfunction of the power plants of the cells called mitochondrions. The role of malnutrition and how it contributes to weight loss is understood only to the extent of the observed loss of appetite and the reduced food intake because of pain, nausea, candidiasis of the mouth, and breathlessness. Evidence is increasing that the environment of the intestinal system could be implicated in cancer cachexia, yet, the possible effect of cancer and the cancer treatment on the intestinal environment is not understood. Thus, large and as yet poorly understood details of this syndrome precede a later weight loss.\n\nExercise training could help restore muscle function and how the chemical reactions works in cancer. In healthy people, and patients with diabetes, cardiovascular disease, and obesity exercise potently improves health. Exercise has been thought to slow down the unwanted effects of cancer cachexia by changing the reactions mentioned above. Thus, there is a tremendous gap in our knowledge of how and if exercise can restore the cells power plants function, muscle mass, strength, and hormone sensitivity in human cachexic skeletal muscle. Tackling that problem and examining potential mechanisms, will enable us to harness the benefits of exercise for optimizing the treatment of patients with cancer.\n\nThe data will provide novel clinical knowledge on cachexia in cancer and therefore addressing a fundamental societal problem.\n\nThree specific aims will be addressed in corresponding work packages (WPs):\n\n* investigate the involvement of hormone sensitivity of insulin and measure the chemical reactions between the cells in patients with lung cancer (NSCLC) and describe the physical performance and measure amount of e.g. muscles and adipose tissue across the 1st type of cancer treatment and understand how that is related to the disease and how patients and informal caregiver feel (WP1).\n* find changes in the chemical reactions in skeletal muscle, adipose tissue (AT), and blood samples in these patients, to understand how to predict how the disease will develop (WP2).\n* measure changes of skeletal muscle tissue in response to exercise and see if it might reverse the hormone insensitivity and improve muscle signaling and function (WP3).\n\nThe investigators believe that:\n\n* the majority of patients with advanced lung cancer, at the time of diagnosis already are in a cachectic state, where they lose appetite, and have hormonal changes, and an overall altered chemical actions between the cells affecting both muscle mass and AT. The investigators propose that all this can predict how the disease will progress, and how patient- and informal caregiver fell and how they rate their quality of life.\n* lung cancer and the treatment thereof is linked with changes in the blood, the muscle tissues, and the adipose tissues, especially in patients experiencing cachexia, that could be targeted to develop new treatment.\n* exercise can restore the muscles and improve insulin sensitivity and improve the function of the cells power plants in patients with lung cancer-associated muscle problems.",[98,99,100,101,102,103,104,105,106,107,108,109,110,111,112,113,114,26],"Cachexia","Neoplasms","Exercise","Metabolism","Body Composition","Insulin Resistance","Physical Functional Performance","Quality of Life","Sarcopenia","Caregivers","Adipose Tissue","Muscle, Skeletal","Patient Reported Outcome Measures","Gastrointestinal Microbiome","Proteomics","Lipidomics","Epigenomics","2022-05-09",{"date":117,"type":37},"2022-05-16",{"date":119,"type":37},"2022-04-01",{"date":121,"type":20},"2028-01-01",{"name":123,"class":44},"University of Copenhagen"]