Mitochondrial Redox Modulation in Newly Diagnosed Type 2 Diabetes: A Randomized Controlled Trial … (NCT07436182) | Clinical Trial Compass
Not Yet RecruitingPhase 4
Mitochondrial Redox Modulation in Newly Diagnosed Type 2 Diabetes: A Randomized Controlled Trial Comparing Imeglimin vs. Metformin Monotherapy
Egypt176 participantsStarted 2026-03-01
Plain-language summary
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:
Does imeglimin improve the fasting plasma pyruvate/lactate ratio (a validated surrogate of mitochondrial NAD⁺/NADH 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?
Researchers 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/lactate ratio, without compromising glycemic efficacy or safety.
Participants will:
Take 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/lactate 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
Who can participate
Age range18 Years
SexALL
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Inclusion criteria
✓. Age 18 or more inclusive, male or female.
✓. Confirmed diagnosis of T2DM within the preceding 12 months prior to screening, established by ADA or WHO criteria: fasting plasma glucose ≥ 126 mg/dL on two separate occasions, and/or 2-hour OGTT plasma glucose ≥ 200 mg/dL, and/or HbA1c ≥ 6.5%, and/or random plasma glucose ≥ 200 mg/dL with classic hyperglycemic symptoms.
✓. HbA1c between 6.5% and 7.5 % inclusive at screening.
✓. Treatment-naive: no prior antidiabetic pharmacological treatment, or any prior antidiabetic treatment discontinued at least 3 months before screening.
✓. Estimated glomerular filtration rate (eGFR) ≥ 45 mL/min/1.73m² by CKD-EPI formula at screening.
✓. Willing and able to provide written informed consent in Arabic or English.
✓. Able to attend all scheduled study visits and comply with study procedures, dietary restrictions, and pre-analytical blood collection requirements.
Exclusion criteria
✕. Type 1 diabetes mellitus, Latent Autoimmune Diabetes in Adults (LADA), or other specific types of diabetes (anti-GAD antibody positivity, monogenic diabetes).
What they're measuring
1
To compare the change in fasting plasma pyruvate/lactate ratio from baseline (Week 0) to the end of the treatment period (Week 12) between patients with newly diagnosed T2DM randomized to imeglimin monotherapy versus metformin monotherapy.
Timeframe: Mitochondrial redox and metabolic assessments will be performed at baseline (Week 0) and at the end of the treatment period (Week 12).
2
Change (Delta) in fasting plasma pyruvate/lactate ratio from Week 0 (Baseline) to Week 12 (end of treatment period).
✕. eGFR \< 45 mL/min/1.73m² - increase risk of drug accumulation and lactic acidosis.
✕. 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.
✕. 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.
✕. Active or recent (within 3 months) use of any antidiabetic pharmacological agent.
✕. Current use of medications known to significantly affect mitochondrial function or lactate/pyruvate metabolism: valproate, linezolid, nucleoside reverse transcriptase inhibitors (NRTIs), phenformin, zidovudine, or high-dose thiamine-depleting regimens.
✕. Pregnancy, planned pregnancy within the trial period, or active breastfeeding.