Leigh syndrome mitochondrial transfer therapy
preclinicaldrug program · high · Tue Sep 10 2024 00:00:00 GMT+0000 (Coordinated Universal Time)
Treat inherited mitochondrial disease, specifically Leigh syndrome, by improving morbidity, mortality, neurological function, and energy metabolism through mitochondria transfer-based approaches.
Mitochondria transfer-based therapy using wild-type or human isolated mitochondria, and bone marrow transplantation associated with extracellular mitochondria transfer, tested in Ndufs4-/- Leigh syndrome mouse models.
2024 publication / LUCA Science news release reported reduced morbidity and mortality of Leigh syndrome in mouse treatment paradigms.
Wild-type bone marrow transplantation ameliorated Leigh syndrome in mice; isolated wild-type mitochondria extended lifespan, improved neurological function, and increased energy expenditure; human mitochondria also improved Leigh syndrome in mice, while Ndufs4-/- mitochondria did not improve neurological function.
Functional mitochondria therapeutic platform
preclinicalplatform · high
Develop functional mitochondria as storable, deliverable biopharmaceutical therapeutic agents for damaged tissues, damaged organs, and mitochondrial dysfunction-related diseases.
Proprietary isolation of high-quality mitochondria / Mitochondria oRganelle Complex from cryopreserved cell stocks, combined with delivery and formulation technology for storage and administration.
2026 publication characterized cryopreserved MRC-Q structural integrity, respiratory capacity, catalase activity, cellular uptake, ATP effects, and oxidative-stress resistance in recipient cells.
MRC-Q maintained high membrane integrity and respiratory capacity after cryopreservation and thawing; in human fibroblasts and vascular endothelial cells it increased respiration, ATP levels, electron transport chain component expression, TFAM expression, and resistance to oxidative stress.
Kyowa Kirin joint research on mitochondrial disease treatment
exploratoryresearch program · medium
Research treatment of mitochondrial disease using a novel mitochondria modality.
Joint research agreement between LUCA Science and Kyowa Kirin on mitochondrial disease treatment with a novel mitochondria modality.
Joint research agreement announced in public news coverage.
Mitochondrial therapy for myocardial infarction / cardiac ischemia-reperfusion injury
preclinicaldrug program · high
Prevent or reduce myocardial ischemia-reperfusion injury and protect cardiomyocytes after cardiac injury.
Administration of freeze-thawed allogeneic mitochondrial organelle complex Q in mouse and porcine cardiac ischemia-reperfusion injury models, with in vitro hypoxia/reoxygenation testing in H9C2 cardiomyocytes.
2026 JACC Asia publication reported cardioprotective effects in mouse and pig preclinical models; earlier joint research with Nagoya University was announced on December 1, 2020.
MRC-Q reduced infarct size, decreased apoptotic cells and circulating cardiac enzymes, improved cardiac function, improved cardiomyocyte viability after hypoxia/reoxygenation, and supported mitochondrial quality control, ATP production, and anti-reactive oxygen species activity.
MRC-Q treatment for adipose tissue remodeling in metabolic disease
preclinicalresearch program · high
Evaluate whether mitochondrial preparation treatment can protect against obesity-related adipose tissue inflammation, remodeling, blood glucose elevation, and glucose intolerance.
Intraperitoneal administration of frozen-thawed isolated mitochondrial preparations every two weeks in a high-fat diet-induced obesity mouse model, with in vitro macrophage polarization experiments.
2025 Circulation Reports publication reported effects of MRC-Q in diet-induced obesity mice and macrophage assays.
MRC-Q reduced adipose tissue amount and body weight, reduced blood glucose, improved glucose tolerance, promoted M2 macrophage polarization, suppressed pro-inflammatory responses in visceral fat, and directly transformed macrophages toward the M2 phenotype in vitro.
