IMEL is developing a novel game-changing mitochondrial replacement approach for cell-based therapies. Its core technology demonstrates a remarkable >90% replacement of dysfunctional mitochondria. Reprogrammed T cells are shown to regain functionality, to overcome exhaustion in elderly people, and recover the ability of immune cells to persist and self-renew. Reprogrammed T cells are shown to regain functionality, to overcome exhaustion in elderly people, and recover the ability of immune cells to persist and self-renew.
Mitochondria are the primary source of energy production in a cell. These organelles are found in almost every cell in the body and are critical for healthy organ function. Additionally, they orchestrate cell fate and are involved in innate and acquired immune systems. Mitochondrial dysfunction is one of the hallmarks of aging that plays a key role in the development of senescence and exhaustion in the T cells of the elderly population.
Cancer can develop at any age, but the incidence of cancer rises dramatically at the latter stage of life. As people age, their T cells become exhausted and are no longer able to fight tumors effectively.
Check point inhibitors resistance in the elderly, partially caused by T cell exhaustion, represents a significant obstacle for therapy.
Elderly patients deserve better therapies!
Naïve (stem-like) T cells, with healthy mitochondria, differentiate to effector cells to meet the demands of the immune system. In the healthy population, some of the differentiated effector T cells regenerate regularly. However, in elderly people, the exhausted effector cells lose the ability to regenerate. They become terminally differentiated with damaged and dysfunctional mitochondria. T cell exhaustion means poor anti-tumor activity. There is a pressing need for a solution to reverse T cell exhaustion.
Acquired mitochondrial dysfunction is involved in many age-related disorders such as neurodegenerative diseases, cancer, and inflammatory diseases.
Inherited mitochondrial disorders are caused by mutations in mitochondrial or nuclear DNA and is involved in more than 50 genetic-related diseases, including:
IMEL cell-based therapy enhances mitochondrial function by replacing dysfunctional mitochondria with young mitochondria. IMEL’s mitochondrial replacement (MirC) process increases the number of healthy mitochondria in a cell. By doing so we restore mitochondrial function to revert T cell exhaustion to a stem-like behavior. The technology can potentially be applied to improve existing T cell-based therapies in solid tumor indications and also be applicable to a wide range of age-associated indications that currently have no treatment options.
We are developing autologous mitochondria-replaced T cells (Mir T Cells) as an intravenously infused cell therapy to reprogram aged immune cells and restore cellular functionality with enhanced agonist activation capacity. The patient’s cells are collected, undergo the mitochondrial replacement process, and returned to the patient.
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