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Enhancement Therapy

Mitochondrial Enhancement for T Cell Reprogramming

Enhancement Therapy

Mitochondrial Enhancement for T Cell Reprogramming

T cell reprogramming by mitochondrial replacement

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.

It is all about the mitochondria

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.

Targeting the growing population of elderly cancer patients

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!

The path to T-cell exhaustion and senescence involves dysfunctional mitochondria

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.

Mitochondrial dysfunction is one of the hallmarks of aging

Acquired mitochondrial dysfunction is involved in many age-related disorders such as neurodegenerative diseases, cancer, and inflammatory diseases.

  • Alzheimer’s disease
  • Immunosenescence
  • Pulmonary fibrosis
  • Chronic kidney disease
  • COPD
  • Metabolic disease
  • Cardiovascular disease
  • Liver disease

Inherited mitochondrial disfunction are manifested in multiple genetic diseases

Inherited mitochondrial disorders are caused by mutations in mitochondrial or nuclear DNA and is involved in more than 50 genetic-related diseases, including:

  • Leigh syndrome
  • LHON
  • cPEO
  • KSS
  • Bath Syndrome
  • Friedreich’s Ataxia

Our approach:
Next-generation T cell reprograming

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.

The new era
of mitochondrial therapies

IMEL’s products: Autologous mitochondria-replaced T cells

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.

1: Collect

Collect blood cells via apheresis

2: Select

Select target cells

3: Replace

Replace target cells with the healthy donor mitochondria

4: Prepare

Prepare cell-based product for treatment

5: Infuse

Mitochondria replaced product

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Board of Directors

Advisory board

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