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The Significant Role of Tregs in Neurodegenerative, Autoimmune, and Metabolic Diseases

Since the discovery of Tregs in 1995 by Dr. Shimon Sakaguchi, a member of our Scientific Advisory Board, we have continued the development and research of Tregs by leveraging the scientific discoveries of Dr. Stanley Appel, who is also a member of our Scientific Advisory Board, and his research team at Houston Methodist Hospital (“Methodist”) in Houston, Texas.


Tregs Overview

Tregs Overview in Neuroinflammation & Neurodegenerative Diseases

Recent scientific evidence from Dr. Appel demonstrates that dysregulation of the immune system negatively impacts the severity and progression of neurodegenerative conditions such as amyotrophic lateral sclerosis (“ALS”), Alzheimer’s disease (“AD”), and frontotemporal dementia (“FTD”). In particular, Dr. Appel discovered that Tregs are both reduced in numbers and function in these patients suffering from neurodegenerative diseases, and more marked reduction could be associated with more rapid disease progression.

 

Discovery that Treg dysfunction is a core driver of Neurodegenerative Disease

Treg Function Predicts ALS Survival, Disease Progression, and Burden of Disease

 Survival  survival
Survival to 100 AALS Points  survival to 100AALS points

Treg dysfunction is also central to Alzheimer’s Disease, Parkinson’s Disease, and Frontotemporal Dementia*


Tregs Overview in Autoimmune and Metabolic Diseases

Dysfunctional Tregs underlie many diseases, driven by the chronic inflammatory environment and high levels of oxidative stress commonly observed autoimmune diseases, metabolic diseases (liver inflammation & fibrosis, systemic sclerosis, aka scleroderma) . Our research suggests, the degree of Treg dysfunction is associated with the severity and progression of serious and life-threatening conditions.

 

 

Treg-Derived Exosome Overview

Orders of magnitude more potent via immunomodulation and immunosuppression than industry standard mesenchymal stem cells

The iscEXOTM Platform: Coya has developed a first-in-class exosome or extracellular vesicle (EV) product
  • Highly suppressive ex vivo expanded immunosuppressive cells (the iscEXOTM Platform)


Most Potent Anti-inflammatory Exosome Platform: derived from two of the most prominent anti-inflammatory and neuroprotective cell types- Tregs and M2 Macrophages
  • Leverage mesenchymal stem cell (MSc) derived EVs
  • EVs are not cells and avoid potential cell-based issues such as immune rejection and polarization to a pro-inflammatory cell type
whatareEVs
Unique and Differentiated Approach:
Compared to MSc Derived Exosomes, iscEXOTM is significantly more immunosuppressive

 

What makes our exosome platform different?

01
Most companies leverage mesenchymal stem cell (MSC) derived exosomes, not Treg derived exosomes
02
Treg derived exosomes have higher suppressive capacity and inflammatory function than MSc derived exosomes
03
Coya has developed the only manufacturing platform to isolate highly neuroprotective Treg derived exosomes (not feasible without Coya’s primary proprietary Treg expansion process)
04
Coya has optimized cryopreservation and full functional stability of Treg exosomes 12+ months post thaw allowing for chronic off the shelf administration
05
Coya’s Manufacturing platform allows isolation, normalization, and expansion of cells while concurrently extracting cellular EV contents.

 

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First in Class Treg Derived Exosomes Platform

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Tregs maintain tolerance to self and limit other immune responses—they achieve this through different mechanisms including the release of exosomes