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Houston-Based Coya Therapeutics To Present Results From ALS Clinical Study Data For Its Investigational Biologic Combination at the 2023 MDA Clinical & Scientific Conference in Dallas

Coya Therapeutics, Inc. (NASDAQ: COYA) recently announced the presentation of results from an academic clinical study in patients with Amyotrophic Lateral Sclerosis (ALS) with Coya’s proprietary investigational biologic combination at the 2023 MDA Clinical & Scientific Conference in Dallas, Texas, to be held in-person and virtually from March 19 to March 22, 2023.

The proof-of-concept open-label clinical study is the first-of-its-kind evaluating a dual-mechanism immunotherapy for the treatment of ALS. Patients in the study received investigational treatment for 12 consecutive months and were evaluated for safety and tolerability, Treg function, serum biomarkers of oxidative stress and inflammation, and clinical functioning as measured by the ALSFRS-R scale. The dual-mechanism investigational biologic combination combines low dose Interleukin-2 that is intended to enhance anti-inflammatory regulatory T cell function with a fusion protein that is intended to suppresses pro-inflammatory cell function and has been designed to be administered subcutaneously to minimize treatment burden for patients and caregivers.

ALS is a disease of the parts of the nervous system that control voluntary muscle movement. In ALS, motor neurons (nerve cells that control muscle cells) are gradually lost. As these motor neurons are lost, the muscles they control become weak and then nonfunctional, thus leading to muscle weakness, disability, and eventually death. ALS is the most common form of motor neuron disease.

The study was conducted at the Houston Methodist Research Institute (Houston, Texas) by Stanley Appel, M.D., Jason Thonhoff, M.D., Ph.D., and David Beers, Ph.D.

Dr. Appel is chair of Coya’s Scientific Advisory Board and is former chair of the Stanley H. Appel Department of Neurology. He is the director of the Ann Kimball & John W. Johnson Center for Cellular Therapeutics, Professor of Neurology at Weill Cornell Medical College, and the Peggy and Gary Edwards Distinguished Chair for the Treatment and Research of ALS at the Houston Methodist Research Institute.

Presentation details are:

  • Title: Novel Treg-modulating Immunotherapy Targets Inflammation in ALS.
  • Date: Tuesday, March 21, 2023, at 11:00 am CST
  • Conference: 2023 MDA Clinical & Scientific Conference (https://www.mdaconference.org)

This article was originally published on Benzinga here.

About Coya Therapeutics, Inc.

Headquartered in Houston, TX, Coya Therapeutics, Inc. (Nasdaq: COYA) is a clinical-stage biotechnology company developing proprietary treatments focused on the biology and potential therapeutic advantages of regulatory T cells (“Tregs”) to target systemic inflammation and neuroinflammation. Dysfunctional Tregs underlie numerous conditions including neurodegenerative, metabolic, and autoimmune diseases, and this cellular dysfunction may lead to a sustained inflammation and oxidative stress resulting in lack of homeostasis of the immune system. Coya’s investigational product candidate pipeline leverages multiple therapeutic modalities aimed at restoring the anti-inflammatory and immunomodulatory functions of Tregs. Coya’s therapeutic platforms include Treg-enhancing biologics, Treg-derived exosomes, and autologous Treg cell therapy. Coya’s 300 Series product candidates, COYA 301 and COYA 302, are biologic therapies intended to enhance Treg function and expand Treg numbers. COYA 301 is a cytokine biologic for subcutaneous administration intended to enhance Treg function and expand Treg numbers in vivo, and COYA 302 is a biologic combination for subcutaneous and/or intravenous administration intended to enhance Treg function while depleting T effector function and activated macrophages. These two mechanisms may be additive or synergistic in suppressing inflammation.

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Contact Details

David S. Snyder

David@coyatherapeutics.com

Company Website

https://coyatherapeutics.com/

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