Joint effort to leverage existing collaboration and non-dilutive grants to advance development of proprietary Treg exosome technology towards a first-in-human clinical study, continue work on validating biomarkers in a variety of neurodegenerative diseases, and explore novel synergistic drug combinations with COYA 301 (proprietary Low Dose Interleukin-2, or LD IL-2)
HOUSTON--(BUSINESS WIRE)-- Coya Therapeutics, Inc. (NASDAQ: COYA) (“Coya” or the “Company”), a clinical-stage biotechnology company developing biologics intended to enhance regulatory T cell (Treg) function, announces the expansion of its research collaboration with the Houston Methodist Research Institute (“HMRI”) through a sponsored research agreement (SRA) covering multiple initiatives.
The development and production of exosomes from patients’ regulatory T cells will be funded by the Johnson Center for Cellular Therapeutics with participation of the SRA from Coya to Dr. Stanley Appel, Director of the Johnson Center and Chair of Coya’s Scientific Advisory Board.
Coya and HMRI will advance the development of multiple patented modalities of exosomes, including full characterization of the nanovesicles, and GMP manufacturing to enable a first-in-human academic clinical study. Furthermore, Coya will continue the characterization and validation of several clinical biomarkers in patients with Amyotrophic Lateral Sclerosis, Alzheimer’s Disease, Frontotemporal Dementia, and Parkinson’s Disease. These proprietary biomarkers will provide valuable tools to better objectively correlate disease status and biological processes, improve the criteria for participation and stratification in clinical studies, and assess treatment response. In addition, Coya and HMRI will continue exploring the potential synergy of COYA 301 (LD IL-2) with other relevant drug products, following the innovative approach of COYA 302 (LD IL-2 + CTLA4-Ig) targeting multiple paths involved in the pathophysiology of severe neurodegenerative and autoimmune diseases. Biologic combinations serve as the cornerstone of Coya’s unique approach in addressing the complex pathophysiology of diseases and offer future opportunities for strategic collaborations.
About COYA 301 COYA 301 is the company’s proprietary investigational low-dose interleukin-2 (IL-2) intended to enhance the anti-inflammatory function of regulatory T Cells and is designed for subcutaneous administration.
About COYA 302 COYA 302 is an investigational and proprietary biologic combination therapy with a dual immunomodulatory mechanism of action intended to enhance the anti-inflammatory function of regulatory T cells (Tregs) and suppress the inflammation produced by activated monocytes and macrophages. COYA 302 is comprised of proprietary low dose interleukin-2 (LD IL-2) and CTLA-4 Ig and is being developed for subcutaneous administration for the treatment of patients with ALS, FTD, and PD. These mechanisms may have additive or synergistic effects.
In February of 2023, Coya announced results from a proof-of-concept, open-label clinical study evaluating commercially available LD IL-2 and CTLA-4 Ig in a small cohort of patients with ALS 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. This study was the first-of-its-kind evaluating this dual-mechanism immunotherapy for the treatment of ALS. Patients in the study received investigational treatment for 48 consecutive weeks 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.
During the 48-week treatment period, the therapy was well tolerated. The most common adverse event was mild injection-site reactions. No patient discontinued the study, and no deaths or other serious adverse events were reported.
Patients' disease progression was measured using the ALSFRS-R scale, a validated rating tool for monitoring the progression of disability in patients with ALS. The mean (±SD) ALSFRS-R scores at week 24 (33.75 ±3.3) and week 48 (32 ±7.8) after initiation of treatment were not statistically different compared to the ALSFRS-R score at baseline (33.5 ±5.9), suggesting significant amelioration in the progression of the disease over the 48-week treatment period.
Treg suppressive function, expressed as percentage of inhibition of proinflammatory T cell proliferation, showed a statistically significant increase over the course of the treatment period and was significantly reduced at the end of the 8-week washout post-treatment period. Treg suppressive function at 24 weeks (79.9 ±9.6) and 48 weeks (89.5 ±4.1) were significantly higher compared to baseline (62.1 ±8.1) (p