Coya Therapeutics Presents Biomarker Data on Neuroinflammatory Pathways in Frontotemporal Dementia (FTD) at the AD/PD 2024 Conference - Seite 2

Results of the study demonstrate that FTD patients exhibit a compromised immunosuppressive function of Tregs, along with increased peripheral levels of inflammatory cytokines and chemokines, dysregulation of peripheral monocyte’s inflammation transcriptome and systemic activation of the inflammatory cascade, supporting the critical role of the immune system in the pathophysiology of FTD. The data in FTD is consistent the Treg dysfunction and increased levels of inflammatory cytokines and chemokines previously reported by Coya in other serious and progressive neurodegenerative diseases and support the multi-pathway combination approach of COYA 302 to target numerous components of the dysfunctional immune system.

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.