Coya Therapeutics Announces Pipeline Expansion of COYA 302 to Include Frontotemporal Dementia and Parkinson’s Disease in Addition to Amyotrophic Lateral Sclerosis - Seite 2

The Company also announces its key milestones and catalysts anticipated in 2024, including:

H1 2024:

• COYA 302 File IND and Initiate Phase 2 Trial in ALS Patients
• COYA 302 Publication of Phase 1 Investigator Initiated Trial clinical data in ALS Patients
• COYA 302 Publication of Longitudinal Biomarker study with correlation to patient survival in ALS Patients
• COYA 302 Presentation on Longitudinal Biomarker Data in ALS Patients at Conference
• COYA 301 Presentation of Phase 1 Investigator Initiated Trial data in AD Patients at 18^th annual AD + PD Conference

H2 2024:

• COYA 302 First patient dosed in Phase 2 Trial in ALS Patients
• COYA 302 File IND and Initiate Phase 2 Trial in FTD Patients
• COYA 302 Animal data released in PD model
• COYA 301 Proof of Concept combination data with Drug X in AD mouse model
• COYA 301 Phase 2 Investigator Initiated Trial Topline AD data Presented (Summer)

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. 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 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.