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

Coya Therapeutics, Inc. (“Coya” or the “Company”), a clinical-stage biotechnology company developing biologics primarily focused on the restoration of regulatory T cell (Treg) immunomodulatory function, announces the presentation of data demonstrating the role of the peripheral immune system in the pathophysiology of Frontotemporal Dementia (FTD) from a biomarker study conducted at the Houston Methodist Hospital by Dr. Stanley Appel and Dr. Alireza Faridar and funded by the Houston Methodist Clinical Scholar Award Program. The poster presentation was shared for the first time today at the AD/PD 2024 Conference in Lisbon, Portugal and can be found here. The poster is titled, “Deciphering the Role of the Peripheral Immune System in the Pathology of Frontotemporal Dementia.”

“The data from this biomarker study clearly depicts a compromised peripheral immune environment present in patients with FTD that, we believe, contributes to the pathophysiology of the disease process. Further, we believe that targeting systemic inflammation with COYA 302 may lower both peripheral and central nervous system inflammatory cell types while enhancing Treg function and may be a meaningful approach for FTD. We intend to file an Investigational New Drug (IND) application with the FDA for COYA 302 in FTD later this year and initiate a Ph. 2 trial in FTD patients shortly thereafter,” stated Fred Grossman, Chief Medical Officer at Coya Therapeutics.

Summary of Study Results

The study was designed to evaluate Treg immunosuppressive function, monocyte mRNA expression, levels of inflammatory cytokines and chemokines, and immune cell markers in peripheral blood mononuclear cells (PBMCs) in blood samples of 22 FTD patients and 11 age-matched healthy individuals as a control group.

Treg Function Compromised: Treg suppressive function was significantly reduced in FTD, compared to controls (p<0.01), demonstrating that Treg immunomodulatory function is negatively impacted in FTD.

Pro-Inflammatory Systemic Immune Activity: Plasma levels of inflammatory chemokines and cytokines, including C-X-C motif chemokine ligand 9 (CXCL9), CXCL10, CXCL11, CXCL12, tumor necrosis factor alpha (TNFα), chemokine (C-C motif) ligand 3 (CCL3), CCL7, and colony stimulating factor 1 (CSF-1) were consistently and significantly increased in FTD patients (p<0.05). In addition, several inflammation transcripts in monocyte genes known to be involved in neuroinflammatory signaling pathways were dysregulated in FTD, compared to controls.