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

HOUSTON, TX — Coya Therapeutics, Inc., 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.

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.

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<0.01), suggesting enhanced and durable Treg suppressive function over the course of treatment. In contrast, Treg suppressive function (mean ±SD) was significantly decreased at the end of the 8-week washout period compared to end-of-treatment at week 48 (70.3 ±8.1 vs. 89.5 ±4.1, p <0.05).

The study also evaluated serum biomarkers of inflammation, oxidative stress, and lipid peroxides. The available data up to 16 weeks after initiation of treatment suggest a decrease in these biomarker levels, which is consistent with the observed enhancement of Treg function. The evaluation of the full biomarker data is ongoing.

COYA 302 is an investigational product not yet approved by the FDA or any other regulatory agency.


About Amyotrophic Lateral Sclerosis

Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s Disease, is a rare neurological disease that affects motor neurons, the nerve cells in the brain and spinal cord that control voluntary muscle movement. About 20,000 people live with ALS in the United States and approximately 5,000 new cases are diagnosed every year. The disease is progressive, meaning the symptoms get worse over time. The functional status of ALS patients declines about 1 point per month on average, as measured by the Revised ALS Function Rating Scale, or ALSFRS-R, a validated tool to monitor the progression of the disease.

ALS has no cure, and the currently approved drug treatments provide limited benefit to patients. ALS is a type of motor neuron disease. As motor neurons degenerate and die, they stop sending messages to the muscles, which causes the muscles to weaken, start to twitch (fasciculations), and waste away (atrophy). Eventually, the brain loses its ability to initiate and control voluntary movements. Most people with ALS die from respiratory failure, usually within three to five years from when the symptoms first appear.


About Frontotemporal Dementia

Frontotemporal dementia (FTD) is the result of damage to neurons in the frontal and temporal lobes of the brain. Many possible symptoms can result, including unusual behaviors, emotional problems, trouble communicating, difficulty with work, or difficulty with walking. FTD is rare and tends to occur at a younger age than other forms of dementia. About 60% of people with FTD are 45 to 64 years old. FTD is progressive, meaning symptoms get worse over time. In the early stages, people may have just one symptom. As the disease progresses, other symptoms appear as more parts of the brain are affected. It is difficult to predict how long someone with FTD will live. Some people live more than 10 years after diagnosis, while others live less than two years after they are diagnosed. There is no cure for FTD, and no treatments slow or stop the progression of the disease.



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