Coya Therapeutics Presents ALS Biomarker Data at Society of Neuroimmune Pharmacology Conference

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 that Dr. Stanley Appel, M.D., Chairman of Coya’s Scientific Advisory Board and Dr. David Beers, Ph.D., Associate Research Professor of Neurology, Houston Methodist, will present biomarker data today as part of a panel presentation at the Society of Neuroimmune Pharmacology Conference.

The data presented highlights the strong predictive value of levels of an oxidative stress biomarker (4-HNE) with the rate of disease progression and survival in 50 ALS patients from a longitudinal patient registry cohort. An additional analysis of another random 50 patients from the same patient registry cohort is being finalized and will be presented in the future. In a proof-of-concept study in patients with ALS, the combination of low dose interleukin-2 (LD IL-2) and CTLA-4 Ig appeared to lower 4-HNE and other proinflammatory biomarker levels. Coya intends to finalize the analysis of the initial 50 patients, as well as the additional 50 ALS patients, and publish the results in a peer review journal in the near future. Furthermore, Coya has filed patent applications relating to the use of the biomarker in ALS. The biomarker data can be viewed here.

Stanley Appel, M.D., Chairman of Coya’s SAB, commented: “We believe these studies of the first set of 50 ALS patients from our database document the correlation of 4-HNE with the progression of disease and patient survival and support the potential importance of 4-HNE as a biomarker.”

Fred Grossman, Chief Medical Officer at Coya, commented, “Based on the strength of the biomarker data, Coya plans to discuss with the FDA the goal of validating 4-HNE as a new potential biomarker for predicting progression and survival in patients with ALS.”

4-HNE Relevance in Disease Pathophysiology

Reactive oxygen species (ROS) are generated mainly as byproducts of mitochondrial respiration and are tightly controlled by multiple anti-oxidant mechanisms. In neurodegenerative diseases, such as ALS, when the antioxidant system is overwhelmed by overproduction of ROS, oxidative stress occurs. 4-HNE, an abundant and reactive oxygen species, is thought to exert neuronal toxicity ultimately through formation of toxic protein aggregates, such as those seen in ALS patients. Additionally, 4-HNE appears to be causally involved in multiple pathophysiologic events associated with disease pathophysiology, including motor neuron death.