Tackling Inflammation With Innovative Alzheimer Disease Treatments: Stanley H. Appel, MD
The director of the Ann Kimball and John W. Johnson Center for Cellular Therapeutics at Houston Methodist Hospital talked about the phase 2 study assessing low-dose COYA 301 in mild-to-moderate Alzheimer disease and the focus on inflammation in this patient population. [WATCH TIME: 5 minutes]
WATCH TIME: 5 minutes
“Our innovative therapy, utilizing low-dose COYA 301, holds the promise of not only slowing the rate of progression but potentially offering better outcomes for patients with neurodegenerative diseases."
COYA 301 (Coya Therapeutics), an investigational interleukin-2 (IL-2) treatment, is a combination immunotherapy designed to lower activated T effector cells and activated macrophages/microglia, while increasing peripheral T cell regulatory (Treg) function and numbers. Previous findings from a proof-of-concept phase 1 study (NCT05821153) assessing the low-dose COYA 301 indicated sustained cognition among patients with Alzheimer disease (AD). The therapy also restored Treg function and ameliorated systemic pro-inflammatory mediators.1
In a recent announcement, the randomized, double-blind, placebo-controlled phase 2 study (NCT06096090) of low-dose COYA 301 in patients with mild-to-moderate AD completed enrollment.2 In this study, investigators will assess the safety and tolerability, biological activity, blood and cerebrospinal fluid biomarkers, neuroimaging, and changes in cognitive function of LD IL-2 compared with the placebo at prespecified timepoints in a 21-week treatment period and at 9 weeks after the last dose administered. According to a recent release, the company noted that the topline results of the study are anticipated to be reported in summer 2024.2
Recently, coprincipal investigator Stanley H. Appel, MD, director of the Ann Kimball and John W. Johnson Center for Cellular Therapeutics at Houston Methodist Hospital, sat down in an interview with NeurologyLive® to discuss how Coya Therapeutics' approach to targeting inflammation differs from the ß-amyloid hypothesis in AD treatment. Appel also talked about the promising results observed in animal models using low-dose IL-2 to enhance regulatory T-cell functionality in AD. In addition, he explained how the research shift from AD to frontotemporal dementia addresses the unmet needs faced in patients with the condition, and the potential anticipated breakthroughs.
