Use of interferon-gamma antibody to reduce damage to the heart after myocardial infarction
NU 2024-243
INVENTORS
SHORT DESCRIPTION
Interferon-gamma antibodies to improve heart function after myocardial infarction (MI)
BACKGROUND
Myocardial infarction (MI) can trigger inflammation that contributes to adverse cardiac remodeling, which increases the risk of heart failure and mortality. The inflammation is primarily due to elevated cytokine activities. Existing therapeutics for MI such as antiplatelets, anticoagulants, and thrombolytics target blood clot prevention and removal, but anti-inflammatory therapies targeting cytokines are still underdeveloped. While IL-1β inhibitors (e.g., canakinumab) have shown promise in improving patient outcomes, other cytokine inhibitors have yielded mixed results, suggesting the need for better therapeutic approaches. Interferon-gamma (IFN-g) is a key pro-inflammatory cytokine in immune cell activation but its role in MI remains understudied.
ABSTRACT
Northwestern researchers have shown that targeting IFN-g signaling is a viable strategy for cardiac protection after MI. They identified the role of tricarboxylic acid (TCA) cycle-related enzymes in heart remodeling, as well as the impact of IFN-g on post-MI inflammation and metabolism. The research identified a disruption in the TCA cycle, specifically affecting α-ketoglutarate dehydrogenase (α-KGDH) due to increased tristetraprolin (TTP) activity, which is driven by elevated interferon-gamma (IFN-γ) levels. They showed that IFN-g neutralizing antibody reduced the inhibition of α-KGDH, thus preserving mitochondrial function and reduced adverse cardiac remodeling. This strategy represents a promising avenue for enhancing cardiac protection and function following MI and reduce healthcare cost.
APPLICATIONS
ADVANTAGES
IP STATUS
A provisional application has been filed.