Heart failure affects over 6 million adults in the US and can lead to irreversible damage to the heart.

The Need

In the realm of cardiovascular health and the management of heart-related disorders, there exists a pressing commercial need for a technology that can effectively address the challenges presented by failing hearts, chronic pressure overload, and cardiac energy metabolism. These conditions necessitate a solution that can enhance cardiac function, reduce hypertrophic markers, and optimize energy utilization with the heart muscle.

The Technology

Researchers at The Ohio State University have developed a gene therapy solution that enables the precise modulation of CPT1a expression, influencing critical cardiac functions and survival mechanisms. CPT1a plays a pivotal role in determining the rate of long-chain fatty acid oxidation in the heart. The OSU researchers have shown that increasing CPT1a expression in the heart offers protection against functional decline during hypertrophic decompensation, leading to improved ejection fraction with chronic pressure overload.

Commercial Applications

• Cardioprotection: By increasing CPT1a expression in the heart, our technology offers protection against functional decline during hypertrophic decompensation, leading to improved ejection fraction with chronic pressure overload.
• Enhanced Energy Utilization: CPT1a modulation ensures the maintenance of long-chain fatty acid oxidation and optimal bioenergetic states in the heart, crucial for sustained energy production.
• Reduction in Hypertrophy: Our technology significantly reduces hypertrophic and profibrotic gene expression, thereby preventing adverse cardiac remodeling.
• Targeted miRNA Regulation: The technology incorporates miR370 regulation, enabling precise control over CPT1a gene expression, further enhancing cardioprotective effects and minimizing adverse cardiac remodeling.

Benefits/Advantages

• Improved Cardiac Function: CPT1a modulation preserves ejection fraction, ensuring better overall heart function during hypertrophic decompensation

• Optimized Energy Production: The technology maintains long-chain fatty acid oxidation and a favorable bioenergetic state, promoting efficient energy utilization under chronic pressure overload

• Reduced Hypertrophy and Fibrosis: By decreasing hypertrophic and profibrotic gene expression, the technology mitigates the risk of adverse cardiac remodeling

Provisional patent application filed