Scientists have uncovered a potential new treatment for heart failure with preserved ejection fraction (HFpEF)—and it’s one that already exists.
Steven Houser, PhD, of the Lewis Katz School of Medicine at Temple University, and colleagues said in their Science Translational Medicine study that rather than start from scratch with a new HFpEF therapy, they’d comb through the vast catalogue of medical drugs already approved for use in clinical practice. Repurposing existing therapies is becoming a more popular practice in a landscape where it costs on average $19 million to push a new drug through to FDA approval.
“Although many people suffer from HFpEF, there are currently no FDA-approved therapies available for the problem,” Houser said in a release.
“We know from previous research that heart cells from patients with HFpEF have abnormalities in the genes that are being activated as well as in the function of the proteins that they encode. The alterations in gene expression and protein activity in these cells involve a group of enzymes known as histone deacetylases (HDACs).”
HDAC-blocking drugs have already been developed to treat other diseases, Houser said, including cancer. One HDAC inhibitor, known as suberoylanilide hydroxamic acid (SAHA) and sold under the brand name Zolinza, looked particularly attractive as a candidate for HFpEF therapy.
Houser and his team tested SAHA, which is currently approved to treat cutaneous T-cell lymphoma, in a group of animals with lab-induced HFpEF. Like humans, the animals’ HFpEF presented with exercise intolerance, shortness of breath and tissue changes including heart remodeling. After treatment with SAHA, there were noticeable differences.
One of the most noticeable improvements with SAHA seemed to be reduced left ventricular hypertrophy, according to the study’s results. The left ventricle in treated animals was also much more relaxed than in untreated animals, allowing the heart to function more normally.
Houser said researchers are still working to determine what exactly makes HFpEF heart cells abnormal, noting that “if we can figure out why, we may be able to find a more targeted approach to develop entirely new treatments for HFpEF.”
“The remarkable thing is that this therapy could be tested in HFpEF patients today,” he said.