In a new study, researchers found that a common form of heart failure could be treated with an already approved anticancer drug.
The research was conducted by scientists at the Lewis Katz School of Medicine at Temple University.
When it comes to finding new treatments for disease, reinventing the wheel is not always necessary—drugs already in use for other conditions may do the job.
And if it turns out that a pre-existing drug works, getting it approved for the treatment of another disease can happen much more quickly than for entirely new drugs never previously tested in people.
This fast-tracking approach may now prove valuable—and potentially life-saving—for patients with a common form of heart failure known as heart failure with preserved ejection fraction (HFpEF).
Many patients with HFpEF feel fine at rest but experience shortness of breath upon physical exertion because their sick heart struggles to pump enough blood to meet the body’s needs.
HFpEF usually worsens over time, leading to major declines in quality of life, and often death.
In the study, the researchers show that a drug already approved for the treatment of some forms of cancer can reverse HFpEF symptoms and improve the heart’s ability to pump blood in an HFpEF animal model.
Previous research has shown 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).
Drugs that block HDAC activity have already been developed for other diseases, including cancer.
The team tested the effects of an HDAC inhibitor known as SAHA on animals with HFpEF.
SAHA, marketed under the name Zolinza, is currently approved for the treatment of a form of cancer known as cutaneous T-cell lymphoma.
The teams found treatment with SAHA showed amazing effects. The left heart ventricle was much more relaxed, enabling the heart to fill and pump more effectively and leading to overall improvements in heart structure and function.
The team now plans to examine what specifically makes heart cells in HFpEF abnormal. They hope to find a more effective approach to develop entirely new treatments for HFpEF.
One author of the study is Steven Houser, Ph.D., FAHA, Senior Associate Dean of Research.
The study is published in Science Translational Medicine.
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