WARF: P120252US02

Treating Heart Failure by Inhibiting Myosin Interaction with a Regulatory Myosin Binding Protein


Richard Moss, Ariel Fernandez

The Wisconsin Alumni Research Foundation (WARF) is seeking commercial partners interested in developing and using peptides that promote cardiac muscle contraction by disrupting the binding of MyBP-C to myosin.
OVERVIEWIn the United States, one in every four deaths is attributed to heart disease. That amounts to about 600,000 people every year. Heart failure can arise due to many causes, such as heart attack and coronary artery disease, and generally is characterized by deficient blood pumping. Diagnosing and supporting patients suffering from these diseases costs hundreds of billions of dollars.

Current medications, like diuretics and beta adrenergic receptor blockers, can have deleterious side effects and do not improve prognosis. Many patients would benefit from new, safe and effective treatment options. One promising approach looks to better understand and harness the molecular mechanisms of heart function.
THE INVENTIONA UW–Madison researcher in collaboration with others has developed peptides for treating and slowing the progression of heart failure. The peptides are designed to disrupt a key interaction involving myosin and Myosin Binding Protein C (MyBP-C).

In healthy hearts, myosin is responsible for generating the force that drives normal cardiac function. It works by continually binding and releasing a protein called actin, in a process that powers heart muscle contractions. In healthy hearts, the process is slowed when myosin is also bound to a regulatory protein, MyBP-C. In compromised hearts, the result of this interaction is to further slow and weaken muscle contractions.

The new peptides target a specific binding site of MyBP-C, thereby blocking attachment to myosin. The peptides could be administered as small-molecule pharmaceuticals in conjunction with other therapies like beta blockers and diuretics.
  • Treating and slowing the progression of heart failure
  • May dramatically improve speed and strength of heart muscle contractions
  • First potential drug of its kind
  • Does not stress or require more energy from cardiac cells
  • Could support longer, healthier lives for heart failure patients
STAGE OF DEVELOPMENTPreliminary in vitro data suggests that cardiac muscle cells treated with the peptides recovered 40 percent of their contractile force.
For More Information About the Inventors
  • Colson B.A., Bekyarova T., Fitzsimons D.P., Irving T.C. and Moss R.L. 2007. Radial Displacement of Myosin Cross-Bridges in Mouse Myocardium Due to Ablation of Myosin Binding Protein-C. J Molec Biol 367, 36-41.
Contact Information
For current licensing status, please contact Rafael Diaz at or 608-960-9847.
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