Windtree Therapeutics announced the company is extending its collaboration with the University of Milan-Bicocca for the discovery and development of new SERCA2a compounds for the potential treatment of chronic and acute human heart failure. Over the next 12 months, the program will focus on the further characterization of Windtree's SERCA2a activators and their interaction with SERCA2a and associated regulatory proteins.
"We are delighted to extend our collaboration with the scientific team at the University in Milan-Bicocca as we continue to develop SERCA2a activators and understand their potential in chronic and acute heart failure," said Steve Simonson, M.D., senior vice president and chief medical officer. "The potential role of SERCA2a activation as a treatment in heart failure (including heart failure with preserved ejection fraction, or HFpEF) has been recognized but successful intervention at this target has been elusive. By utilizing a novel approach to SERCA2a activation, Windtree has developed a portfolio of oral (and i.v.) SERCA2a activitors which are progressing through pre-clinical testing and development. This collaboration strengthens and extends the SERCA2a program and will provide important scientific support to Windtree efforts to bring these compounds forward."
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Two aspects of SERCA modulation to be explored under the terms of this collaboration include the antiarrhythmic potential and modulation of smooth muscle activity resulting from SERCA2a activation. Ahead of this preclinical research, Windtree is advancing istaroxime, a first-in-class, dual action, luso-inotropic agent for the treatment of acute decompensated heart failure. Istaroxime is currently being assessed in a Phase 2 study in patients experiencing early cardiogenic shock and has been granted Fast Track designation by the FDA based on positive Phase 2a and Phase 2b trial results in patients with acute heart failure. Istaroxime has a dual mechanism of action including inhibition of the sodium-potasium ATPase and activation of SERCA2a.