Data on vericiguat, investigational heart failure medicine, to be presented as late-breaking clinical trial at the 2015 AHA Scientific Sessions
Vericiguat study in patients with worsening chronic heart failure and reduced ejection fraction.
Bayer and Merck (MDS outside the Us and Canada) have announced that new data on vericiguat (BAY 1021189), an investigational oral sGC (soluble guanylate cyclase) stimulator being codeveloped by Bayer and Merck for chronic heart failure and reduced left ventricular ejection fraction (HFrEF), will be presented at the upcoming American Heart Association (AHA) Scientific Sessions to be held 7–11 November 2015 in Orlando, Florida. The data were accepted as a late-breaking clinical trial presentation and are the results of the Phase IIb SOCRATES-REDUCED study. The objective of the study was to investigate the change over 12 weeks in NT-pro BNP (a blood marker of heart failure) to determine the appropriate dose of vericiguat for consideration in a Phase III clinical trial in patients with chronic HFrEF in addition to standard therapy.
The following data will be presented at AHA Scientific Sessions 2015:
Vericiguat Data Analysis
“Of the millions who suffer from heart failure, approximately half are estimated to have heart failure with reduced ejection fraction,” said Dr Daniel Bloomfield, vice president, Cardiovascular Diseases, Merck Research Laboratories. “As a company, we feel it’s important to research additional treatment options for this disease.”
“Heart failure with reduced ejection fraction is an area of unmet need,” said Dario Mirski, vice president of US medical affairs, Bayer Pharmaceuticals. “At Bayer we’re committed to researching and advancing new therapies to help people with this condition.”
Vericiguat is part of a worldwide development collaboration between Merck and Bayer in the field of sGC modulation, which seeks to target a distinct molecular mechanism that is associated with the underlying pathophysiology of heart failure. The soluble guanylate cyclase (sGC) enzyme, which is important for the function of both the blood vessels and the heart, is insufficiently stimulated in heart failure due to impaired NO (nitric oxide) availability and endothelial dysfunction.
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