ARCA biopharma, Inc. (Nasdaq: ABIO), a biopharmaceutical company developing genetically-targeted therapies for atrial fibrillation and other cardiovascular diseases, today announced that the paper "Combinatorial pharmacogenetic interactions of bucindolol (Gencaro) and beta-1, alpha-2c adrenergic receptor polymorphisms” was published in PLOS ONE (
), an international, peer-reviewed, open-access, online publication.
Analyses in the paper demonstrate that two previously described adrenergic receptor polymorphisms that have been shown to pharmacogenetically interact with the anti-adrenergic agent and beta-blocker Gencaro (bucindolol hydrochloride) appeared to behave in specific, pharmacologically-determined ways when individual genetic monotypes are combined.
The paper details the combined research efforts of three leading cardiologists and/or pharmacogeneticists:
- Christopher O'Connor, M.D., Professor of Medicine, Director of the Duke Heart Center, Duke University Medical Center, Lead Author of the paper;
- Steven Liggett, M.D., Associate Vice President for Personalized Medicine, Morsani College of Medicine University of South Florida in Tampa, a senior author of the paper whose laboratory discovered and characterized the two adrenergic receptor polymorphisms; and,
- Michael Bristow, M.D., Ph.D., President and CEO of ARCA biopharma and Professor of Medicine (Cardiology) at the University of Colorado Anschutz Medical Campus, the senior author of the paper in whose academic laboratory the mechanism for the described pharmacogenetic interaction was discovered and characterized.
Dr. Bristow commented, “These data demonstrate that combinatorial pharmacogenetic interactions may be used to increase the predictive power of genetic biomarkers to identify subpopulations of patients that appear to respond either better or worse than the general population of patients. In the case of Gencaro, in this review of study data, adrenergic receptor combinatorial pharmacogenetics appear to identify a substantial subpopulation of patients in the study, approximately 45-50% of the total, in which responses appear to exceed outcomes reported for other studies with other beta-blockers in U.S. heart failure populations. These pharmacogenetic findings also identify a smaller subpopulation, approximately 10-15%, where the drug did not appear to be useful in preventing heart failure in this study. The ability to identify these subpopulations may allow for more efficient drug development and potentially improved targeted therapies for cardiovascular patients, if regulatory approval is obtained."