Renovacor Announces Pipeline Expansion with New Research Program for Multiple Genetic Segments of Arrhythmogenic Cardiomyopathy
Renovacor has expanded its pipeline by collaborating with the University of Utah to develop an AAV gene therapy for arrhythmogenic cardiomyopathy (ACM). This partnership focuses on three significant genetic segments of ACM: plakophilin-2, desmoglein-2, and desmoplakin. The program aims to restore gap junction protein trafficking and communication among heart muscle cells, addressing life-threatening arrhythmias. The collaboration stems from promising proof-of-concept data demonstrating reduced premature ventricular contractions in genetic mouse models.
- Expansion of pipeline with an AAV gene therapy program for ACM.
- Partnership with University of Utah aids research development.
- Focus on three major genetic segments brings targeted approach.
- Promising proof-of-concept data showing reduced PVCs.
- None.
Research collaboration with the
The research collaboration will focus on a protein discovered by
The collaboration leverages positive proof-of-concept data generated in a genetic mouse model of ACM that was performed by the
“Renovacor’s pipeline expansion with this new AAV gene therapy research program for multiple genetic segments of ACM further demonstrates our precision medicine approach to develop potentially transformative therapies that target core biological drivers of serious cardiovascular diseases,” said
“We are thrilled to have
Arrhythmogenic cardiomyopathy (ACM) is a heritable heart muscle disorder that can affect the left and right ventricle. It is characterized by a heightened risk of potentially lethal ventricular arrhythmias, fibrofatty replacement of myocardial tissue, and in some patients, heart failure.(1,2) It is recognized as a disease of the desmosome, with well-defined genetic drivers. The prevalence of ACM is estimated to range from 1 case in 1,000 persons to 1 case in 5,000, with an average age of diagnosis of approximately 30 years.(1-3) Current treatment options aim to prevent potentially life-threatening arrhythmias and progression to end-stage disease, but they do not target the underlying genetics or disease biology and, as such, patients can continue to experience serious breakthrough events.(1-2)
About
About the
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1. | Austin KM et al Nat Rev Cardiol. 2019 Sep; 16(9): 519–537 |
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2. | Corrado D, et. al, N Engl J Med 2017;376:61-72 |
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3. | McNally E (2017) in: Adam MP, Mirzaa GM, Pagon RA, GeneReviews® |
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