Cardiovascular and Metabolic Diseases

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Novartis has a longstanding commitment to cardiovascular and metabolic disease, and has developed major medicines in the field including the angiotensin receptor blocker valsartan for hypertension and the DPPIV inhibitor vildagliptin for diabetes. Its angiotensin receptor neprilysin inhibitor LCZ696 is in development for chronic heart failure.

Despite a wide range of medicines available for cardiovascular and metabolic disorders, these diseases remain the number one cause of death in the developed world, and prevalence is increasing rapidly in developing nations. Our Cardiovascular and Metabolic (CVM) research focuses on discovering and developing innovative mechanism-based compounds for novel targets in relevant disease processes.

Our CVM strategy is to go beyond current palliative therapies or lifestyle modifiers and directly address the pathobiology at the site of disease. The primary goal is to identify and develop true disease modifying therapies that preserve or restore beta cell function, preserve cardiac function, restore vascular function, protect from renal damage, and reduce cardiovascular mortality.

Our CVM research concentrates on dyslipidemia, atherosclerosis and vascular diseases, type 2 diabetes, heart failure, cardiac arrhythmias and associated disorders.

 

Selected publications

The DGAT1 inhibitor Pradigastat Decreases Chylomicron Secretion and Prevents Postprandial Triglyceride Elevation in Humans. Meyers CD, Serrano-Wu M, Amer A, Chen J, Rocheford E, Commerford R, Hubbard B, Brousseau M, Li L, Meihui P, Chatelain R, Dardik B. J Clin Lipidol. 2013. 7(3):285.

Wolfram syndrome 1 and adenylyl cyclase 8 interact at the plasma membrane to regulate insulin production and secretion. Fonseca SG, Urano F, Weir GC, Gromada J, Burcin M. Nat Cell Biol. 2012. 14(10):1105-1112.

Genome-wide association mapping of quantitative traits in outbred mice. Zhang W, Korstanje R, Thaisz J, Staedtler F, Harttman N, Xu L, Feng M, Yanas L, Yang H, Valdar W, Churchill GA, DiPetrillo K. G3:Genes, Genomics, Genetics. 2012. 2(2):167-174.