A new article using JQ1 in pre-clinical models highlights the potential for BET bromodomain inhibition in treating heart failure. This research was primarily done at University of Californina, San-Francisco School of Medicine and the Gladstone Institute of Cardiovascular Disease.

BET bromodomain inhibition suppresses innate inflammatory and profibrotic transcriptional networks in heart failure

Here's a brief summary:

BETting on a new heart failure treatment

Heart failure remains a common and difficult-to-treat medical condition with a high mortality, and there is a great need for more effective therapeutics. Duan et al. determined that a small molecule called JQ1, which was originally developed for cancer therapy, may be an effective treatment for heart failure. Bromodomain-containing protein 4, a member of the BET family of epigenetic regulators and the target of JQ1, plays a role in the development of heart failure and contributes to cardiomyocyte hypertrophy. The authors used a combination of mouse and human induced pluripotent stem cell–derived cardiomyocyte models to show that JQ1 can reverse the detrimental effects of this protein and improve cardiac structure and function even in the setting of prolonged and severe disease. They also found that JQ1 did not interfere with physiological cardiac hypertrophy that occurs in response to exercise, supporting the safety of this approach.