Prof. Ray gives a presentation on the rationale, design and CV outcomes of the BETonMACE trial, in which the BET inhibitor apabetalone was evaluated compared to placebo in high-risk patients.
AHA 2019 The BETonMACE trial evaluating apabetalone did not reduce the primary composite efficacy outcome, nor key secondary outcomes, in T2DM patients with recent ACS and low HDL-c.
Prof. Ray describes the high residual CV risk in post-ACS diabetes patients, and how BET inhibition with apabetalone may reduce this residual risk and thereby prevent CV events.
The phase 3 BETonMACE trial did not meet the primary endpoint, a reduction in MACE with apabetalone, in high CV risk patients.
Prof. Jukema explains the mechanism of epigenetics and how the BET inhibitor apabetalone can potentially impact CVD. In addition, he presents findings of first clinical studies with apabetalone.
Prof. Libby discusses the inflammatory residual risk in diabetes patients and explains how epigenetic modulation of (inflammatory) gene transcription can potentially reduce CV risk.
Alkaline phosphatase (ALP) is a potential novel treatment target for CVD in CKD. Dr. Haarhaus discusses ALP-related mechanisms of increased CV risk and beneficial effects of the BET inhibitor apabetalone.
Epigenetic processes are involved in renal damage. Marta Ruiz-Ortega describes the role of vascular calcification and alkaline phosphatase (ALP) in CKD and effects of BET inhibition on vascular calcification.
ERA-EDTA 2019 Epigenetics contribute to vascular calcification, which is a hallmark of CVD in CKD. Prof. Brandenburg explains how BET inhibition can interfere with factors and pathways associated with vascular calcification.
BET proteins can stimulate inflammatory processes by regulating genes. Prof. Kausik Ray discusses the role of BET inhibition in reducing CVD risk in patients with diabetes.
Prof. Jorge Plutzky explains BET inhibition as a novel therapeutic strategy for controlling pathologic cardiovascular responses.
Professor Erik Stroes gives an overview of evidence that inflammation plays a role in CVD and diabetes and considers options to target the hyperactive inflammatory state to lower residual CV risk.