There's a ton of information and research out there that underpins Apabetalone's MoA. Here's one:

https://f1000research.com/articles/6-1015/v1

"We previously showed that JQ1 prevents several hallmarks of heart failure, including cardiomyocyte hypertrophy, cardiac fibrosis, and systolic dysfunction, in a mouse model of aortic constriction-induced left ventricular pressure overload30–32. We found that, mechanistically, BRD4 promotes cardiomyocyte hypertrophy by triggering RNA Pol II pause release at promoters of pro-hypertrophic genes30 and by contributing to the formation of long-range super-enhancers (SEs) associated with these genes33; SEs are thought to signal to proximal promoters to stabilize coactivator complexes near transcription start sites and facilitate P-TEFb–mediated Pol II phosphorylation and transcription elongation34–36. Intriguingly, in addition to controlling pro-growth genes, many of the BRD4-enriched SEs identified in cardiomyocytes were associated with pro-fibrotic genes, including those encoding the secreted factors connective tissue growth factor (CTGF), plasminogen activator inhibitor-1 (PAI-1/Serpine1), and TGF-β233. These findings suggest the possibility that BRD4 signaling in cardiomyocytes regulates expression of paracrine factors that crosstalk with fibroblasts and other stress-activated cell types in the heart to elicit fibrotic remodeling.

More recently, we have found that late administration of JQ1 also attenuates cardiac dysfunction both in the murine transverse aortic constriction (TAC) model and in post-MI cardiac remodeling37. In addition, JQ1 blocked agonist-induced pathological hypertrophy and brain natriuretic peptide (BNP) expression in human induced pluripotent stem (iPS) cell-derived cardiomoycytes. Integrated transcriptomic analyses across rodent and human iPS cell models have made clear that JQ1 preferentially suppresses transactivation of a broad pro-fibrotic and pro-inflammatory gene program. Although precise delineation of cell type–specific effects in vivo will require the development of conditional and inducible genetic loss-of-function models for the BET alleles, the transcriptomic analysis of mouse bulk LV tissue revealed a strong suppression of myofibroblast activation by JQ1. Consistent with this, using cultured primary cardiac fibroblasts, we have found that BRD4 coordinates TGF-β–mediated pro-fibrotic gene expression and myofibroblast differentiation (unpublished data). Thus, BRD4 appears to play a crucial role in cardiac fibrosis by regulating fibrogenic gene expression in both cardiomyocytes and resident cardiac fibroblasts and possibly other cell types that populate the stressed myocardium."