Great replies by Fouremm and Tada in this thread. I'll throw in a few more reasons into the mix that may be holding back interest.

1) Safety: Will the rise in liver transaminases be an issue? DSMB hasn't disclosed any concerns, but that doesn't mean apabetalone in BETonMACE isn't eliciting the same effects on liver transaminases as seen in prior trials. 

2) Moving target: Before it was a bromodomain-2 selective BET inhibitor beneficially effecting several cardiometabolic readouts via an epigenetic mechansim, it was a small molecule that simply raised apo-AI/HDL-C via an unknown mechansim at the time that CETP inhibitors were failing in the clinic.  BET proteins are critical components of the transcriptional machinery that regulates gene expression. Many may be hesitant to invest in an epigenetic therapy because of being concerned about the clinical viability of epigenetic drugs with such widespread and understudied effects.

3) Failed/disappointing Phase 2s and MACE: The effects on apo-AI/HDL-C in ASSERT and SUSTAIN (both trials succeeded) were pretty modest, at least relative to CETP inhibitors. Then, ASSURE failed to meet its primary endpoint of plaque reduction by IVUS. Yes, post-hoc of MACE looks promising and clearly low-HDL diabetics seem, to respond better than normal HDL non-diabetics. And there may be some rosuvastatin synergy going on too. But those MACE post-hocs are primarily based upon the two "soft" 5-point MACE events: coronary revascularization/hospitalization for unstable angina or heart failure. Very few 3-point MACE events (CVD death, non-fatal MI, non-fatal stroke) in those analyses. Basing BETonMACE (3-point MACE endpoint) on post-hocs comprised primarily of non 3-point MACE events is risky. 

BearDownAZ