Tada wrote "CS99 - I have heard DM say that apabetalone tells the body to produce new flat HDL particles that pick-up stuff on the artery walls a number of times in the past."

CS99 wrote "Yes, that’s how apabetalone works, which makes good sense of course as a strategy to increase circulating HDL particle number."

This exemplifies my point "d"

"d) Most may view it as an apo-AI and HDL drug. The HDL hypothesis lacks support and has been tarnished by the CETP story. All major trials of apabetalone prior to BETonMACE have been based on the modest ability of apabetalone to raise apo-AI and HDL. Phase 2 ASSERT and Phase 2 SUSTAIN had only modest changes in the primary endpoint of apo-AI and/or HDL-C modulation."

Apabetalone was discovered and developed in Phase 1 and Phase 2 as an apo-AI/HDL drug. The announcement that apabetalone is a BET bromodomain inhibitor that affects many other pathways didn't come until very late in the game (April 2012). This was after ASSERT trial results and just before SUSTAIN top-line (August 2012); ASSURE was well underway by this point too. First impressions are hard to break. Even though WE all know it does much more than modulate apo-AI/HDL, many probably still think of it as just an apo-AI/HDL drug.

These topics have been thoroughly presented in these two posts:

How to best promote apabetalone? aka Evolution of Apabetalone

The Evolution of Apabetalone, Redux

This is even further exemplified by the March 2019 video presentation by Dr. Basil Lewis that Growacet shared. Dr. Lewis, who is one of the BETonMACE clinical investigators, unfairly and inappropriately mis-labeled apabetalone as just a lipid modifying therapy (apo-AI/HDL modulator) categorizing in alongside CETP inhibitors and apo-AI infusions without hardly acknowledging its revised mechanism of action as a BET bromodomain inhibitor that had been known for seven years now or the other non-apo-AI/HDL affected pathways.

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