Golfyeti,

I was thinking more along the lines of Resverlogix being able to tie together a secondary outcome to the CVOT data. If Resverlogix's BETonMACE succeeds, one challenge is how to explain its beneficial effects. Apabetalone is an epigenetic drug, eliciting effects on many cardioprotective pathways. Which one(s) are responsible for the potential cardoprotective effects of apabetalone?

SGLT2 inhibitors and GLP-1R agonists were tested, approved and marketed for blood glucose lowering in diabetics long before the CVOT results started coming out.

The LDL-C lowering therapies (i.e. statins, ezetimibe, PCSK9s, bempedoic acid) were tested, approved and marketed for LDL-C lowering (bempedoic acid not approved yet) long before the CVOT results started coming out. Note: some of these (statins, bempedoic acid) also lower hsCRP.

The omega-3 fatty acids trials, including the recent REDUCE-IT using Amarin's Vascepa, were tested, approved and marketed for plasma triglyceride lowering long before the CVOT results started coming out.

Canakinumab was developed and validated to be an anti-IL-1B antibody and approved for some inflammatory conditions before the CANTOS CVOT trial was done.

CETP inhibitors were shown to greatly and reproducibly elevate HDL-C long before the CVOT results (failed) started coming out.

Low-dose methotrexate was widely tested and approved as an anti-inflammatory for rhematoid arthritis long before the CIRT trial was started.

How will the picture of apabetalone mechanism of action be painted? What modulated secondary outcomes from BETonMACE will they tie together with the hopefully stellar MACE outcomes? Will BETonMACE reveal changes in glucose, insulin, serum lipids (TG, HDL-C, LDL-C), and inflammatory markers that will show changes that rival those elicited by the above mentioned therapies. That was my thought process. 

BearDownAZ