BDAZ this is very interesting.

Assuming the 77% RRR in DM patients with CVD and low HDL treated with rvx-208 and Crestor can be replicated in phase lll BETonMACE, then, while we know that rvx-208 raises ApoA-l (good, functional, non oxidized cholesterol) the other cascading epigenetic effects must either account or augment in an interactive manner such that MACE reduction is dramatic.

This seems to imply that increased HDL is only part of the solution and that rvx-208 goes much further in solving the MACE problems.

My apologies to readers for this awkward description. Science people please let me know if I am on track or misguided here.

At least RVX knows with a high probability of certainty (and nothing in life is certain) that rvx-208 reduced MACE in a specific, large and growing patient population. We also know this requires experimental replication.

Regards

Toinv