ETC-216 was actually a mimic of preß-HDL comprised of a synthetic version of apo-a1 Milano and a synthetic phospholipid. It was ultimately impossible to manufacture at commercial quantities.
In theory, the "increase in HDL" with ETC-216 would have been equal to the number of viable drug particles that survived the infusion process since preß-HDL counts as HDL.
If you want to talk about what the increase in the larger a1-HDL particles would be, it would likely be similar -- minus some completely unknown percentage for the number of ETC-216 particles that could not mature into a1-HDL due to lack of available mediators like LCAT.
RVX-208 attempts to back up one step further by spurring the liver into producing apo-a1, which they hope matures into preß-HDL via ABCA1 and other mediators.
It's clear the drug produces apo-a1. Whether it creates enough of it and/or whether the creation triggers the beneficial cascade that results in maturity to a1-HDL that can uptake fats and offload them into the liver is what ASSURE will tell us.
The Phase III trials will tell us whether that process converts into morbidity and mortaility benefits as the post-hoc, retrospective analyses of a generation of lipid trials suggest.
Unless otherwise indicated, this is the personal viewpoint of David
Miller and not necessarily that of Biotech Stock Research, LLC.
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