I don't want to spend too much time on this, since this topic has been discussed ad nauseam on this forum and Stockhouse for several years now. Just a few points. Not all strategies to raise HDL or HDL-cholesterol are created equal. The HDL-cholesterol hypothesis does seem to have a lot of holes poked in it with the failure of CETP inhibitors and niacin therapy to consistently, if even at all, reduce cardiovascular risk despite significant increases in HDL-cholesterol. However, just because the HDL-cholesterol hypothesis has holes in it doesn't mean that other HDL-particle or HDL-function hypotheses are defunct. Recall that apabetalone, unlike other HDL-cholesterol raising therapies, not only increases HDL-cholesterol but also increases apo-AI synthesis, circulating apo-AI levels, HDL particle number, number of large HDL particles and average HDL particle size. Some of these effects of apabetalone on HDL parameters seem to be especially prevalent in those patients with pre-existing low-HDL levels. So it's not just about HDL-cholesterol, but more about the number, size and function of the HDL-particles.

BearDownAZ