RE: RE: RE: RE: RE: Biotech 777..FYIA couple of really good posts. Lots of information in both. As far as angiograms, yes, I have seen many angiograms. Once you get above 50% stenosis where you will see lumen reduction on an angiogram, you typically have a more calcific plaque that has formed with a cap on the endoluminal side. Apoa-1 and rHDL have not been shown to be very effective on this type of plaque. It is more effective on the softer lipid, earlier stage fibrocalcific stuff that forms in the media. Ironically, once you have a more calcicified cap exposed to the endoluminal side, you also have a much, much less risk for plaque rupture and subsequent heart attack. So there is less need to try and stabilize the plaque but rather deal with the stenosis. For stenosis greater than 50% that requires intervention and patients have significant pain and fatigue, RVX or any HDL based therapy may not work for that. HDL based therapies I believe are more appropriately targeted towards those earlier stage plaques that are more often asymptomatic and do not require intervention angiographically speaking. As far as inflammation goes, I was not referring to autoimmune disorders but rather to vascular inflammation that is caused often during the acute phase response following an event. While we used to think that heart attacks were simply caused by years and years of plaque buildup, most data now suggests that this is not the case. The conversion from stable to unstable of vascular plaques seems to be mediated by an inflammatory process. This is the primary reason that recurrent events are so common following a heart attack or other ischemic event. For those who are more clinically oriented, this is the exact issue with reperfusion injury post intervention.Anyway, as far as the business side, I think parsing out the applications is a fairly common tactic. You see this on the cell based therapies as well. The question realistically is whether a small company can advance any of those other indications. I think Alzheimers is quite interesting as the beta amyloid plaques due seem to have some similarities to atherosclerotic plaques, but this is all small animal data.I actually think the best application for RVX besides treating the ACS patient is mild aortic stenosis. This is the patient subset for which there is no treatment until they are severely calcified, the plaque composition is quite similar and it is largely an inflammatory mediated progressive process. This is the area I would be looking at if I were designing their next clinical trial (after post NONSTEMI MI of course).I think the pairing with statins is simply to try and get the attention of the few big pharma players who either need to extend patent protection or simply want to get into this space. Unfortunately, all of these ideas or opportunities are moot if they do not show success in this trial. If they fail their primary endpoints, I think it will be quite difficult to raise additional funds even if there are hints of data.Let's hope for some + data and soon!