RE: RE: RE: Biotech 777..FYIMy short answer is that you can see double that level of circulating HDL particle increases from high doses of Niacin alone so I fear that big pharma will see this as an Amarin AMR101 like treatment. Having said that, they are spending the money and we will see if there is regression, but keep in mind, regression alone really means nothing clinically. At a minimum you would want to see plaque stabilization or regression of vary specific types of plaque. There is often a misconception that this plaque buildup interferes with blood flow. Often the plaque lesions that are vulnerable to rupture are asymptomatic. This is where I think OCT would have been a better choice, but again, I understand the timing issue.As far as how much regression would be enough, that is obviously a tough question. My gut says both Nissen and other cardiologists will be looking for something near 4-5%. This is tricky though as the type of plaque morphology changes may be just as important. Additionally there will be a desire to extrapolate out whatever regression is seen and ask the question of whether this effect will be seen if dosed over a longer period of time. It certainly might be, but it is also possible that it will not. In many animal studies, you can see a rapid and early regression and then very minimal to no regression after the high doses are given. This is probably due to the type of plaque that apao-1 binds most effectively with.I think the financial fund raising and the personnel stability are very good things particularly with a small company, but I am hesitant to read much more into it as everyone knows the potential, now only the data will speak. There is little insight that even insiders will have regarding this. I personally have done a number of apao-1 related work, so along with everyone else, I just want to see the data.