RE:RE:RE:RE:RE:NISSEN INTERVIEW DURING. THIS MONTHS ACC
Apoa-1/ HDL still has a cloud hanging over its head in the scientific community. The Cerenis PII trial results released in January that failed to meet endpoints is case in point. So thats billions spent on CETP inhibitors, failed Niacin trials, RVX fails and then Cerenis fails. None of this looks good with all different approaches.
As far as a poster presentation being something that is negotiated. I would doubt that. Poster's presentations are great ways for companies to get data out that isn't able to be presented live. It sounds a lot better to say as presented at ACC (even as a poster presentation) than as released on newswire. RVX wanted to get their positive spin on the data in a scientific setting that would enable them to speak about it publicly.
With regards to Nissen not being a part of a future RVX study. I have no idea, but it would not surprise me if he wasnt. Not because of any issues but simply because they are shifting endpoints. Nissen and the CC have been known as the gold standard core lab for IVUS. If you are doing a CV IVUS study, you want them as your core lab. If you are not, there may not be a reason to have them involved.
As far as MDCO and their rHDL product. I agree that this would be good for field if they are successful, but I would stop short of saying that if theirs works that 208 will work. Very different compounds. MDCO uses the Milano mutation which causes the protein to dimerize (couple). They then complex this with a phospholipid to make a form of HDL that is most able to remove cholesterol. Most studies have shown a improvement in cholesterol efflux from ApoA-1 Milano versus wild type ApoA-1. 208 stimulates the production of wild type. However, the main reason I would stop short of comparing the two is dosing. MDCO doses at extremely amounts of ApoA-1. Their study doses have been in the 20-40 mg/kg of body weight. This translates into gram quantities of ApoA-1 being administered at one time versus nanogram quantities of improvements. Of course it is an extremely expensive therapy and will likely only be used acutely in the 30 -90 days post ischemic event. So may not be so competitive to 208. This is one of those that may work but probably only has real market potential in the US and Europe direct countries whereas 208 could have broad market appeal in emerging markets.