Scott still gets his Big Pharma fix—AtheroGenics partnered in December 2005 with AstraZeneca to commercialize AG-1067—but the South Africa native feels right at home working for a smaller operation—on a bigtime project.
Pharm Exec: When did you first know that Lipitor was going to be successful?Rob Scott: We used to hold these R&D days at Pfizer, when we'd talk about where we should be going, which drugs we should be trying to develop, which approaches we should be trying to follow. About a year before we did the deal [Pfizer acquired Parke-Davis, developer of Lipitor, when it bought Warner-Lambert in 2000], we were reviewing a bunch of approaches that Pfizer had. And every time we looked at an approach, people would say, "Well, that's not going to work out so well if Lipitor makes it to the market." And then somebody in the room said, "Well, we should try and get Lipitor, then."
We were going to be launching against other companies with deep pockets, that had outcomes data for their statins. So we were realistic at the time, but I think that both Merck and BMS missed the opportunity to blunt the launch of Lipitor.
Compare that with where you sit today, with the drug you have in development.
Lipitor was going to be the fifth statin on the market. In some respects, that makes life easier, because you know the approach is going to work, and that there's a high degree of acceptance in the marketplace. But we didn't have anything really exciting to talk about. We could say that we lowered LDL more than the competitors, but that's not really sexy.
AGI-1067 is a brand-new approach. There are no other drugs in this class. When we launch, we're going to have to persuade people—make them understand how the drug works.
How was 1067 born?
Back in about 1992, the two scientific co-founders of AtheroGenics, Wayne Alexander and Russ Medford [current CEO], came up with a very novel concept. The first thing they said is that atherosclerosis is mainly an inflammatory disease. That was something people were starting to talk about, but it wasn't widely accepted.
[The founders] said that there are certain intracellular mechanisms that turn on the inflammation, and that these mechanisms can be blocked with an antioxidant—that was the basic technology. AtheroGenics was formed out of that idea.
The way 1067 works is that it's absorbed into cells, and it blocks a message that comes from outside the cell to the nucleus that tells the cell to turn on various inflammatory processes. What gets this message going are all of the current risk factors. So if you have hypertension, high blood pressure, high glucose with diabetes, high lipids, if you smoke, have a bad diet and lifestyle—all of those things turn on this oxidant signaling that tells a cell to go into the more inflammatory state. 1067 acts on that signaling. Instead of focusing on individual risk factors, we're trying to block the next step down from that.