It’s not every day that you see one Big Pharma company handing an award to another, but that’s just what happened yesterday at the New York Academy of Sciences. New Brunswick, NJ-based Johnson & Johnson (NYSE: [[ticker:JNJ]]) gave its Dr. Paul Janssen Award for Biomedical Research to Napoleone Ferrara, the Genentech scientist whose discoveries contributed to the development of the blockbuster cancer drug bevacizumab (Avastin), and a related treatment, ranibizumab (Lucentis), for the blinding disease macular degeneration. Genentech, based in South San Francisco, is a unit of the Swiss drug giant Roche.
In conjunction with the award presentation, J&J convened a top-flight group of scientists for a day-long scientific symposium on the future of treatments such as those that Ferrara spearheaded. Ferrara is most famous for his work with vascular endothelial growth factor (VEGF), a protein that promotes blood-vessel growth. His findings contributed to the birth to a new class of drugs—anti-VEGF compounds that starve tumors by cutting off their blood supply, and preserve sight by drying up the leaky blood vessels that cause macular degeneration.
The success of anti-VEGF drugs has brought a mix of celebration and criticism to Genentech. Sales of the cancer product hit $7.5 billion last year, while the macular degeneration drug brought in about $1.6 billion in sales. But late last year, an advisory panel to the FDA recommended the agency revoke its approval for the cancer product to be used in treating breast cancer, based on clinical trial results that suggested it didn’t work more effectively than other treatments. Genentech appealed the decision. Meanwhile, ranibizumab has been under pressure from eye doctors because of its $2,000-per-dose price tag. Many are choosing to use tiny doses of bevacizumab instead, which they can get for $20 to $50 per dose.
Although the commercial controversies did play into the discussion at the award presentation, the scientists chose to focus more closely on work being done to better define VEGF—and hence to improve treatments designed to block it. Ferrara described work in his lab to understand
