Pricing: Prove It

Fragile Shoots: Extending the Tree of Life for Cancer Patients

To do that, Avastin will not only need to secure additional FDA and EMEA approvals, but also demonstrate better efficacy as an early stage inhibitor of tumor growth—a big if, according to some cancer specialists. "Validating patient benefit to drive the payer investment is at the heart of the debate here," argues Karol Sikora, a practicing oncologist and former professor of cancer medicine at London's Imperial College. "Right now, if you can afford it, Avastin is probably worth the price. But assuming continued growth through additional indications, Roche could halve the price and still double its revenues."

Philippe Bishop , VP, Clinical Development, Avastin

For Roche, the answer depends on grafting broader applications to backstop Avastin's ability to score against multiple cancers. Company researchers are looking to its potential as an overall early-stage treatment, an inhibitor of post-surgery tumor relapse, a cancer maintenance therapy—even as a preventive. One little-understood aspect of Avastin is that in contrast to many cancer drugs it is well tolerated by patients, over a longer period of time. This might enhance its value as a micro-tumor growth suppressor when used in combination with drugs that target other aspects of cancer biology.

Skeptics Pan a New Path

The rationale for rewarding drug innovation starts with three metrics: time, money, and opportunity. Avastin's storyline is a long one, emerging over three decades from a heretical concept in the biology of vascular cell growth to commercial breakthrough that blocked cancer's spread through the blood supply. The journey began in 1971 with publication in The New England Journal of Medicine of a paper by Harvard professor Judah Folkman positing that cancer cells secrete excess amounts of a molecular substance—Vascular Endothelial Growth Factor (VEGF)—which promotes proliferation of blood vessels that feed tumors and help them metastasize. Folkman dubbed the process angiogenesis, a combination of the Greek words for "vessel" and "birth." His practical conclusion was that if VEGF could be controlled, it could beat back or even render dormant the cancerous growths whose spread depends on their ability to stimulate the formation of new blood vessels.

The cancer community found Folkman's paper fanciful, even threatening. This was especially true for the many researchers trained in the laboratory rather than in the real world setting where Folkman worked as a surgeon, in regular contact with patients suffering from perversely healthy, blood-rich tumors. Plagued by the "not in my back yard" syndrome, Folkman found little institutional support for his conclusions, and it was left to circumstance whether others might take up the challenge of transforming his theory into medical practice.