Angiogenesis Inhibitors

When they learned about angiogenesis, scientists recognized a potential avenue for stopping the spread of cancer.  The body makes chemicals that promote angiogenesis and other chemicals that stop it. Like most physiological processes, angiogenesis is subject to a feedback system.  Doctors thought – if we can make the body’s anti-angiogenesis signal chemicals and supply it in excess to the patient, we can stop the growth of blood vessels in the body.  And that would prevent the growth of tumors. Anti-angiogenesis therapy, also called angiogenesis inhibitor therapy, could theoretically be effective in fighting solid tumor cancer.  It wouldn’t be relevant to leukemia and lymphomas but if the strategy worked on solid cancers, it would be a huge boon to oncology.

The angiogenesis inhibitors could be those the body naturally makes – produced by genetic engineering techniques in the lab – or synthetic inhibitors.  Either way, these inhibitors would be tested and proven as drugs. No angiogenesis inhibitor drugs existed yet, so it was a whole new category of anti-cancer medicines.  There was a good deal of excitement in the 1990s about this approach to fighting cancer.

A flurry of activity by the pharmaceutical companies to develop these medicines followed. Bevacizumab, sold under the brand name Avastin, was the first drug of this class approved by the FDA.  Several others followed. Disappointingly these did not turn out to be the wonder drugs people had hoped for. They show some efficacy (otherwise the FDA would not approve them), but they typically only add a few months to a patient’s life expectancy, and oncologists typically give them in conjunction with older style cytotoxic drugs.