The History of Herceptin

Herceptin (chemical name: trastuzumab) got its start in the 1970s, when researchers began using the new tools of molecular biology to find the genes that trigger various cancers. One scientist discovered a gene, called HER2/neu, or HER2, that directed the production of a protein that seemed to cause cancer in mice.

Then in the late 1980s, researcher Dr. Dennis Slamon showed that the aggressiveness of certain kinds of breast cancers was linked to how many copies of the HER2 gene they had. Breast cancers with the most copies of the HER2 gene spread the fastest. These tumors produced the most HER2 proteins, also called HER2 receptors.

Dr. Slamon reasoned that if the HER2 receptors are associated with the aggressive spread of breast cancer, then a drug that could block the action of those receptors might block or slow down the growth of the cancer. He convinced researchers at a biotechnology drug company to make an antibody that could target the HER2 receptors. The antibody latches on to the HER2 receptors in breast cancer cells, and stops them from receiving signals that tell the cancer cells to grow. The antibody also alerts the immune system to selectively destroy the tumor cells to which it binds.

Tests of this antibody showed that it was effective at stopping or slowing the spread of breast cancer for many women with metastatic tumors that made too many HER2 receptors. In 1998 these tests led the U.S. Food and Drug Administration (FDA) to approve Herceptin for the treatment of such women. Since that time, the FDA has approved Herceptin as adjuvant treatment (treatment after initial treatment, such as surgery) either alone or as part of a regimen containing Adriamycin (chemical name: doxorubicin), Cytoxan (chemical name: cyclophosphamide), and Taxol (chemical name: paclitaxel) for women with earlier stages of HER2-positive disease.

Herceptin gives women with HER2-positive breast cancer an important treatment option.