trace amounts of the hormone. Another is by blocking an enzyme called CYP17 that allows the body to make small amounts of testosterone in adrenal glands, which can happen even while standard hormone-blocking drugs are essentially instructing the brain not to produce any testosterone, Montgomery says. The other way Tokai fights the cancer is by reducing the number of hormone receptors in prostate cancer tumors, essentially so they can’t vacuum up any testosterone in the body, Montgomery says.
One potential side effect to watch for will be if the drug turns off a lot of the normal ability of the adrenal system, Montgomery says. “What if you can’t make cortisol?” he asked, noting that would be a problem since cortisol is involved in the body’s natural response to stress and anxiety.
But there’s plenty of enthusiasm in the medical community for what Tokai is doing, Montgomery says. The Phase I/II clinical trial is being conducted at leading cancer centers like the University of Washington/Fred Hutchinson Cancer Research Center, the Sidney Kimmel Comprehensive Cancer Center, UCLA, Dana-Farber Cancer Institute, Roswell Park Cancer Institute, and others. “There’s excitement that this could be the beginning of what proves to be a very effective drug, perhaps the likes of which we haven’t seen before,” Montgomery says.
The technology for what became Tokai has its roots in the medicinal chemistry lab of Angela Brodie at the University of Maryland School of Medicine in Baltimore, says Tokai’s Harrison. Venture capitalists have been encouraged by the triple-threat mechanism of action of the company’s drug in animal tests, and they will hope to see at least a few anecdotal cases early on of the lower PSA scores that are a good sign that a patient is improving, Harrison says.
If all goes well, Tokai may have some preliminary evidence from its first clinical trial to present this June at the American Society of Clinical Oncology, Harrison says.
