about Velcade in the maintenance setting. One, called Hovon, will be presented Sunday, Dec. 5 at 5:15 pm Eastern. The second, called Upfront, will come out Monday Dec. 6 at 2:45 pm Eastern.
—The “empowered antibody” against lymphomas. This is a drug developed by Seattle Genetics, known as SGN-35 or brentuximab vedotin. It’s an antibody designed to seek out specific cancer cells, while being combined with a potent dose of chemotherapy to give the package extra tumor-killing kick. Seattle Genetics (NASDAQ: [[ticker:SGEN]]) retains complete commercial rights to this drug in North America, but Millennium has obtained the rights in Europe and other parts of the world. The companies have already told investors that this drug hit its tumor shrinkage goals in studies of patients with relapsed forms of Hodgkin’s disease and anaplastic large cell lymphoma.
The results of the studies were remarkable—about 75 percent of Hodgkin’s patients had their tumors shrink, while 86 percent of anaplastic large cell lymphoma patients did that well. If the drug had performed that well for 30 percent of patients, it would have been good enough to take to the FDA for approval. But the main questions Seattle Genetics and Millennium will get at ASH are the kind that companies dream of fielding: How many patients had complete remissions versus partial remissions? How long did the remissions last? How does that square with the side effect profile? How long did patients actually live on the drug, compared with their life expectancy on standard meds? (It’s still too early to answer that one).
The big presentation of this drug in Hodgkin’s patients will be at 7 am Eastern on Monday Dec. 7, while the anaplastic large cell lymphoma talk will come later, at 7:30 am on Tuesday, Dec. 8.
“The overall response rate was very impressive. To see that level of activity in patients who don’t have a lot of other options, it’s very exciting. It will be a really important overall finding at ASH,” Simonian says.
—What else is coming in the Millennium pipeline? Ever since the Takeda takeover, Millennium has been set up to be the company’s global center for cancer R&D, which ultimately means it will be judged on whether it can deliver more drugs like Velcade and brentuximab vedotin to the marketplace. Millennium CEO Deborah Dunsire and other executives talked in some detail about this in an R&D overview in Japan back in March 2009.
One of those drugs highlighted back then, MLN-4924, is starting to show enough early signs of activity to get a hearing on the big stage of ASH. This drug, as I described back then, blocks the Nedd8 activating enzyme, a novel target discovered by Millennium scientists. This small-molecule drug is supposed to block pathways that are critical to cancer cell growth and survival.
Researchers are expected to present data from the first of three phases of clinical trials generally required for FDA approval, so this one is still at an early stage of the game. Its key data will come at 7 am Eastern on Monday Dec. 6.
“There’s very novel biology here, there’s biomarker work built into the study, and there are already signs of activity in patients with AML (acute myeloid leukemia). You’ll be hearing a lot about that,” Simonian says.
A little science background is required to understand why this matters. Velcade is what’s known as a proteasome inhibitor, which showed that if you can make a drug to inhibit these enzymes (which act as a cellular garbage disposal), then you might block the release of certain proteins that cancer cells secrete to grow and resist conventional chemotherapies. The new Millennium molecule is seeking to build on this philosophy, approaching it from a slightly different angle.
“It’s a new way to think about treating cancer—going after the infrastructure,” Simonian says. Rather than just focusing on mutations that stand out as specific targets on tumors, Millennium is looking at how the cell adapts to survive or regulate itself while under enhanced stress from something like chemotherapy. A slight change on how those proteins function may be enough to coax the cancer cell into a state of self-destruction, known as apoptosis, Simonian says.
