among patients on the experimental treatment, and Seattle Genetics is hoping to add a couple extra months of median survival time, without any serious added side effects, Siegall says.
The trial is designed in such a way that researchers, and the company, are blinded to the results to prevent any biases that might skew the study until at least 186 patients who entered the study have died. Then, statisticians will look at which patients got the new drug compared with the standard therapy, to see if there was any benefit. The initial findings will be issued by press release, and then the company will go into more detail at a medical meeting, Siegall says.
It’s possible that if the data for the Seattle Genetics drug is compelling enough from this single study, the company could use it as the basis to whip up an application to the FDA, Siegall says. It’s also possible that it could form part of a body of evidence for the drug, and provide the spark for another rigorous study to prove the drug’s worth, he says.
There are no other drugs on the market for acute myeloid leukemia that hit the same target as the Seattle Genetics drug, since Pfizer announced yesterday that it is pulling gemtuzumab ozogamicin (Mylotarg) off the market.
Strangely enough, the Pfizer drug was a trailblazer in the field of “empowered antibodies” that Seattle Genetics is seeking to reinvent today with a next-generation form of the technology. The scientists at what was then Wyeth created Mylotarg as a way to combine the targeting ability of an antibody with a potent toxin attached to give it more tumor-killing kick. The drug ultimately was a poor seller, partly because the linker wasn’t really stable enough to ensure the toxin got exactly where it needed to go in the tumor.
A decade of research and development later, Seattle Genetics has applied new chemistry techniques for empowered antibodies for a variety of forms of cancer. But with acute myeloid leukemia, among elderly patients who are especially frail, the notion is that a simpler “naked” antibody like lintuzumab, without any extra toxin, might be an effective way to disrupt tumors without causing serious side effects.
The company has spent a lot of time and money on getting this answer, as it completed enrollment in the study in February 2009, and stopped treating the last patient 12 months later. Suspense, naturally, is building at the company on whether this dark horse drug candidate is a winner or not.
“Our goal is to see a meaningful improvement in survival,” Siegall says.
