Author: Ben Butkus
Pfizer said last week that it will provide $14 million over three years to the first phase of public-private research consortium project designed to investigate the regulatory mechanisms involved in human energy metabolism and potentially uncover ways to treat diabetes and obesity.
The Insulin Resistance Pathway project, which could eventually receive additional funding from the pharma giant,
comprises scientists from biotech firm Entelos, the University of California-Santa Barbara, the California Institute of
Technology, the Massachusetts Institute of Technology, and the University of Massachusetts. It plans to take a
systems-biology approach to help it better characterize the basic biology of insulin signaling in adipose cells.
According to officials on both sides of the agreement, the consortium will seek to protect the interests of the academic
parties by allowing them to freely publish and patent any discoveries, although Pfizer will have first rights to review
these discoveries and an option to license them for further development.
“The idea generally is that in order to get the deal to go, we protect the academics and let them do what they have to do
to be successful, which is to publish and patent,” Preston Hensley, senior director of worldwide exploratory science and
technology at Pfizer, and head of the IRP project, told BTW this week.
“We encourage them to do that, and the only thing we want is to see manuscripts 30 days before they go out just to
make sure that there is nothing we need to worry about in there,” Hensley added. “And then if there are any patents, we have the right to license them either exclusively or non-exclusively, depending on the patent.”
Frank Doyle, a professor of chemical engineering at UCSB and associate director of the ICB, said that the 5-year-old institute receives about $10 million in annual funding from the Army, and has traditionally focused on biosensors,
medical systems, and biological materials, although more recently it has developed a systems biology core in its
network sciences division.
“The team really grew from a dialogue between the core academics and researchers at Pfizer,” Doyle said. “Pretty soon we had shaped the proverbial ‘A team’ to attack the problem [using] a balance of computational biology,
high-throughput biological assays, and clever experimental protocols.”
More specifically, Doyle said that the team will be taking a systems-biology approach to investigate the linkage between insulin binding to the outside of an adipocyte, and the end process of that cascade, which is the mobilization of GLUT4 transporters to the cell wall so glucose can enter the cell.
“One of the key paradigms that people use to describe systems biology is this iterative process of going from data to models to new experiments to better models, and so on,” Doyle said. “The model is not the end goal; it is a tool that sheds light on the system, much like proteomics and genomics shed light on the system. So this is one more tool in the tool kit to shed light and understanding on the network.”
Pfizer will fund the consortium for three years and $14 million initially. If the first phase of the project proves successful, Pfizer said, it will fund a second, two-year phase that will extend the studies to other insulin-sensitive tissues such as liver, muscle, and possibly hypothalamic or beta cells.
Hensley said that Pfizer, Entelos, and the academic collaborators jointly developed a basic research strategy and list of milestones at the onset. The completion of those milestones will help determine whether Pfizer will fund the second leg of the project.
Navigating the potential intellectual property roadblocks that could arise from a public-private collaboration of this size will undoubtedly be challenging. However, according to UCSB’s Doyle, the basic nature of the research has lent an air of true cooperation to the consortium that is somewhat unusual in industry-sponsored research.
Doyle added that the early-stage nature of the research “allowed all of the sides here to recognize that we’re really going to be writing papers about the molecular biology of adipocytes, shedding light on fundamental biology, and that the translational piece of that is further down the road.”
“I want to be clear that all sides were very open and negotiable here,” he said. “You have a lot of different stakes on IP in play here, yet everybody recognized that this was something big and exciting, and it was the beginning, and we should see where we run with this, and in subsequent phases we can worry about carving out those strategic IP
domains.”
Similarly, Sherylle Mills Englander, director of the Office of Technology & Industry Alliances at UCSB, which is handling the sponsored research contract negotiations on behalf of UCSB and the ICB, said that Pfizer has “set an example” for developing large-scale industry-academic collaborations.
Englander acknowledged that the pharmaceutical industry is often painted as being difficult to work with by academic tech-transfer offices, and vice-versa. However, Englander said that Pfizer was “absolutely exceptional” during the negotiations, and were not at all difficult to work with when they could have been.
“They really listened to the universities’ needs, and really came to the middle, rather than having a take-it-or-leave-it attitude,” Englander said. “For a collaboration of this scope, that’s really admirable. They did make sure that their critical needs were addressed, but made absolutely sure that the contract did not become an obstacle to the scientists working together.”
According to Pfizer’s Hensley, IP-development and licensing issues might not even come into play. “My secret feeling is that there will not be much need for that,” he said. “Usually Pfizer is not in the business of patenting targets, unless something extraordinary comes out of this.
“In a sense what we’re doing is playing the role of the National Institutes of Health,” he added. “We’re funding focused research to understand the pathobiology of, in this case, diabetes. If we know that there are five redundant pathways that link insulin binding to glucose transport in adipocytes, and we understand how one might modulate those pathways to restore insulin sensitivity, for example, that’s all we care about.”
(Source: BiotechTech Transfer Week - April 30, 2008)