Infinity Pharma, Intellikine Strike Deal to Make Cancer Drugs Against Hot Target

Cambridge, MA-based Infinity Pharmaceuticals seeks to stay on the leading edge of cancer research, and today it has found something it likes in San Diego. Infinity (NASDAQ: [[ticker:INFI]]) has struck a global development and commercialization deal with San Diego-based Intellikine to pursue drugs aimed at one of the emerging hot targets in  biology of cancer and autoimmune diseases.

Infinity agreed to pay Intellikine $13.5 million upfront, as much as $25 million in milestone payments for two drug candidates, and potentially $450 million more if two drugs can win regulatory approval and reach the marketplace. Intellikine stands to receive royalties on product sales, although at the end of mid-stage clinical trials to test the drugs’ effectiveness for cancer, it will have the option to take a 50/50 split of the U.S. profits.

Infinity has no products on the market generating cash to finance a deal like this, and it stumbled more than a year ago when a clinical trial of its lead cancer drug at the time, IPI-504, was halted because of adverse events. Yet Infinity, led by CEO Adelene Perkins and Julian Adams, its president of R&D, has been able to buffer itself somewhat through a lucrative partnership with Purdue Pharma and Mundipharma struck in late 2008. Even though today’s deal means that Infinity will exceed its R&D budget forecast for this year, the company still has enough cash to operate into 2013, the company says.

That relative financial stability is part of what put Infinity in position to obtain what Intellikine has to offer. The venture-backed San Diego company is one of the emerging players seeking to make drugs that hit the PI3 kinase pathway. Researchers say that pathway plays a key role in critical cell processes like proliferation, migration, and survival. Those normal functions are flipped into an overactive mode in cancer cells, so shutting off the switch that controls them is thought to be a promising new drug development strategy.

Adelene Perkins
Adelene Perkins

“This agreement is emblematic of Infinity’s strategy to use our scientific expertise and financial strength to expand our portfolio of high-quality development programs in areas where there is a significant unmet medical need and for which Infinity is well positioned to reveal—and then realize—the potential of such programs,” Perkins said in a statement.

Besides the PI3K pathway’s importance for cancer, researchers also say it could hold potential for the treatment of autoimmune disease, in which overactive immune system cells attack healthy tissues like a virus. Intellikine’s lead drug candidate mentioned in today’s release is INK1197, an oral pill that’s being primed for its first clinical trials in 2011.

As with any hot field, there are a lot of competitors battling for the lead in the PI3K development race. GlaxoSmithKline, Novartis, Roche, South San Francisco-based Exelixis (NASDAQ: [[ticker:EXEL]]]), and Seattle-based Calistoga Pharmaceuticals are a few of best-known contenders. Intellikine CEO Troy Wilson, in an exclusive interview last August, said what differentiates Intellikine is its investment in basic biology to characterize the four different variants of the PI3 kinase pathway, combined with a prolific chemistry team that has created 1,500 different drug candidates to block those targets.

Author: Luke Timmerman

Luke is an award-winning journalist specializing in life sciences. He has served as national biotechnology editor for Xconomy and national biotechnology reporter for Bloomberg News. Luke got started covering life sciences at The Seattle Times, where he was the lead reporter on an investigation of doctors who leaked confidential information about clinical trials to investors. The story won the Scripps Howard National Journalism Award and several other national prizes. Luke holds a bachelor’s degree in journalism from the University of Wisconsin-Madison, and during the 2005-2006 academic year, he was a Knight Science Journalism Fellow at MIT.