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promise of” linking our drugs to other molecules to deliver them to cells.
When Fambrough took to the fund-raising trail after he became the CEO in May, he did so with a lot of experience with both the company and venture investing. He was a founding investor in Dicerna and a general partner at Boston’s Oxford, which led Dicerna’s $21.4 million Series A round in November 2007. During his Oxford days, Fambrough also made a successful bet on the RNAi drug developer Sirna, which Whitehouse Station, NJ-based Merck (NYSE:MRK) scooped up for $1.1 billion in 2006.
Despite the influx of capital, Fambrough said the company doesn’t plan to go it alone. The company’s strategy is to form collaborations with outside drug companies around specific uses of the startup’s technology. (The CEO declined to say how long he expected the second-round dollars to support his firm’s operations.) In January, Dicerna revealed its first collaboration with a major drugmaker, Japan-based Kyowa Hakko Kirin, initially to develop an RNAi drug against an undisclosed cancer target. That deal brought in $4 million in cash upfront, with the potential to bring in up to $1.4 billion in milestone payments. The firm’s Ipsen collaboration was announced in March, but no financial figures were provided.
Indeed, many major drug companies have struck deals with RNAi firms or formed research groups to gain a foothold in RNAi. Alnylam, for example, has either licensed its RNAi technology or partnered with such giant drugmakers as GlaxoSmithKline, Novartis, Roche, and Takeda Pharmaceutical. Before its deal with Dicerna, Kyowa hooked up with Alnylam in June 2008 to develop and potentially sell Alnylam’s experimental RNAi drug for respiratory syncytial virus infection in Asian markets.
Still, Dicerna says it has always believed that its gene-silencing method offers a separate and unique door into RNAi. Also, its gene-silencing drugs hold promise to knock down disease targets which previous drugs have been unable to hit. In lab mice, for instance, Dicerna has shown that its gene-silencing molecules can block expression of a cancer gene called KRAS that has evaded small molecule drugs. The gene plays a key role in cancer progression in leukemia as well as solid tumors of the lung, colon, rectum, and pancreas.