Less than five years after betting $1.1 billion on the power of RNA-interference (RNAi) to treat disease, pharmaceutical powerhouse Merck is shutting down the San Francisco research facility it acquired when it purchased Sirna Therapeutics, a biotechnology firm that specialized in RNAi, in 2006.
The announcement, first reported last week by Xconomy, is another blow to a young field that has been pummeled over the past year. In November, Swiss pharma firm Roche announced that it was pulling out of RNAi after investing $500 million over three years, and Novartis, another Swiss pharmaceutical giant, elected not to extend a partnership with Alnylam, an RNAi biotechnology company in Cambridge, Massachusetts. In February, the New York Times reported that Pfizer and Abbott Laboratories were also cutting back on their RNAi investments.
Nevertheless, Merck spokesman Ian McConnell says that the company will continue to have over 100 scientists working on RNA-based treatments. “Merck continues to invest significantly in RNAi therapuetics,” he says, noting that since the acquisition of Sirna, Merck has been steadily integrating the technology into its other research programs. The closure of the Sirna lab, which currently houses about 50 scientists, is an effort to trim the budget by eliminating the cost of maintaining a separate RNAi facility, McConnell says.
Delivery of RNA-based drugs to target organs remains a critical stumbling block, and the industry pull-backs come as proponents eagerly await early clinical trial results of systemically-delivered RNAi therapies. Today, Alnylam announced the completion of its phase 1 trials of ALN–VSP, a treatment that has shown early promise against liver cancer. In June, UK-based Silence Therapeutics also reported promising but very preliminary clinical trial results of its RNAi-based tumour treatment. And Alnylam also plans to announce early clinical trial results for two other therapies this year: one against high cholesterol, and the other against a rare genetic disease called TTR-mediated amyloidosis.