Neurogenesis drug hits trials

BrainCells, a company that stakes its existence on the once-heretical notion of linkurl:adult neurogenesis,;http://www.the-scientist.com/article/display/12172/ is finally taking its novel treatment for depression into a phase II trial, CEO Jim Schoeneck told me at a neurotechnology meeting in Boston yesterday (May 8). Researchers have recently begun to suspect that treating depression requires neurogenesis. Drugs such as Prozac, though, stimulate nerve growth via the serotonin pathway, which

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BrainCells, a company that stakes its existence on the once-heretical notion of linkurl:adult neurogenesis,;http://www.the-scientist.com/article/display/12172/ is finally taking its novel treatment for depression into a phase II trial, CEO Jim Schoeneck told me at a neurotechnology meeting in Boston yesterday (May 8). Researchers have recently begun to suspect that treating depression requires neurogenesis. Drugs such as Prozac, though, stimulate nerve growth via the serotonin pathway, which may be what causes the side effects many patients experience. Last year, The Scientist linkurl:reported on BrainCells' work;http://www.the-scientist.com/article/daily/52980/ on a compound called BCI540 that spurred neurogenesis via a different pathway and improved symptoms of depression in an animal model. When I caught up with Schoeneck for an update on the work, he told me that that the company had kicked off a Phase 2 trial of the compound in April, and had secured $50 million in funding to continue its work. BrainCells' mode of operation is to take a closer look at compounds that have been already undergone human testing for safety, but that failed to show efficacy for indications as diverse as cardiovascular and respiratory illnesses, and test them for their ability to stimulate nerve growth; BCI540 had originally been tested as a treatment for Alzheimer's disease. In the last year, Schoeneck told me, the company has focused on testing combinations of these compounds, with surprising results. Single molecules might be mildly neurogenic, or not at all, but paired, some show a markedly strong potency. "This is totally unanticipated," he said. Combinations can have the opposite effect, too. "A compound may have an effect in itself, but combined with another one, it just crashes," he said. All of this hints at how little researchers know about how the molecules used in treatment actually act. In fact, Schoeneck said, 10-15% of the combinations they tried cut down on neurogenesis. That could explain the high rate of non-responders in clinical trials, he said, since enrolled patients might be taking any number of other drugs for unrelated conditions. "Anything we're taking into the clinic, we're running against a panel of 70 or 80 or so other drugs," he said. "If I was in big pharma, I would be wanting to run this."
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