With a $44 million investment, a group of investors is betting that a Stanford University spinout has a drug that potentially could interfere earlier in the process of knotty neurodegenerative diseases such as Alzheimer’s.

Annexon Biosciences Inc. of South San Francisco will use the money to push two drugs — ANX-005 against Alzheimer’s and Huntington’s diseases and ANX-007 in glaucoma — into clinical trials next year. Data from Alzheimer’s and Huntington’s patients is expected by late 2017.

The Series B funding was led by new investor New Enterprise Associates and included participation by Correlation Ventures. Existing investors Novartis Venture Fund, Clarus and Satter Investment Management LLC also were involved.

In all, Annexon has raised at least $78 million since its formation in 2013 by Stanford neurobiology professor Dr. Ben Barres and Rinat Neuroscience cofounder Arnon Rosenthal.

Alzheimer’s is not an easy space for drug developers. No one really knows what causes the memory-robbing disease, but researchers have paid a lot of attention to two proteins, amyloid and tau. Medivation Inc. of San Francisco, for example,famously failed a late-stage Alzheimer’s study before it was rescued by the success of the prostate cancer drug Xtandi.

But Annexon is taking another approach to neurodegeneration, focusing on a protein called C1q, which normally initiates an immune response called the “complement cascade” that rids the brain of dead cells or bacteria. The problem is that C1q can accumulate at junctions where neurons meet, called synapses, and start to break down these important message-distribution centers in the brain.

ANX-005 is designed to inhibit C1q.

“We are stopping the assault on synapses and stopping them from going into disease,” said Annexon CEO Doug Love, a former executive vice president of Elan Pharmaceuticals.

There are a few big questions: Will zeroing in on C1q allow Annexon’s Alzheimer’s ambitions to succeed where other companies have flamed out over the past decade or more? Will ANX-005 not only work at stopping or slowing neurodegeneration but also prevent damage and allow synapses to repair themselves? And can ANX-005 pull off the difficult balancing act of stopping the bad activity of the C1q protein without throwing out of whack the innate immune system, the body’s first line of defense against viruses and other invaders?

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Source: American City Business Journals 

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