Biogen’s Alzheimer’s drug aducanumab implodes in a PhIII disaster — putting them at a perilous crossroads

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by John Carroll — on March 21, 2019 07:13 AM EDT
Updated: 02:05 PM

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Biogen’s big late-stage play in Alzheimer’s has just crashed. And the damage will be extensive.

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There are 4 comments by 3 users. Read the comments or add your own?

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Nancy Curran ago ↷

I have been on Biogen for 3&1/2 years and was devastated by your report! HOPE has just washed down the drain!

rb woodward ago ↷

Aducanumab does not get into the brain. This is true of all the antibodies pharma has been developing for Alzheimer's disease.
This is also true of the cytokines GDNF, BDNF and leptin. Clinical trial failure of a large molecule (biologic, antibody, cytokine, protein) is not an apt test of the amyloid hypothesis...or an apt test of any hypothesis for that matter. The failure is simply a lack of brain exposure. The same can be said for 'gene therapy', 'stem cell therapy', and CRISPR. Only small molecules penetrate the blood-brain barrier to access brain targets. But, it seems that nothing can stop the march of the immunologists. I'm quite sure we'll be hearing about intracranial delivery systems, skull drilling, shunts and ports in the future.

Anonymous ago ↷rb woodward

Of course antibodies DO penetrate the blood brain barrier. Typically 0.1-0.2% of serum levels are achieved in the brain. Dosing clearly is a challenge for all of the AD antibodies currently being tested clinically, because none of them is selective for the low concentration amyloid beta oligomers, which are the cause of memory failure and neuronal degeneration. Most non-specific amyloid targeting antibodies are completely consumed by the tremendous quantities of amyloid plaque and amyloid monomer that reside in AD brain tissue, so little if any of the drug can neutralize the toxic amyloid oligomers. Look for BAN2401 and Crenezumab to fail as well.

rb woodward ago ↷Anonymous

I agree! Your reply spotlights the problem of poor brain exposure: "0.1-0.2% of serum levels" and "completely consumed by the tremendous quantities of amyloid plaque and amyloid monomer". And, I also agree, soluble amyloid oligomers are the true synaptotoxins. The neuronal receptors of amyloid oligomers are the most tractable targets for AD drugs.

Biogen’s Alzheimer’s drug aducanumab implodes in a PhIII disaster — putting them at a perilous crossroads

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