Next Alzheimer's Hope Step Forward

There is some buzz in the news today about an eagerly awaited Alzheimer's drug, bapineuzumab, as it progresses in a pivotal phase III trial. The drug is being developed by Elan/J&J and Pfizer. The popular press is touting the drug as a potential - 1st drug - to treat Alzheimer's rather than just ameliorate symptoms for relatively short periods.  It may be the first drug approved that can delay or prevent disease progression.  It does this by binding the amyloid beta protein.  We'll see as the trial results become available as to its effectiveness.

I can understand the anxiousness involved with possibly having an actual treatment for Alzheimer's but I think people need to keep perspective until the trial results are available to assess that it actually works -- or on which sub-populations it actually works. Alzheimer's is a tough area.  Just this past summer, Lilly's semagacestat went down and out in a pivotal phase III trial.  This drug too was aimed at preventing amyloid beta plaques --  though it is a gamma secretase inhibitor and worked by blocking an amyloid forming enzyme. 

Bapineuzumab is a mAb that works by binding a soluble form of the amyloid beta protein in the blood.  Thus, has a different mechanism of action from semagacestat.  Lilly does have another direct rival drug to bapineuzumab, called solanezumab, that is also in pivotal phase III trials.  Solanezumab puportedly will work with a wider patient sub-population and has a somewhat better safety profile though that too needs to be proven by the trial data. See Fierce Biotech and The Daily Mail.

Both newer drugs are touted as mega-blockbusters with peak revenue predictions ranging to the $3 billion plus annually.  However, both need to make it through their respective trials and to market through the appropriate regulatory agencies.  Until then, let's keep our enthusiasm tempered. See Investor Village link to Datamonitor report.

 
Posted by Bruce Lehr April 25th 2011.

Comments

[gup1138]

My also-flawed understanding agrees @bigredbrurce - the mAb is targeted at soluble A-beta, thus helping it to be 'cleared' out of the body - and preventing it 1) from participating in plaque formation AS WELL AS 2) interfering with synaptic communications (which apparently the soluble forms - 'dimers' of two A-beta proteins - and more, 'oligomers' - do very effectively, disrupting synaptic transmission).

[bigredbruce]

My understanding may be flawed but I believe the mAb is directed at soluble amyloid beta in the blood and thus renders this circulating material unavailable to participate in plaque formation.

[Fai]

i still cannot understand how does an antibody cross the blood brain barrier. I think modular antibody will have better chance. We had discussion about this drug like 7-8 years ago, and most of us don't think it is possible at the time to work. I hope it work, cause AD is a horrible disease.