Roche pulls another major piece out of the wobbly Alzheimer’s jenga, shuttering crenezumab PhIIIs

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by Amber Tong — on January 30, 2019 05:55 AM EDT
Updated: 10:58 AM

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When AC Immune announced two years ago that its partners at Genentech is launching a second Phase III for its Alzheimer’s drug, CEO Andrew Pfeifer touted crenezumab as a “distinct” hope amid disappointing results of other anti-amyloid beta therapies, given at higher doses and targeting earlier stages of the disease.

Today crenezumab has become a big disappointment itself — marking another prominent failure in a frustration-prone field.

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Anonymous ago ↷

Crenezumab is routinely referred to as an Abeta oligomer-specific antibody. However, it was selected based on its ability to bind multiple Abeta species. No difference in binding to oligomers, monomers, and fibrils were in fact reported (J. Neurosci. (2012) 32(28):9677-9689). The bottom line: This antibody is not oligomer specific, and the toxic forms are not likely targeted at all. Its inability to affect plaque load also suggests that it does not even reach the brain in therapeutically relevant amounts. This is thus yet another example of the futility of targeting Abeta indiscriminately.

rb woodward ago ↷

Antibodies do not get into the brain. Biologics, generally, do not get into the brain. The previous failures of GDNF, BDNF, leptin, and all the other antibodies targeting Alzheimer's disease should have made that clear by now. The lack of brain exposure is the crux of the problem and so, in fact, this study does not “meaningfully contribute to our understanding of Alzheimer’s disease”. It is not a rigorous test of the amyloid hypothesis. It does not comment meaningfully on the central role of amyloid oligomers. What it does tell us, once again, is that Alzheimer's disease requires brain permeable small molecule drug candidates...Pills and capsules.

Anonymous ago ↷rb woodward

I beg to differ. Immunotherapy is the only form of therapy that has shown any signs whatsoever of disease modification. All other attempts have failed miserably, most notably small molecules that not only have proven ineffective but usually also toxic. Perhaps the disease modification observed in e.g. Aducanumab is too small to be clinically significant, but efficacy should be increased by honing in on what appears to be the most toxic - oligomers - and until this has been tried in the clinic we will not know for sure. This is why it is important not to call something "oligomer specific" when it is not. Crenezumab says nothing about the potential therapeutic efficacy of targeting toxic Abeta specifically. The only thing that has been learned here is that one cannot compensate for a lack of oligomer specificity by simply increasing the dose - the antibody will still not reach its target.

Roche pulls another major piece out of the wobbly Alzheimer’s jenga, shuttering crenezumab PhIIIs

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