For $300m Biogen beefs up its Alzheimer’s attack
Biogen’s decision to spend $300m to license in a phase I anti-tau antibody from Bristol-Myers Squibb shows that repeated failure seems to be no impediment to continued development of Alzheimer’s disease projects.
The deal brings to five the number of assets for the neurodegenerative condition held by the Massachusetts-based biotech, and its second project targeting tau deposits rather than amyloid plaques (see table below). Meanwhile, Bristol signalled its withdrawal from Alzheimer’s development, and in so doing sold at a profit an agent it bought with Ipierian for $175m three years ago (Development-stage M&A premiums reward very patient investors, May 7, 2014).
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The Alzheimer’s project is BMS-986168; it has completed phase I safety studies, and is ready for phase II in Alzheimer’s and progressive supranuclear palsy. In Biogen’s pipeline it will join the phase III sset aducanumab, phase I BIIB076, and the Eisai-partnered elenbecestat, and BAN2401.
While aducanumab and the Eisai collaborations all seek to inhibit the neural damage caused by accumulation of amyloid plaques, BIIB076 and the Bristol project target a second protein, tau, that is deposited in the brains of Alzheimer’s patients and is also thought to contribute to the condition. In tau inhibition, Biogen recently put BIIB076 into phase I, according to the project’s originator, Switzerland-based Neurimmune; both ‘076 and ‘168 are antibodies.
In this space Abbvie has a slight lead – it initiated a phase II trial in January for ABBV-8E12 in early Alzheimer’s disease, and this will enrol 400 patients and measure disease progression over two years. Presumably Biogen’s assets will follow a similar strategy.
|Clinical stage tau-targeting Alzheimer's disease projects|
|Phase II||ABBV-8E12||Abbvie/C2N Diagnostics|
|Tau MAb Research Program||Lilly|
|Anti-tau pS422 MAb|
|Phase I||RG7345||Roche/AC Immune|
|Phase I||ACI-35||Johnson & Johnson/AC Immune|
|Beta-amyloid, tau & alpha-synuclein aggregation inhibitor|
|Phase I||NPT088||Proclara Biosciences|
|Tau aggregation inhibitor|
|Phase III||LMTX||Bayer/TauRX Pharmaceuticals|
|Phase II||PBT2||Prana Biotechnology|
|Phase I||AADvac2||Axon Neuroscience|
|Tau protein modulator|
|Phase II||AADvac1||Axon Neuroscience|
Biogen’s development strategy appears to be to cover the waterfront with mechanisms of action. And with ‘168 it also has the advantage of using orphan drug regulation to speed to market early while Alzheimer’s data mature. Progressive supranuclear palsy is estimated to affect between three and six in 10,000.
Bristol, meanwhile, has profited today from pipeline optimisation efforts. It also sold rights to BMS-986089 (myostatin adnectin), a fusion protein blocking-myostatin, in development for Duchenne muscular dystrophy, to Roche, for $170m.
Both of these deals appear sensible. Bristol is a small player in neurological diseases, deriving just $13m a year from central nervous system drugs, according to EvaluatePharma. Alzheimer’s is a huge market, but is also one of the highest-risk therapy areas, with billions of dollars spent on failed clinical trials in recent years.
And while Duchenne has shown itself to be a more favourable area of development thanks to Sarepta’s Exondys 51, ‘089 is probably better placed in the pipeline of Roche, which could be looking to build its CNS commercial presence now that its multiple sclerosis therapy Ocrevus is approved.
With Bristol investors likely looking for the group to make some strategic moves to offset Opdivo’s disappointment in first-line lung cancer, an extra $470m could come in handy if it goes into deal-making mode.