Anavex Life Sciences Corp (AVXL)

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Here's the new drug abstract.

http://www.nature.com/articles/nature19323.epdf?referrer_access_token=NlkTxpKe9jieJVRiNIWQpdRgN0jAjWel9jnR3ZoTv0OqjsrnqFbRwzkQCJeuXdT6QH-vYxB4jJOOZP2j6zdaACbVctHYuYUBdTerwRAH4-9AvWn-rZW1e88pDQ-9j2ONjQx5pobaT4LZQhagK-bt5kDJTOGoEjUkQeALjRPkHEo5nwBQkwDupCBeexDHofPnatBCXPjW9NQLXHqRe-5ox4HJH6DuNVulLwXtiQ0ikVOT4348mlnFP7Vng20hazxImXT5VJdjf2dsy7tcj6wJuNCNQf_cISY0zsY6QpnVZBU%3D&tracking_referrer=www.telegraph.co.uk

Alzheimer’s disease (AD) is characterized by deposition of amyloid-ß (Aß) plaques and neurofibrillary tangles in the brain, accompanied by synaptic dysfunction and neurodegeneration. Antibody-based immunotherapy against Aß to trigger its clearance or mitigate its neurotoxicity has so far been unsuccessful. Here we report the generation of aducanumab, a human monoclonal antibody that selectively targets aggregated Aß. In a transgenic mouse model of AD, aducanumab is shown to enter the brain, bind parenchymal Aß, and reduce soluble and insoluble Aß in a dose-dependent manner.

In patients with prodromal or mild AD, one year of monthly intravenous infusions of aducanumab reduces brain Aß in a dose- and time-dependent manner. This is accompanied by a slowing of clinical decline measured by Clinical Dementia Rating—Sum of Boxes and Mini Mental State Examination scores. The main safety and tolerability findings are amyloid-related imaging abnormalities. These results justify further development of aducanumab for the treatment of AD. Should the slowing of clinical decline be confirmed in ongoing phase 3 clinical trials, it would provide compelling support for the amyloid hypothesis.

Can aducanumab be an Anavex 2-73 competitor? Several observations.

1. The drug is claimed to present "... a slowing of clinical decline...." Presently, no claim is made that that it holds things at baseline; merely that it slows decline (similar to Aricept, but apparently for a longer duration). Preliminary (but valid) Anavex 2-73 results from the Australian human trial show both stabilization at initial baseline, or for some, actual reduction in Alzheimer's symptoms.

2. The drug is a unique human monoclonal antibody, expressing immunotherapeutic actions. Well and good; except that monoclonal antibodies frequently cause adverse events, affecting not just the target molecules (in this cases, solely beta-amyloids), but other molecules or organelles. A comprehensive Phase 3 study will determine this. The record of immunotherapies for Alzheimer's, as the abstract states, " Antibody-based immunotherapy against Aß to trigger its clearance or mitigate its neurotoxicity has so far been unsuccessful."

Billions of dollars have been spent so far in unsuccessful immunotherapies for Alzheimer's. All have failed.

3. Aducanumab must be administered by IV infusion (drip), on a monthly basis. Anavex 2-73 is efficiently absorbed and crosses the blood/brain barrier by simple oral administration, something that can be done without professional guidance or travel (no nurse or physician or infusion center visit needed).

4. Crucially, there is no mention of tau-tangle absorption or removal by aducanumab. Tangles of waste tau proteins are the second recognized cause of Alzheimer's symptoms. Aducanumab apparently helps clear beta-amyloid accumulations; but over time, will the remaining, un-touched tau tangles complicate recovery?

Apparently aducanumab is owned by Biogen. I won't be buying any Biogen shares any time soon.