Anavex Life Sciences Corp (AVXL)

[TrueTrades]

Yes...5 days until we present in Greece and we're one of the few who don't have an abstract available. Hope it helps keep things mellow.

AAT: 14th International Athens/Springfield Symposium on Advances in Alzheimer Therapy
SPEAKERS 2016
Christopher U. Missling*
UPDATE ON ON-GOING PHASE 2A TRIAL OF NEW EXPLORATORY ALZHEIMER’S
DRUG ANAVEX 2-73
(Abstract not available at time of publication)

The other two are:

Suzanne Craft*
INSULIN THERAPY IN ALZHEIMER’S DISEASE: EVIDENCE OF CLINICAL EFFECT
(Abstract not available at time of publication)

Looks like PO results for SNIFF Study:
https://clinicaltrials.gov/ct2/show/NCT01767909
Headed up by Paul Aisen and USC

and

Lon Schneider*
THE BEST TREATMENT? ONE THAT WILL WORK
(Abstract not available at time of publication)

Dr Schneider is also from USC. I could not ascertain what he might be presenting on specifically.

I'm fine with the 3-71 poster:

"There is no cure for Alzheimer’s disease (AD), making it one of the largest unmet medical needs in
neurology. AF710B is a novel selective M1 muscarinic receptor allosteric agonist and sigma-1 receptor
agonist. In vitro, it rescues synaptic loss and reduces oxidative stress and apoptosis. In 3xTg-AD
mice, AF710B mitigated cognitive deficits and decreased AD-like hallmarks (e.g. BACE1, GSK3beta
activity, p25/CDK5, neuro-inflammation, Amyloid-beta, plaques and tau pathologies) [Fisher et
al, 2015 Neurodegener Dis. DOI:10.1159/000440864]. In a further extension, we tested whether
AF710B can reduce AD-like neuropathology and alleviate cognitive impairment in McGill-R-Thy1-
APP transgenic (tg) rats. Tg versus wild type (wt) rats of 12 months of age were orally treated with
either AF710B (10µg/kg) or vehicle (PBS) daily for 4.5 months. To establish whether AF710B may
hold true disease-modifying properties, we implemented a unique experimental design where the
treatment was interrupted for 5 weeks before submitting rats to behavioral tests designed to assess
cognition. Long-term chronic treatment with AF710B was capable of fully reverting the cognitive
deficits at later stages of the AD-like Amyloid-beta neuropathology in the McGill-R-Thy1-APP tg
rats, as evidenced by a complete reversal of the deficit measured by the Novel Object Recognition
and Morris Water Maze tasks. Importantly, this effect was maintained following a 5-week interruption
in the treatment, suggesting true disease-modifying properties of AF710B. An ELISA performed
on cortical samples showed a trend towards a decrease in Amyloid-beta 42 soluble and
insoluble fractions in treated tg rats, supporting a possible shift in the APP processing towards
a non-amyloidogenic pathway. Notably, McGill-R-Thy1-APP rats display overt signs of neuro-inflammation
making this model ideally suited to test AF710B on this aspect of the disease. With M1/
sigma-1 activity as well as putative disease-modifying properties at very low doses, AF710B is a
promising novel therapeutic agent for the treatment of AD."

Some A2-73 mouse model study data for Novel Object Recognition is here:

http://www.anavex.com/files/AAIC_Poster_Tangui_tau_July_2011.pdf

Some A2-73 mouse model study data for Morris Water Maze is here:

http://www.anavex.com/files/1311_Poster_Val_Def_final.pdf

Perhaps we'll be able to compare those charts with the A3-71 poster.
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