
The Causes of NEURODEGENERATION
and How We Work to Limit Its Progress
WHAT IS NEURODEGENERATION

Normal Axonal Function and The Onset of Neurodegeneration
A normal nerve cell receives signals, processes them in the cell body and transports them through the axon, a long-arm nerve fiber that extends out from the cell body and connects to the synapses, or fingers. When brain cells become injured or stressed, their first response is the reduction and impairment of axonal transport along the axon's "Informational Highway". If the insult persists it can lead to depression (serotonin), anxiety and insomnia (GABA), cognitive impairment, such as AD (acetylcholine), and movement disorders, such as PD (dopamine).

The buildup of neurotoxic proteins impede healthy axonal transport
NORMAL BRAIN
with normal levels of AB, tau and αSYN.
BRAIN DAMAGE
with an increase in aggregating proteins
reduces neurotoxic proteins and improves brain chemistry


Our Solution to Reverse Neurodegeneration
ANVS401 is a small lipophilic molecule that is orally available and readily enters the brain as demonstrated by pharmacokinetic analyses showing brain concentrations approximately 6 to 8 times higher than plasma concentrations. ANVS401 has a unique mechanism of action in that it inhibited the translation and, therefore, the levels of several key neurotoxic proteins both in vitro and in vivo including APP, tau and αSYN.
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Brain injuries and stresses lead to increases in neurotoxic proteins, impaired axonal transport and nerve cell death – neurodegenerative diseases
OUR MECHANISMS OF ACTION
A Three-Prong Attack on AD and PD
We believe ANVS401 is the only drug in development that targets multiple neurotoxic proteins and inflammation to improve axonal transport in AD, AD-DS and PD. The multiple conditions we will target include;



We Are Dedicated to Reversing Debilitating Neurodegenerative Diseases

By targeting multiple neurotoxic proteins, ANVS401 resembles a combination therapy approach, with the added convenience of being a single drug with a single drug target. Therefore, we have worked to understand how ANVS401 is able to inhibit the translation of more than one neurotoxic protein.
DOCUMENT LIBRARY
Current Presentations
2019 Posiphen Investigator Brochure
2015 Posiphen Investigator Brochure
Publications
2020 Chen Transport in Down Syndrome
2019 Kuo to PD aSYN
2019 Chen Transport Review, Converging Insights into AD
2018 Turcato et. al Posiphen Study
2013 Yu Posiphen and metabolites
2013 Bandyopadhyay, novel UTR inhibitors
2012 Mikkilineni Translation Blockers of aSYN
2007 Marutle Neural stem cells
Scientific Presentations​
2020 Wharton Entrepreneurship
2020 UPenn Rethinking PD Talk
2018 Cleveland Clinic Talk
2017 Alzheimer's Association International Conference - Down Syndrome
2016 Military Health System Research Symposium – Traumatic Brain Injury
Patents
2018 Use of MOA for Prevention and Treatment Application
2017 US 20180228771 Acute brain and nerve injuries Application
2012 US Patent 8,258,172 Dementia
2012 US 20120225922 Neurodegeneration Application
2010 US Patent 7,786,162 Methods for Treating Dementia
2009 US Patent 7,625,942 Down Syndrome