The Causes of NEURODEGENERATION
and How We Work to Limit Its Progress
MECHANISM OF ACTION OF OUR PLATFORM
Buntanetap (previously known as ANVS401 or Posiphen) is our lead compound. It is being developed for the treatment of Alzheimer’s disease (AD), Parkinson’s disease (PD) and other neurodegenerative disorders such as Alzheimer’s in DS (AD-DS). It is a translational inhibitor of neurotoxic aggregating proteins (TINAPs).
Alzheimer’s - Parkinson’s
Parkinson’s - Alzheimer’s
Tauopathies - AD, PD, FTD, CTE
ALS, AD, PD, FTD, CTE
Chronic and acute brain insults lead to high levels of neurotoxic proteins, inflammation and neurodegeneration.
Attacking one neurotoxic protein results in minimal effect.
Buntanetap is the only drug to attack multiple neurotoxic proteins simultaneously.
Buntanetap inhibits the translation of neurotoxic proteins by increasing the binding of a special mRNA sequence that is preserved among neurotoxic aggregating proteins and its binding protein that keeps it from going to the ribosome and being translated.
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.
Neurotoxic Proteins Impair Axonal Transport Causing a Toxic Cascade
When brain cells become injured or stressed, their first response is 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). At high levels, neurotoxic proteins damage the central and peripheral nervous system. The presence of high levels of neurotoxic proteins creates a toxic cascade leading to faulty nerve cell function.
Our Solution to Reverse Neurodegeneration
Lowering the levels of neurotoxic proteins restores axonal transport to normal speed.
In several studies, we have shown that buntanetap and/or ANVS405 improved all the functions that are negatively affected by disturbances of axonal transport. Buntanetap, and where noted, buntanetap and/or ANVS405 reverse the whole toxic cascade leading to nerve cell death.
Our research consistently shows that by reducing APP, tau and αSYN levels, Buntanetap treatment improves axonal transport and impedes the toxic cascade which leads to neurodegeneration, thereby improving or restoring the affected function.
Annovis - Corporate Presentation - November 2022
Phase II Data in Alzheimer's & Parkinson’s Data - AD-PD 2022
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
2006 Salehi Mobley DS-NGF transport
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
2012 World Pharma Congress - Inflammation
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
2006 US Patent 7,153,882 Pos Composition + Use