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.