Platform Compound

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Buntanetap (previously known as ANVS401 or Posiphen) is our lead compound. It is a translational inhibitor of neurotoxic aggregating proteins (TINAPs). Different from monoclonal antibody therapies, buntanetap is an orally available small molecule, and its unique mechanism of action allows it to inhibit multiple neurotoxic proteins at once. Recent research has shown that multiple neurotoxic proteins are at play in all neurodegenerative diseases. Buntanetap is the only drug to attack multiple neurotoxic proteins simultaneously.

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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.

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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. Details see: Cheng 2021‍

Buntanetap, thus, offers a transformative and superior mechanism to treat neurodegenerative disorders. It is being developed for Alzheimer’s disease, Parkinson’s disease, and other neurodegenerative conditions.

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 ANVS405 improve all the functions that are negatively affected by disturbances of axonal transport. 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.

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Safety Profile

Clean Safety Profile

Safety was evaluated in all three studies and buntanetap pattern of adverse events (AEs) was similar to that seen in typical studies in healthy normal volunteers, with an overall incidence rate of 33.3% among placebo-treated subjects and 35% for all buntanetap treatment groups combined. In the single ascending dose study, the 160mg/day group - the highest dose group in the study – had a treatment-related AE rate of 31.7%. In the multiple ascending and in the POC study there were no dose-related AEs. Most AEs were of short duration, mild or moderate in severity, and resolved without medical intervention. These data were* reported to the FDA in SN 0016 and SN 0018.

Clean safety profile up to 160mg, which is a dose that is expected to be about 10 times higher than the efficacious dose.
Reversal of Toxic Cascade

Buntanetap, and where noted, buntanetap and/or ANVS405, reduced multiple neurotoxic proteins and therefore, rescued neuronal health and restored animals’ normal functions.

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Lowered levels of neurotoxic proteins (ANIMAL):

  • AD mice – lowered levels of APP and improved its fragments with full recovery of memory, learning and brain function [Teich at al. 2018]
  • DS trisomic mice – lowered levels of APP and recovered memory and learning [Chen et al. 2020]
  • PD mice – lowered levels of αSYN in brain and gut and regulated gut motility [Kuo et al. 2019]
  • MCI patients – lowered levels of APP, tau and αSYN [Maccecchini et al. 2012]

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Improved retrograde and anterograde axonal transport (ANIMAL):

  • DS trisomic mice fully differentiated nerve cells – buntanetap treatment increased velocity by 70% and decreased pause time by 29% [Chen et al. 2020]

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Increased synaptic transmission in (ANIMAL):

  • AD mice – had similar long-term potentiation as healthy, wild-type mice after treatment with buntanetap [Teich et al. 2018]

Increased neurotransmitter release in (ANIMAL):

  • TBI rats – after traumatic brain injury, ANVS405 restored dopamine levels in the striatum [Chesselet UCLA, submitted for publication]

Increased levels of neurogenesis and BDNF in (ANIMAL):

  • AD mice brains [Lijia et al. 2013]

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Buntanetap and ANVS405 lowered inflammation in (MCI HUMANS and ANIMAL):

  • MCI humans – in CSF of MCI patients, inflammatory markers were reduced [Maccecchini et al. 2012]
  • TBI rats – in the brains of treated rats the microglia were not activated showing that there was no inflammation after TBI [Chesselet UCLA, in preparation]

ANVS405 protected nerve cells in (ANIMAL):

  • TBI rats – staining in the substantia nigra for dead cells, showed that treated rats had similar stain signal to non-TBI rats. [Chesselet UCLA, submitted for publication]
  • Retina of rats with acute glaucoma – ANVS405 protected 67% the retina [Sundstrom, Hershey Medical, unpublished]

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In summary buntanetap improves or restores the affect function in seven different animal models:

In four models of memory and learning: AD mice [Teich at al. 2018]; Down syndrome mice [Chen et al. 2020]; stroke mice [Turcato et al 2018]; traumatic brain injury rats [Chesselet UCLA, submitted for publication]


In two models of movement disorder: PD mice [Kuo et al. 2019] and in FTD mice.


Finally, it protects the retina and eyesight in acute glaucoma rats.

Toxic Cascade

Neurotoxic Proteins Impair Axonal Transport and Cause a TOXIC CASCADE

High levels of neurotoxic proteins create a toxic cascade leading to faulty nerve cell functioning

Buntanetap Improves Axonal Transport and IMPEDES THE TOXIC CASCADE

Lowering levels of neurotoxic proteins impedes the cascade-effect of neurodegeneration. Buntanetap...