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About Our Science.

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We are developing an innovative therapy for Alzheimer’s disease (AD). Our lead candidate, buntanetap, simultaneously inhibits the production of multiple neurotoxic brain proteins that have been shown to impair axonal transport and lead to nerve cell death. Specifically, it inhibits the synthesis of amyloid, Tau and α-Synuclein. It is distinct from other AD drugs in development, because rather than just removing one toxic protein, buntanetap inhibits all major toxic proteins before they can form.

This page describes the phase 2/3 Alzheimer's study in moderate Alzheimer patients with MMSE of 14 to 24. By submitting your email you are agreeing to be contacted about the study.  All information provided is confidential and does not imply that you want to participate.

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IRB approved Alzheimer Study Flyer: Buntanetap in Treating Alzheimer’s and Parkinson’s Disease   


The data from our phase 2 study in Alzheimer’s and Parkinson’s patients was published in JPAD (Journal of Prevention of Alzheimer’s Disease) and we have attached the paper. Here is a summary of what we found and why we have progressed our drug into phase 3.
Buntanetap is an orally available small molecule that inhibits the translation of multiple neurotoxic aggregating proteins only under conditions where their translation is elevated – in sick nerve cells. Because it only affects these neurotoxic proteins when they are overexpressed, it restores their normal levels without affecting other proteins and restores homeostasis in the brain.
Both Alzheimer’s disease and Parkinson’s disease have been shown to have mixed pathology and mixed proteinopathy. All four
neurotoxic aggregating proteins are present in the brain of Alzheimer and Parkinson patients – Aβ forms plaques, tau forms tangles, alpha-synuclein forms Lewy bodies, and TDP43 forms its aggregates.

Amyloid β
Alzheimer’s - Parkinson’s

Annovis Bio Amyloid

Tauopathies - AD, PD, FTD, CTE


Parkinson’s - Alzheimer’s




Buntanetap inhibits translation of all the above four neurotoxic proteins,  thus is well positioned to treat both diseases, which is an advantage compared to removing a single neurotoxic protein alone. In a double-blind, placebo-controlled, multi-center phase 2, study we enrolled 14 early AD and 54 early PD participants who were treated for 25 days with buntanetap or placebo. Buntanetap was safe and well tolerated. Biomarker data indicated a trend in lowering levels of neurotoxic proteins and inflammatory factors and improving axonal integrity and synaptic function in both AD and PD cohorts, confirming target and pathway engagement of buntanetap. Psychometric tests showed statistically significant improvements in ADAS-Cog11 and WAIS coding in AD patients and MDS-UPDRS and WAIS coding in PD patients. These findings support the hypothesis that lowering levels of neurotoxic aggregating proteins leads to stabilization and  improvement in cognition and motor function.     

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