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Ask us about our clinical trials
This page describes a double-blind dual Phase 3 study which aims to assess safety and efficacy of buntanetap in participants with early AD. 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.
Both Alzheimer’s and Parkinson’s diseases have been shown to have mixed pathology and proteinopathy, characterized by the presence of several neurotoxic aggregating proteins – beta amyloid, tau, alpha-synuclein, and TDP43. Buntanetap is an orally available small molecule that inhibits the translation of these 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 normalizes homeostasis in the brain.
In the Phase 2/3 study, we showed that early AD patients (MMSE 21-24) exhibited dose-dependent, statistically significant improvements from placebo in the two higher concentrations (15mg, p=0.042; 30mg, p=0.015) while all doses showed significant improvement over baseline (7.5mg, p= 0.013; 15mgp=0.001; 30mg p<0.001). Further, we demonstrated that APOE4 carriers respond well to the drug improving by 3 - 4 points in ADAS-Cog11, similar to the response seen in non-carriers. More information can be found in the company’s Corporate Presentation, which you can find under the “Investors” tab on our website.
Find more information at ClinicalTrials.gov
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.
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