What side effects are associated with this type of intervention?

Common treatments for Alzheimer's Disease that target amyloid-beta and tau proteins include aducanumab and other amyloid-focused therapeutics. Known side effects of aducanumab include amyloid-related imaging abnormalities (ARIA), which can manifest as brain swelling or small brain bleeds, headache, falls, diarrhea, and confusion. These side effects are more frequent in patients with the APOE ε4 gene variant. Other amyloid-targeting treatments have also faced issues with side effects and have not consistently demonstrated clinical benefits.

What prior FDA approvals exist?

The FDA has approved several drugs for the treatment of Alzheimer's Disease that target amyloid-beta aggregation. One notable example is aducanumab, which is an anti-amyloid monoclonal antibody designed to reduce amyloid plaques in the brain. Other treatments include vitamin E, which has antioxidant properties and has shown modest benefits in delaying functional progression in patients with mild to moderate Alzheimer's Disease. These treatments share a common goal with Buntanetap, which is to inhibit the aggregation of amyloid-beta and tau proteins, thereby potentially slowing the progression of the disease.

What other types of research exist?

Promising novel alternatives to Buntanetap for Alzheimer's Disease patients include: 1) Anti-amyloid monoclonal antibodies like aducanumab and lecanemab, which target amyloid-beta plaques. 2) Tau aggregation inhibitors such as semorinemab. 3) BACE inhibitors like verubecestat, which reduce amyloid-beta production. 4) Anti-inflammatory agents targeting neuroinflammation, such as ALZT-OP1. 5) Neuroprotective agents like neurotrophic factors or small molecules that enhance synaptic function and neuronal survival.

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Buntanetap for Alzheimer's Disease

Phase 2 & 3

Recruiting

Research Sponsored by Annovis Bio Inc.

Eligibility Criteria Checklist

Specific guidelines that determine who can or cannot participate in a clinical trial

Must have

Be older than 18 years old

Timeline

Screening 1 day

Treatment 12 weeks

Follow Up 1 day

Summary

This trial tests buntanetap, a medication, on people with mild to moderate Alzheimer's disease. It aims to find out if different doses of the medication are effective and safe. Participants will take the medication daily for a few months, and their progress will be monitored through various assessments.

Who is the study for?

This trial is for people aged 55-85 with mild to moderate Alzheimer's, as per NIA criteria. They must have a study partner, be in good health without diseases affecting the study, and not at risk of self-harm. Women of childbearing age need a negative pregnancy test and agree to contraception; men must also agree to contraceptive measures.

What is being tested?

The trial tests Buntanetap's effectiveness and safety against a placebo in those with Alzheimer's over 12 weeks at home. Participants will undergo screening for up to 42 days before treatment starts, followed by four clinic visits and one phone call over approximately five months.

What are the potential side effects?

While specific side effects are not listed here, participants will be monitored for any adverse reactions due to Buntanetap or the placebo during their treatment period which includes regular in-clinic visits.

Timeline

Screening ~ 1 day1 visit

Treatment ~ 12 weeks3 visits

Follow Up ~ 1 day1 visit

Screening ~ 1 day

Treatment ~ 12 weeks

Follow Up ~1 day

This trial's timeline: 1 day for screening, 12 weeks for treatment, and 1 day for reporting.

Treatment Details

Study Objectives

Study objectives can provide a clearer picture of what you can expect from a treatment.

Primary study objectives

Alzheimer's Disease Assessment Scale-Cognitive Subscale 11

Alzheimer's Disease Cooperative Study-Clinical Global Impression of Change

Secondary study objectives

Alzheimer's Disease Cooperative Study-Instrumental Activities of Daily Living Scale

Digital Symbol Substitution Test

Mini Mental State Examination Score

Side effects data

From 2022 Phase 1 & 2 trial • 75 Patients • NCT04524351

10%

procedural headache

10%

paraesthesia

10%

back pain

10%

headache

10%

constipation

10%

post lumbar puncture syndrome

10%

erythema

100%

80%

60%

40%

20%

Study treatment Arm

Posiphen, 40mg (Parkinson's Participants)

Posiphen, 20mg (Parkinson's Participants)

Posiphen, 10mg (Parkinson's Participants)

Posiphen, 80mg (Parkinson's Participants)

Posiphen, 5mg (Parkinson's Participants)

Placebo (Parkinson's Participants)

Placebo (Alzheimer's Participants)

Posiphen, 80mg (Alzheimer's Participants)

Trial Design

4Treatment groups

Experimental Treatment

Placebo Group

Group I: 7.5mg BuntanetapExperimental Treatment1 Intervention

Buntanetap 7.5mg oral capsule with daily administration for a period of 12 weeks

Group II: 30mg BuntanetapExperimental Treatment1 Intervention

Buntanetap 30mg oral capsule with daily administration for a period of 12 weeks

Group III: 15mg BuntanetapExperimental Treatment1 Intervention

Buntanetap 15mg oral capsule with daily administration for a period of 12 weeks

Group IV: PlaceboPlacebo Group1 Intervention

Placebo oral capsule with daily administration for a period of 12 weeks

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Research Highlights

Information in this section is not a recommendation. We encourage patients to speak with their healthcare team when evaluating any treatment decision.

Mechanism Of Action

Side Effect Profile

Prior Approvals

Other Research

The most common treatments for Alzheimer's Disease (AD) include cholinesterase inhibitors (e.g., donepezil, rivastigmine) and NMDA receptor antagonists (e.g., memantine). Cholinesterase inhibitors work by preventing the breakdown of acetylcholine, a neurotransmitter important for learning and memory, thereby enhancing cholinergic function. NMDA receptor antagonists help regulate glutamate activity to prevent excitotoxicity, which can damage neurons. Buntanetap, similar to other investigational drugs, aims to inhibit the aggregation of amyloid-beta and tau proteins, which are believed to form toxic plaques and tangles in the brain, contributing to neuronal death and cognitive decline. This mechanism is crucial as it targets the underlying pathology of AD, potentially slowing disease progression and improving patient outcomes.