What side effects are associated with this type of intervention?

Common treatments for Alzheimer's Disease that target amyloid plaques, tau proteins, or neuroinflammation include aducanumab, vitamin E, and anti-inflammatory drugs. Aducanumab can cause amyloid-related imaging abnormalities (ARIA), headaches, falls, diarrhea, and confusion. Vitamin E is generally well-tolerated but may offer only modest benefits. Anti-inflammatory drugs, such as NSAIDs, have not shown significant benefits in clinical trials and can increase the risk of cardiovascular events and other adverse effects. These treatments aim to modify disease progression but come with varying degrees of side effects and efficacy.

What prior FDA approvals exist?

Several FDA-approved treatments for Alzheimer's Disease target amyloid plaques, tau proteins, or neuroinflammation. Aducanumab, an anti-amyloid monoclonal antibody, targets amyloid-beta plaques and was approved for its potential to slow cognitive decline. Other drugs like donepezil and galantamine, which are acetylcholinesterase inhibitors, have shown promise in managing symptoms by enhancing cholinergic function. Additionally, memantine, an NMDA receptor antagonist, helps regulate glutamate activity to protect neurons. These treatments aim to modify disease progression or manage symptoms, aligning with the mechanisms being studied in the TB006 trial.

What other types of research exist?

Promising novel alternatives to TB006 for Alzheimer's Disease treatment include: 1) Solanezumab, which targets amyloid-beta monomers; 2) Aducanumab, which targets amyloid-beta oligomers and plaques; 3) Crenezumab, which targets amyloid-beta oligomers; and 4) Gantenerumab, which targets amyloid-beta fibrils. These monoclonal antibodies are in advanced stages of clinical trials and focus on amyloid-related mechanisms. Additionally, natural products and semi-synthetic compounds are being explored as potential sources for new AD drugs.

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Monoclonal Antibodies

TB006 for Alzheimer's Disease

Phase 2

Waitlist Available

Research Sponsored by TrueBinding, 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 3 weeks

Treatment Varies

Follow Up baseline and up to 113 weeks

Awards & highlights

No Placebo-Only Group

Summary

This trial is testing TB006, a treatment for Alzheimer's disease. It includes people who were part of a previous study or were eligible for it. Researchers want to see how safe TB006 is, how it moves through the body, and its effects on Alzheimer's symptoms over time. T-006, a small-molecule compound derived from tetramethylpyrazine (TMP), has potential for the treatment of neurological diseases.

Who is the study for?

This trial is for adults with Alzheimer's who finished the TB006AD2102 study or could have joined it. They must be able to understand the study, follow visit schedules, and use contraception if needed. New participants should be over 50 years old, weigh at least 50 kg, have a BMI of 18-35 kg/m^2, an MMSE score of 24 or less, and be able to walk.

What is being tested?

The trial tests TB006's safety and effects in Alzheimer's patients over up to 113 weeks. It looks at how the body processes the drug (pharmacokinetics) and its impact on disease markers (pharmacodynamics). Everyone gets TB006 since it’s an open-label extension study.

What are the potential side effects?

Specific side effects aren't listed here but generally include any negative reactions experienced by participants during previous studies with TB006 or might arise from long-term use.

Timeline

Screening ~ 3 weeks3 visits

Treatment ~ Varies

Follow Up ~ baseline and up to 113 weeks

Screening ~ 3 weeks

Treatment ~ Varies

Follow Up ~baseline and up to 113 weeks

This trial's timeline: 3 weeks for screening, Varies for treatment, and baseline and up to 113 weeks for reporting.

Treatment Details

Study Objectives

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

Primary study objectives

Change from Baseline in Columbia Suicide Severity Rating Scale (C-SSRS)

Secondary study objectives

Change from Baseline in Clinical Dementia Rating Scale-Sum of Boxes (CDR SB) score

Change from Baseline in EuroQol 5 Dimension 5-Level quality of life (EQ 5D 5L QoL) total score

Change from Baseline in Mini Mental State Examination (MMSE) score

+2 more

Side effects data

From 2022 Phase 1 & 2 trial • 154 Patients • NCT05074498

14%

Thyroid function test abnormal

14%

Pyrexia

14%

Blood urea increased

14%

Gastroenteritis

14%

Sinus tachycardia

14%

Nausea

14%

Asthenia

14%

Fatigue

14%

COVID-19

14%

Insomnia

100%

80%

60%

40%

20%

Study treatment Arm

Part 2: Placebo

Part 1: TB006 140 Milligrams (mg) Weekly (qw)

Part 1: Placebo

Part 1: TB006 420 mg qw

Part 2: TB006 1000 mg qw

Part 1: TB006 1000 mg qw

Awards & Highlights

No Placebo-Only Group

All patients enrolled in this study will receive some form of active treatment.

Trial Design

1Treatment groups

Experimental Treatment

Group I: TB006 4000 mgExperimental Treatment1 Intervention

TB006 4000 milligram (mg) via a 1-hour continuous intravenous (IV) infusion will be administered once every 28 day

Treatment

First Studied

Drug Approval Stage

How many patients have taken this drug

TB006

2021

Completed Phase 2

~160

Do I qualify?Apply below to find out

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

Common treatments for Alzheimer's Disease often target amyloid plaques, tau proteins, and neuroinflammation. Amyloid-targeting therapies, such as aducanumab, aim to reduce amyloid-beta plaques in the brain, which are believed to contribute to neuronal damage and cognitive decline. Tau protein-targeting treatments focus on preventing the formation of neurofibrillary tangles, another hallmark of AD that disrupts neuronal function. Anti-inflammatory approaches aim to reduce neuroinflammation, which is thought to exacerbate neuronal damage. These mechanisms are crucial as they address the underlying pathophysiological processes of AD, potentially slowing disease progression and improving cognitive function in patients.

Disease modifying strategies for the treatment of Alzheimer's disease targeted at modulating levels of the beta-amyloid peptide.