TB006 is a monoclonal antibody targeting Galectin-3 (LGALS3), a beta-galactoside-binding lectin that plays a central role in chronic neuroinflammation and the inflammaging process underlying neurodegenerative disease progression. Developed by TrueBinding, Inc., TB006 is currently in a Phase 2a multicenter, randomized, double-blind, placebo-controlled clinical trial for Parkinson's disease (PD)[1].
This trial represents a novel therapeutic approach that differs fundamentally from dopaminergic replacement strategies: rather than compensating for dopamine loss, TB006 aims to modify disease progression by resolving chronic neuroinflammation through Galectin-3 neutralization[2].
The trial is actively recruiting 62 participants with early-stage PD at 14 sites across the United States, with an expected completion date of March 2026[1:1].
| Attribute | Details |
|---|---|
| NCT Number | NCT06773962 |
| Phase | Phase 2a |
| Status | Recruiting |
| Study ID | TB006PD2101 |
| Sponsor | TrueBinding, Inc. |
| Start Date | March 2025 |
| Primary Completion | March 2026 |
| Enrollment | 62 participants (estimated) |
| Design | Randomized, double-blind, placebo-controlled, parallel group |
| Duration | 28 weeks |
| Route | Intravenous (IV) infusion |
| Arm | Type | Intervention |
|---|---|---|
| TB006 | Experimental | TB006 via IV infusion |
| Placebo | Placebo Comparator | Placebo via IV infusion |
The primary objectives are to assess the efficacy of TB006 in improving motor function and to assess the safety of TB006 in participants with Parkinson's disease[1:2].
(To be confirmed from full eligibility criteria — see ClinicalTrials.gov for complete list)
The inclusion of early-stage PD patients (within 5 years of diagnosis) reflects the growing recognition that neuroinflammatory processes are most active in the early disease phase when there is still substantial dopaminergic neuron survival in the substantia nigra pars compacta. Targeting inflammation at this stage may provide maximal neuroprotective benefit before significant neuronal loss has occurred.
| Site | City | State |
|---|---|---|
| Parkinson's Research Centers of America — Orange County | Aliso Viejo | California |
| Parkinson's Research Centers of America — Palo Alto | Palo Alto | California |
| CenExel Rocky Mountain Clinical Research | Englewood | Colorado |
| Parkinson's Disease and Movement Disorders Center of Boca Raton | Boca Raton | Florida |
| University of Miami | Miami | Florida |
| University of South Florida Parkinson's and Movement Disorders Center | Tampa | Florida |
| Consultants in Neurology, Ltd | Northbrook | Illinois |
| Josephson Wallack Munshower Neurology — Southeast | Indianapolis | Indiana |
| University of Kansas Medical Center | Kansas City | Kansas |
| Quest Research Institute | Farmington Hills | Michigan |
| Parkinson's Research Centers of America — Long Island | Commack | New York |
| NYU Langone Health | Patchogue | New York |
| Oregon Health & Science University | Portland | Oregon |
| Central Texas Neurology Consultants | Round Rock | Texas |
Contact: TrueBinding, Inc. — clinicaltrial@truebinding.com — 650-847-1117
Galectin-3 (LGALS3) is a unique member of the galectin family distinguished by its N-terminal proline-rich domain, which enables its involvement in diverse cellular processes. In the central nervous system, Galectin-3 is primarily expressed in microglia, the brain's resident immune cells[3].
Galectin-3 serves as a key marker of disease-associated microglia (DAM) or neurodegenerative microglia — a microglial activation state driven by chronic neuroinflammation. Elevated Galectin-3 levels have been documented in postmortem brain tissue from both Alzheimer's disease and Parkinson's disease patients, and in CSF and blood from living patients[4].
TB006 is a monoclonal antibody designed to neutralize Galectin-3, thereby resolving the chronic neuroinflammation characteristic of neurodegenerative disease[2:1].
Key mechanisms:
Microglial phenotype modulation — Galectin-3 promotes pro-inflammatory (M1) microglial activation. Antibody neutralization shifts microglia toward an anti-inflammatory, neuroprotective (M2) phenotype, reducing secretion of IL-1β, TNF-α, and other pro-inflammatory cytokines[5].
Phagocytosis enhancement — Galectin-3 inhibits the clearance of pathological protein aggregates (alpha-synuclein, amyloid-beta, tau). Neutralizing Galectin-3 restores microglial phagocytic function, enhancing clearance of alpha-synuclein aggregates and potentially slowing Lewy body formation[3:1].
Inflammasome inhibition — Galectin-3 activates the NLRP3 inflammasome, a key driver of chronic neuroinflammation. TB006 blocks this activation, reducing caspase-1 activation and IL-1β release[4:1].
Inflammaging resolution — The concept of "inflammaging" refers to chronic, low-grade systemic inflammation that accelerates aging processes and neurodegeneration. TrueBinding's approach specifically targets Galectin-3 as a master regulator of this inflammaging process[(@truebinding2025)].
TB006's PD trial follows a Phase 1b/2a trial in Alzheimer's disease, which showed improvements in Clinical Dementia Rating-Sum of Boxes (CDR-SB) scores in patients[(@truebinding2025)]. This provides early human proof-of-concept for the anti-inflammaging approach in neurodegeneration.
TrueBinding has received FDA Expanded Access Program (EAP) authorization for TB006 in dementia including Alzheimer's disease, allowing patient access outside the clinical trial setting[(@truebinding2025)].
The fact that the same Galectin-3 targeting approach shows signals in both Alzheimer's and Parkinson's disease is significant, as it suggests chronic neuroinflammation and inflammaging may represent a shared upstream driver across multiple neurodegenerative conditions. This aligns with the growing body of evidence supporting a central role for neuroinflammation in Alzheimer's and Parkinson's disease as both a cause and consequence of pathology[(@joachim2024)].
| Agent | Target | Mechanism | Trial Status |
|---|---|---|---|
| TB006 | Galectin-3 | mAb neutralization | Phase 2a (NCT06773962) |
| Exenatide | GLP-1R | Agonist, anti-inflammatory | Phase 3 complete |
| AMBX-0035 | NLRP3 | Small molecule inhibitor | Phase 2 planned |
| BIA 28-6156 | GBA | Small molecule | Phase 1/2 (NCT05967842) |
| Cinumercept | Nogo receptor | Fusion protein | Phase 2 (NCT04449485) |
TB006 represents one of the most direct anti-inflammatory approaches in PD, targeting a specific mediator (Galectin-3) rather than a receptor or broader inflammatory pathway. The antibody format (IV infusion) may provide advantages in CNS penetration compared to small molecules.
A Phase 2a Multicenter Clinical Trial of TB006 in Participants With Parkinson's Disease (NCT06773962). 2025. ↩︎ ↩︎ ↩︎
TrueBinding Official Website. 2025. ↩︎ ↩︎
Beraud M, et al. Galectin-3 in neurodegenerative disease pathogenesis and therapeutic potential. Journal of Neurochemistry. 2024. ↩︎ ↩︎
Joachim SC, et al. Galectin-3 as a therapeutic target in neuroinflammation. Trends in Neurosciences. 2024. ↩︎ ↩︎
Pasternak O, et al. Galectin-3 inhibition reduces neuroinflammation and improves cognitive outcomes. Neurobiology of Disease. 2022. ↩︎