TB-006: A Galectin-3-Targeting Monoclonal Antibody for Neurodegenerative and Neuroinflammatory Disorders

I. Executive Summary

TB-006 is an investigational humanized monoclonal antibody developed by TrueBinding, Inc., designed to target Galectin-3 (Gal3).[1] This protein is increasingly recognized for its role in the pathogenesis of various neurological disorders, primarily through its involvement in neuroinflammation and the aggregation of pathological proteins. The primary clinical focus for TB-006 has been Alzheimer's Disease (AD), where early-phase clinical trials have suggested potential for cognitive improvement and disease modification.[4] Beyond AD, TrueBinding is actively expanding the development of TB-006 into other neurological conditions, including Parkinson's Disease (PD), Autism Spectrum Disorder (ASD), and Acute Ischemic Stroke (AIS), with preclinical interest in Amyotrophic Lateral Sclerosis (ALS) and Glioblastoma.[2] Currently, TB-006 is in various stages of Phase 2 clinical development for these indications and is available for AD patients through an Expanded Access Program (EAP) in the U.S. and a Named Patient Program (NPP) in Hong Kong.[7] The therapeutic strategy of targeting Galectin-3 aims to address common underlying pathological mechanisms, particularly neuroinflammation and protein misfolding, which are implicated across this spectrum of diverse neurological diseases. This approach, if validated through ongoing and future clinical trials, could establish TB-006 as a significant and versatile therapeutic agent for conditions with high unmet medical needs.

The selection of Galectin-3 as a therapeutic target is based on its multifaceted role in disease pathology. Galectin-3 is implicated not only in the aggregation of amyloid-beta (Aβ) and phosphorylated Tau (pTau), the hallmark proteins of AD, but also alpha-synuclein, which is central to PD.[1] Furthermore, Galectin-3 is a known mediator of neuroinflammatory processes, including microglial activation, which is a common feature in AD, PD, ASD, and the acute damage following a stroke.[1] By developing a monoclonal antibody that inhibits Galectin-3, TrueBinding is pursuing a strategy that could potentially modulate these fundamental disease processes. This broad therapeutic hypothesis is reflected in the concurrent clinical development programs across these distinct neurological disorders. The success of this strategy hinges on demonstrating robust clinical efficacy and safety in larger, well-controlled trials, building upon the preliminary, encouraging signals observed to date.

II. Introduction to TB-006

TB-006 (also referred to as TB006) is an investigational therapeutic agent currently under development by TrueBinding, Inc..[1] TrueBinding, Inc., headquartered in Foster City, California, USA, is a clinical-stage biopharmaceutical company focused on creating novel therapies for neurodegenerative diseases, stroke, oncology, and other conditions with significant unmet medical needs.[1] The company is led by key personnel including Dr. Dongxu Sun, Ph.D., as Chief Executive Officer, George Hong as CEO and Co-Founder, and Alan K. Jacobs, M.D., FAAN, as Chief Medical Officer.[1]

TB-006 is classified as a humanized monoclonal antibody.[1] The process of "humanization" is a critical step in the development of therapeutic antibodies that originate from non-human species, such as mice. Murine antibodies, if administered to humans, can elicit an immune response, often termed a Human Anti-Mouse Antibody (HAMA) response. This immunogenicity can lead to reduced efficacy due to neutralization or rapid clearance of the therapeutic antibody, and can also cause adverse reactions. Humanization involves genetically engineering the antibody to replace most of the non-human protein sequences with human sequences, while retaining the specific antigen-binding regions (complementarity-determining regions, or CDRs). This modification significantly reduces the likelihood of an immune response, thereby enhancing the safety profile and allowing for more sustained therapeutic activity, which is particularly important for drugs intended for chronic conditions such as Alzheimer's Disease.

Table 1: TB-006 Key Drug Information

Feature	Description	Supporting Snippets
Official Name	TB-006	3
Developer	TrueBinding, Inc.	1
Drug Class	Humanized Monoclonal Antibody	1
Biological Target	Galectin-3 (Gal3)	1

The primary biological target of TB-006 is Galectin-3 (Gal3).[3] This targeted approach forms the basis of its proposed therapeutic effects across a range of neurological disorders.

III. Mechanism of Action

The therapeutic strategy of TB-006 centers on its ability to specifically bind to and modulate the activity of Galectin-3 (Gal3), a protein implicated in a variety of pathological processes within the central nervous system.

Target: Galectin-3 (Gal3)

TB-006 is a humanized monoclonal antibody engineered for high specificity and affinity towards Galectin-3.9 Gal3, a member of the β-galactoside-binding lectin family, is found to be abnormally upregulated in the brains of patients with Alzheimer's Disease and is also implicated in the pathology of other neurodegenerative conditions.9

The pathological roles attributed to Galectin-3 are multifaceted:

1. Promotion of Pathological Protein Aggregation: Gal3 has been described as acting like a "glue" or "molecular scaffold" that facilitates the aggregation of key pathological proteins. This includes amyloid-beta (Aβ) and phosphorylated Tau (pTau) in Alzheimer's Disease, and alpha-synuclein in Parkinson's Disease, leading to the formation of toxic oligomers and plaques/tangles.[1] These aggregates are known to disrupt neuronal communication and contribute to cognitive decline.
2. Driver of Neuroinflammation: Galectin-3 plays a significant role in neuroinflammatory pathways. It is involved in the sustained release of pro-inflammatory molecules such as cytokines and chemokines, and contributes to the activation of microglia, the brain's resident immune cells.[1] Notably, Gal3 has been identified as a novel endogenous ligand for TREM2 (Triggering Receptor Expressed on Myeloid cells 2), a key receptor on microglia that detrimentally regulates the inflammatory response in AD.[9]

Pharmacodynamics: How TB-006 Works

By binding to and neutralizing Galectin-3, TB-006 is hypothesized to exert its therapeutic effects through several mechanisms:

1. Inhibition of Protein Aggregation: TB-006 is designed to disrupt the formation of Aβ plaques and Tau tangles by blocking Gal3's scaffolding function.[1] This action prevents the self-assembly of these proteins into neurotoxic species.
2. Dissolution of Existing Aggregates: There is also a suggestion that TB-006 may weaken the bonds within existing protein aggregates, potentially facilitating their dissolution and clearance.[17]
3. Reduction of Neuroinflammation: By inhibiting Gal3, TB-006 aims to mitigate neuroinflammation. This is achieved by reducing Gal3-driven microglial activation and the subsequent release of harmful pro-inflammatory cytokines and chemokines.[1]
4. Restoration of Neuronal Function: The combined effect of reducing protein aggregation and neuroinflammation is expected to restore synaptic integrity, allow neurons to resume normal communication, and consequently improve cognitive function and potentially reverse symptoms associated with these neurological disorders.[16]

This mechanism of targeting Galectin-3 is distinct from many current Alzheimer's therapies that directly target amyloid-beta, such as aducanumab (Aduhelm®) or lecanemab (Leqembi®).[4] While those antibodies focus on Aβ, TB-006's inhibition of Gal3 is proposed to impact a broader array of pathogenic factors including Aβ, Tau, alpha-synuclein, and APOE4, in addition to neuroinflammation.[4] This broader mechanistic scope suggests potential applicability in a wider range of patients, including those who may be amyloid-negative, a significant departure from amyloid-centric therapies.[4]

The targeting of Galectin-3 represents a potentially more upstream intervention in neurodegenerative pathways. Pathological protein aggregation and neuroinflammation are complex, interconnected processes. Galectin-3 appears to sit at a nexus, influencing both. By inhibiting a protein that acts as a common facilitator for multiple types of pathological protein aggregates and as a driver of neuroinflammation, TB-006 may offer a more comprehensive therapeutic effect than agents targeting a single downstream element (e.g., only Aβ). This multi-faceted impact could explain the rationale for investigating TB-006 across diverse neurological conditions like AD (amyloid and tau pathology), PD (alpha-synucleinopathy), and ASD/stroke (where neuroinflammation is a key component).

Furthermore, the reported potential efficacy of TB-006 in AD patients irrespective of their amyloid plaque status is a noteworthy claim.[4] Current leading AD therapies often require PET imaging to confirm amyloid pathology for patient eligibility. If TB-006 demonstrates efficacy in both amyloid-positive and amyloid-negative individuals, it would imply that Galectin-3-mediated neuroinflammation or non-amyloid proteinopathies (such as Tau pathology) are significant, and perhaps partially independent, drivers of cognitive decline in a broader AD population. This could substantially expand the treatable patient population for AD and potentially simplify diagnostic and patient selection criteria by reducing the reliance on amyloid PET imaging.

Potential for Disease Modification and Reversal

A key aspiration for TB-006 is its potential not only to manage symptoms but to modify the underlying disease course and possibly reverse existing symptoms.4 This is based on its mechanism of addressing what are considered root causes of these neurodegenerative diseases, namely protein aggregation and chronic neuroinflammation.17

IV. Preclinical Development

The progression of TB-006 into clinical trials was underpinned by a series of preclinical studies, primarily in animal models of Alzheimer's Disease, which indicated its therapeutic potential.

Summary of In Vitro and In Vivo (Animal Model) Studies

TrueBinding has reported strong preclinical data from AD animal models supporting the efficacy of TB-006.21 In some of these studies, a surrogate antibody, mTB001 (presumably a murine version or precursor to the humanized TB-006), was utilized in transgenic mouse models of AD (such as APPSwe and 5xFAD lines, which develop amyloid pathology) and in models where Aβ is directly injected into the brain.21

Key Efficacy Findings from Preclinical Studies

The preclinical research highlighted several positive effects of Galectin-3 inhibition:

• Reduction of Pathological Protein Aggregates: Treatment with TB-006 or its surrogate led to a significant reduction in total Aβ plaques and other neurodegeneration-associated biomarkers. These effects were observed even after relatively short treatment durations, such as two weeks in some mouse model experiments.[1] The mechanism is believed to involve preventing the aggregation of Aβ and facilitating the dissolution of existing plaques.[21] Additionally, preclinical evaluations indicated that Galectin-3 intrinsically promotes the aggregation of Tau proteins, and TB-006 showed capabilities in reducing this aggregation.[1] There is also preclinical evidence suggesting TB-006 may prevent the formation of alpha-synuclein aggregates, a pathology central to Parkinson's Disease.[10]
• Mitigation of Neuroinflammation: A core aspect of TB-006's proposed mechanism is its ability to reduce neuroinflammation. Preclinical studies demonstrated that targeting Galectin-3 leads to a significant reduction in neuroinflammatory markers.[1]
• Improvement in Cognitive Function: Corresponding with the observed reductions in pathological proteins and neuroinflammation, treatment with TB-006 or its surrogate resulted in significant improvements in cognitive performance in AD animal models, particularly in tasks related to hippocampal-dependent spatial memory.[1]
• Potential for Neurogenesis: Some preclinical AD studies have also suggested that treatment with TB-006 might lead to an increase in neurogenesis, or the growth of new brain cells.[30]

The multifaceted preclinical efficacy profile, demonstrating impacts on amyloid pathology, tau pathology, neuroinflammation, and even potentially neurogenesis, strongly supports the therapeutic hypothesis centered on Galectin-3. Galectin-3's involvement in these diverse pathological pathways provides a rationale for these broad effects. The observation of significant improvements in animal models after short treatment durations (e.g., two weeks) is particularly noteworthy and may have informed the design of early human clinical trials, such as the one-month treatment regimen used in the Phase 1b/2a study for Alzheimer's Disease.

Pharmacokinetics and Toxicology Highlights

Detailed peer-reviewed publications on the specific preclinical pharmacokinetics (PK) and toxicology (Tox) of TB-006 are not extensively covered in the provided materials. However, general statements indicate a favorable safety profile. The Alzheimer's Discovery Foundation's review of Galectin-3 inhibitors (a class to which TB-006 belongs, though it is an antibody and administered intravenously) mentions that clinically tested inhibitors generally show good safety, although the profile can depend on the route of administration (oral formulations showing gastrointestinal effects).19 TB-006 itself is administered intravenously.14 Human safety of TB-006 was initially established in a single, escalating dose safety and tolerability study in healthy volunteers, where doses up to 5000 mg were reported as safe and well-tolerated.5

Publications

Several publications and presentations allude to the preclinical work on TB-006 and Galectin-3:

• A key publication appears to be from Rasool, Patel, Johansson, Voloboueva, Lee, Sun, Lan, Ahmed, and Dongxu Sun (CEO of TrueBinding) in Alzheimer's & Dementia (2022), titled "Potential Reversal of Alzheimer's Disease pathology by Antibody TB006 Targeting Galectin‐3, the Root Cause of Oligomerization of Amyloid Proteins".[15] This likely contains significant preclinical data.
• A bioRxiv preprint by Boza-Serrano et al. (2025), "Galectin-3 deletion modulates microglial phenotype and Aβ response via TREM2 activation while attenuating neuroinflammation," references the promising Phase 1b/2a clinical trial results of TrueBinding's TB006 (NCT05074498) and underscores Galectin-3 as a critical mediator in microglial response and AD pathology.[12] While this paper focuses on Gal3 deletion, its mention of TB006 highlights the antibody's relevance in the field.

V. Clinical Development Program

TrueBinding, Inc. is pursuing a broad clinical development program for TB-006, investigating its therapeutic potential across several neurological disorders. The strategy leverages the hypothesis that Galectin-3 plays a pivotal role in shared pathological mechanisms, such as neuroinflammation and protein aggregation, common to these conditions. Alzheimer's Disease represents the most advanced program, with other indications including Parkinson's Disease, Autism Spectrum Disorder, and Acute Ischemic Stroke also in clinical phases.

Table 2: TB-006 Clinical Trial Overview

NCT Number	Indication	Phase	Trial Title/Brief Description	Status (as of latest info)	Sponsor/Collaborator	Key Objectives/Endpoints (Selected)	No. of Participants	Start Date	Est. Primary Completion
NCT04920786	Healthy Volunteers (AD Program)	Phase 1	Safety and Tolerability of TB006	Completed	TrueBinding, Inc.	Safety, Tolerability	N/A	Summer 2021	N/A
NCT05074498	Alzheimer's Disease (Mild to Severe)	Phase 1b/2a	Safety, Tolerability, PK, PD, and Efficacy of TB006	Completed	TrueBinding, Inc.	CDR-SB, MMSE, Safety, Biomarkers (Aβ42 plasma, Imaging)	157	Oct 2021	N/A (Results announced Nov 2022)
N/A (OLE for NCT05074498)	Alzheimer's Disease	Open Label Extension	Long-term Safety, Tolerability, PK, PD of TB006	Active, Not Recruiting (Recruitment completed)	TrueBinding, Inc.	Long-term safety, CDR-SB, Cognitive/Functional measures	~150-180 (119 treated for avg. 8 mo)	Sep 2022	Up to 2 years per participant
N/A (Planned)	Alzheimer's Disease	Phase 2b	Longer-term Efficacy and Safety	Planned (as of Mar 2023)	TrueBinding, Inc.	N/A	N/A	N/A	N/A
NCT05959239	Alzheimer's Disease & Related Dementias	Expanded Access Program	Compassionate Use of TB006	Active	TrueBinding, Inc.	Provide access, Monitor AEs/SAEs	No limit (Open Access)	Dec 09, 2024 (Actual)	N/A
NCT06773962	Parkinson's Disease (Early to Mild)	Phase 2A	Safety and Efficacy of TB006 on Motor Function	Recruiting (IND cleared Nov 2024)	TrueBinding, Inc.	Change in Parkinson's Disease Rating Scale Score, AEs/SAEs	62 (Est.)	Jan 14, 2025 (Est.)	Q1 2026 / Dec 29, 2025 (Est.)
NCT06500637	Autism Spectrum Disorder (Adults)	Phase 2 (IIT)	Safety and Efficacy of TB006 on Core ASD Symptoms	Recruiting (IND approved July 2024)	TrueBinding, Inc. (IIT)	Improvement in core/associated behavioral symptoms, Safety	N/A	N/A	July 31, 2026 (Est.)
NCT05156827	Acute Ischemic Stroke	Phase 2	Safety and Efficacy of TB006	Status Unclear (IND approved Feb 2022, no recent updates in snippets)	TrueBinding, Inc.	Safety and Efficacy	N/A	N/A	N/A

N/A: Not Available in provided snippets. Status and dates are based on the latest information within the research material and may require direct verification from ClinicalTrials.gov for real-time accuracy.

A. Alzheimer's Disease (AD)

The Alzheimer's Disease program for TB-006 is the most advanced for TrueBinding.

• Phase 1 Trial (Healthy Volunteers - NCT04920786): This initial study, commenced in the summer of 2021, aimed to establish the safety and tolerability of TB-006 in healthy individuals.23 It was reported that single, escalating doses up to 5000 mg were safe and well-tolerated, providing the foundational human safety data necessary to proceed to patient trials.5
• Phase 1b/2a Trial (NCT05074498): "A Seamless Phase 1b/2a Double-blind, Randomized, Multiple dose, Multi-center, Sequential Dose-escalation Study to Assess the Safety, Tolerability, Pharmacokinetics, Pharmacodynamics and Efficacy of TB006 in Patients with Mild to Severe Alzheimer's Disease".[33]
• Status: This trial is completed. Patient recruitment was finished by May 20, 2022, and topline results were announced in November 2022.[5]
• Design: The study was conducted at 15 active sites in the U.S. The Phase 1b portion involved sequential dose escalation (140 mg, 420 mg, 1000 mg weekly for one month). The Phase 2a portion randomized patients (1:1) to receive either TB-006 (1000 mg) or placebo, administered weekly for one month.[5]
• Patient Population: A total of 157 patients with mild to severe AD, confirmed by a screening Mini-Mental State Examination (MMSE) score of ≤24, were enrolled. Notably, amyloid positivity (confirmed by PET imaging or CSF analysis) was not an inclusion criterion, allowing for a broader patient population.[4]
• Key Efficacy Endpoints & Results:
• The primary endpoint was the change from baseline on the Clinical Dementia Rating-Sum of Boxes (CDR-SB) score through Day 104. The results showed a reduction in the CDR-SB score for the TB-006 group compared to placebo, with a reported treatment difference of 63% (score change of -0.44 points). This finding trended toward statistical significance (p=0.08) in the intent-to-treat (ITT) population, which is an encouraging signal given the short one-month treatment duration.[4] Improvements on the CDR-SB were observed as early as 15 days after the first treatment and continued through Day 36, diminishing after treatment cessation.[24]
• A key secondary endpoint, the MMSE, demonstrated a statistically significant improvement (p=0.02) in the TB-006 group at Day 36, with a 1.02 point improvement compared to placebo.[5]
• Biomarker analyses indicated that TB-006 significantly reduced plasma levels of Aβ42.[5] Furthermore, improvements in PET and MR imaging were reported, consistent with the dissolution of toxic amyloid plaques, as suggested by preclinical studies.[7]
• Subgroup analyses suggested that patients with mild AD experienced more pronounced and sustained improvements, while the mild-to-moderate AD group also showed signs of disease reversal with statistically significant outcomes on some measures.[9]
• Safety: TB-006 was reported to be safe and well-tolerated throughout the 3.5-month observation period. The most common adverse event (AE) was infusion reaction, which was generally minor. Importantly, no treatment-related serious adverse events (SAEs) and no imaging-related abnormalities, such as Amyloid-Related Imaging Abnormalities (ARIA-E or ARIA-H), were detected through clinical laboratory evaluations, imaging, or ECGs.[4]
• Open Label Extension (OLE) Study (for NCT05074498): "A Long-term Extension study to Assess the Safety of TB006 in Participants with Alzheimer's Disease".[36]
• Purpose: This ongoing study aims to evaluate the long-term safety, tolerability, pharmacokinetics (PK), and pharmacodynamics (PD) of TB-006 in participants who completed the lead-in Phase 1b/2a study, as well as in some de novo participants.[36]
• Status: The OLE study commenced in September 2022.[25] Recruitment is completed, with over 100 participants enrolled, including 119 patients who had been treated for an average of 8 months as of early 2025 reports.[9] The study will follow participants for up to two years, with a total study duration of up to 113 weeks.[25]
• Patient Population: The study includes 100-120 participants from the NCT05074498 trial and up to 50 de novo participants, for a total of approximately 150-180 individuals.[36]
• Dosage: Participants receive TB-006 at a dose of 4000 mg via intravenous (IV) infusion every 28 days.[24]
• Key Reported Outcomes (Early/Interim): Early results from the OLE study, particularly from a cohort of 79 participants who completed at least three months of treatment, have been encouraging. Among these, 47% showed signs of disease reversal or cognitive improvement, and an additional 28% exhibited disease stabilization, resulting in a positive response in the majority (75%) of these participants.[4] Across the broader OLE population (119 patients treated for an average of 8 months), CDR-SB scores were reported to be well-maintained around baseline levels.[9] Lower levels of inflammation have also been anecdotally reported.[25]
• Safety: The OLE study has continued to demonstrate a favorable safety profile, with no significant adverse events reported.[4]
• Planned/Ongoing Phase 2b Trial: TrueBinding has indicated plans to initiate a longer-term, 12-month, randomized, placebo-controlled Phase 2b trial for AD.1 As of early 2023, this trial was stated to "soon commence." However, specific details regarding its official start date or an NCT identifier were not found in the 2024-2025 updates within the provided research material.7 One news report from March 2025 mentioned that "Soon RB006 will start phase three of clinical trials".25 This statement requires clarification, as it could refer to the advanced Phase 2b study or a distinct Phase 3 trial. No official announcement or ClinicalTrials.gov registration for a Phase 3 trial for TB-006 in AD was identified for 2024 or 2025 within the provided snippets.39
• Expanded Access Program (EAP)/Compassionate Use (NCT05959239): "Expanded Access With TB006 Treatment in Adults With Alzheimer's Disease and Related Dementias".[31]
• Purpose: This program provides access to TB-006 for patients diagnosed with symptomatic AD or related dementias who have no other satisfactory treatment options and are unable or ineligible to participate in ongoing clinical trials.[11]
• Status: The EAP is active. It received initial FDA approval in May 2023 and was granted renewal approval by the FDA in May 2024.[7] The actual start date listed on ClinicalTrials.gov is December 09, 2024.[31] The program is open-access with no specified limit on the number of participants.[45]
• Eligibility: Key criteria include patients aged >55 years with symptomatic AD or related dementia (MMSE score ≤ 24), stable and well-managed comorbid medical conditions, and documentation showing they are unable to receive or have failed current anti-AD medications (including aducanumab and lecanemab), and are unable/ineligible for other AD clinical trials.[25]
• Dosage: Participants receive TB-006 at a dose of 4,000 mg IV every 28 days (± 5 days).[31]
• Data Collection: The sponsor, TrueBinding, primarily collects AE and SAE data from this program. Efficacy data collection is not a primary objective of the EAP from the sponsor's perspective, though treating physicians will monitor patient progress.[45]

Table 3: Summary of Key Efficacy Results from TB-006 Alzheimer's Disease Trials

Trial Phase/Study	Endpoint	TB-006 Result	Placebo Result	Treatment Difference/Effect Size	p-value	Timepoint	Patient Population	Supporting Snippets
Phase 1b/2a (NCT05074498)	CDR-SB (Primary)	Improvement trend		-0.44 points (63% diff. vs placebo)	0.08	Day 104 (after 1-month treatment)	Mild to Severe AD (ITT)	5
Phase 1b/2a (NCT05074498)	MMSE (Secondary)	Improvement		1.02 points better than placebo	0.02	Day 36 (after 1-month treatment)	Mild to Severe AD	5
Phase 1b/2a (NCT05074498)	Aβ42 Plasma Levels	Significant reduction		N/A	Significant	N/A	Mild to Severe AD	5
Phase 1b/2a (NCT05074498)	PET/MRI Imaging	Improvements consistent with amyloid plaque dissolution		N/A	N/A	N/A	Mild to Severe AD	7
OLE (following NCT05074498)	Cognitive Improvement / Disease Reversal	47% of participants	N/A (Open Label)	N/A	N/A	After 3 months treatment	Participants from Phase 2a and de novo	4
OLE (following NCT05074498)	Disease Stabilization	28% of participants	N/A (Open Label)	N/A	N/A	After 3 months treatment	Participants from Phase 2a and de novo	4
OLE (following NCT05074498)	CDR-SB	Maintained around baseline	N/A (Open Label)	N/A	N/A	Average 8 months treatment (119 patients)	Participants from Phase 2a and de novo	9

B. Parkinson's Disease (PD)

The development of TB-006 for Parkinson's Disease marks an expansion of TrueBinding's focus on Galectin-3 inhibition for neurodegenerative conditions characterized by protein misfolding (alpha-synuclein in PD) and neuroinflammation.

• Phase 2A Trial (NCT06773962): "A Phase 2a, Multicenter, Randomized, Double-Blind, Placebo-Controlled Study of the Safety and Efficacy of TB006 in Participants With Parkinson's Disease".[46]
• Status: The FDA cleared the Investigational New Drug (IND) application for this trial on November 18, 2024.[7] The trial is planned to be initiated in the U.S. and is listed with an estimated start date of January 14, 2025. The estimated primary completion date is Q1 2026 or December 29, 2025.[14] As of the latest information, results have not yet been posted.[46]
• Design: This is a multicenter, randomized, double-blind, placebo-controlled study.[14]
• Objectives: The primary objectives are to assess the efficacy of TB-006 in improving motor function and to evaluate its safety in participants with PD.[32]
• Patient Population: The trial aims to enroll approximately 62 adults, aged 50 to 80 years, diagnosed with early-stage PD (Hoehn and Yahr stage 1 or 2). Participants should be less than 5 years from their initial PD diagnosis and either on no other PD medications or only on immediate-release Levodopa-carbidopa/benserazide therapy.[14]
• Intervention: Participants will receive either TB-006 via IV infusion or a placebo IV infusion.[32]
• Primary Outcome Measures: The primary outcomes include the change from baseline in a Parkinson's Disease Rating Scale score and the number of participants experiencing adverse events (AEs) and serious adverse events (SAEs), all assessed at 28 weeks.[46]

C. Autism Spectrum Disorder (ASD)

The investigation of TB-006 in Autism Spectrum Disorder suggests a focus on the neuroinflammatory component of Galectin-3's activity, as ASD is increasingly understood to involve immune dysregulation.

• Phase 2 Investigator Initiated Trial (IIT) (NCT06500637): "A Multi-center Double Blind Placebo Controlled Study to Assess the Safety and Efficacy of TB006 for Improving Core Symptoms in Adults With Autism Spectrum Disorder".[3]
• Status: The FDA approved the IND for this Investigator Initiated Trial on July 9, 2024.[7] The trial is currently listed as recruiting.[3] The estimated study completion date is July 31, 2026.[52]
• Design: This is a 14-week prospective, multicenter, double-blind, placebo-controlled, parallel-group, randomized (2:1, TB-006:placebo) clinical trial. It includes a 14-week open-label extension phase for participants who initially received placebo.[51]
• Objectives: The primary goals are to evaluate the efficacy of TB-006 in improving core and associated behavioral symptoms of ASD in adults and to assess its safety and tolerability in this population.[52]
• Patient Population: The trial is enrolling adults diagnosed with ASD.[3]

D. Acute Ischemic Stroke (AIS)

The development of TB-006 for AIS likely targets the acute neuroinflammatory response and neuronal damage that occurs following a stroke.

• Phase 2 Trial (NCT05156827):
• Status: The FDA approved the IND for this Phase 2 trial on February 8, 2022.[3] Synapse lists the drug in Phase 2 for AIS.[3] However, the provided news snippets from late 2023 through 2025 do not contain recent updates on the recruitment status, progress, or results of this trial.[7] Direct verification via ClinicalTrials.gov would be necessary for the most current information.[53]
• Objectives: The trial aims to evaluate the safety and efficacy of TB-006 in patients who have experienced an Acute Ischemic Stroke.[7]

The expansion of TB-006 development into PD and ASD, following the initial focus on AD, underscores TrueBinding's confidence in the broad applicability of the Galectin-3 inhibitory mechanism. The use of an Investigator-Initiated Trial for ASD may represent a strategic, resource-efficient approach to gather preliminary human efficacy and safety data in a new indication, potentially leveraging external clinical expertise and infrastructure. Conversely, the absence of recent public updates regarding the Phase 2 trial for Acute Ischemic Stroke (NCT05156827) since its IND approval in early 2022 is notable. While clinical development timelines can be extensive and periods of silence are not uncommon, the lack of any news (positive or negative) for over two to three years for a Phase 2 study warrants attention. This could be due to various factors, such as the trial proceeding as planned without public milestones yet being reached, challenges in recruitment, a strategic deprioritization, or results that are pending analysis or publication. Without direct access to the current status on ClinicalTrials.gov, this remains an area requiring further information.

E. Other Potential Indications (ALS, Glioblastoma)

• Current Development Stage: TB-006 is listed in the preclinical stage of development for Amyotrophic Lateral Sclerosis (ALS) and Glioblastoma Multiforme (GBM).[2]
• Plans for Clinical Progression: The provided news snippets, particularly those from late 2023 to 2025, do not mention specific plans or timelines for advancing these preclinical programs into human clinical trials.[7] Other snippets found [5] discuss these diseases generally or refer to research by other entities or on different therapeutic agents, not specifically TrueBinding's TB-006 clinical advancement plans.

VI. Safety and Tolerability Profile

The safety and tolerability of TB-006 have been evaluated in healthy volunteers and in patients with Alzheimer's Disease across its Phase 1 and Phase 1b/2a trials, as well as in the ongoing Open Label Extension study and Expanded Access Program.

Summary of Safety Data Across Clinical Trials (Primarily AD):

TB-006 has generally been reported as well-tolerated. In the Phase 1 study involving healthy volunteers, single escalating doses up to 5000 mg were found to be safe.5 This favorable early safety profile extended into the Phase 1b/2a trial in patients with mild to severe Alzheimer's Disease.4 Anecdotal reports from compassionate use contexts also suggest a good safety record, with one source mentioning administration to over 300 patients with no adverse side effects reported, though this is outside the rigorous monitoring of a controlled trial.25

Common Adverse Events (AEs) and Serious Adverse Events (SAEs):

In the Phase 1b/2a AD trial, adverse events were generally minor. The most frequently reported AE was infusion reaction.5 Importantly, no treatment-related Serious Adverse Events (SAEs) were reported in this trial or in the early data from the Open Label Extension study.4

Incidence of Specific AEs of Interest (ARIA):

A significant finding from the AD clinical trials of TB-006 is the reported absence of Amyloid-Related Imaging Abnormalities (ARIA).5 ARIA, which can manifest as ARIA-E (edema/effusions) or ARIA-H (microhemorrhages/superficial siderosis), is a known class effect and a significant safety concern for many amyloid-beta targeting monoclonal antibodies used in AD treatment.40 The lack of ARIA with TB-006, if confirmed in larger and longer trials, would represent a major safety advantage. This distinction suggests that TB-006's mechanism of action, targeting Galectin-3 rather than directly binding to and clearing amyloid plaques in a manner that might disrupt vascular integrity, could circumvent the pathways leading to ARIA. This could simplify patient monitoring (reducing the need for frequent MRI scans specifically for ARIA) and improve the overall risk-benefit profile, potentially making the therapy suitable for a broader AD patient population, including those with cerebrovascular comorbidities who might be at higher risk for ARIA with other agents.

Safety Monitoring in EAP (NCT05959239):

The Expanded Access Program protocol includes recommendations for safety monitoring, such as clinical chemistry, hematology, and urinalysis; vital signs; electrocardiograms (ECGs); and brain MRIs to monitor for ARIA, although ARIA has not been associated with TB-006 to date.45

Table 4: Summary of Safety Profile of TB-006 in Alzheimer's Disease Trials

Trial/Study	Adverse Event Category	Frequency/Incidence in TB-006 group	Frequency/Incidence in Placebo group	Severity	Relatedness to Drug	Supporting Snippets
Phase 1 (Healthy Volunteers)	General Safety	Doses up to 5000 mg safe and well tolerated	N/A	N/A	N/A	5
Phase 1b/2a AD (NCT05074498)	Infusion Reaction	Most common AE	N/A (specific frequency not detailed)	Minor	N/A	5
Phase 1b/2a AD (NCT05074498)	Serious Adverse Events (SAEs)	None reported	None reported	N/A	No treatment-related SAEs	5
Phase 1b/2a AD (NCT05074498)	Amyloid-Related Imaging Abnormalities (ARIA)	None reported	None reported	N/A	N/A	5
OLE (following NCT05074498)	Significant Adverse Events	None reported	N/A (Open Label)	N/A	No drug-related SAEs	4
EAP (NCT05959239)	General Safety	Over 300 patients administered with "no adverse side effects reported" (compassionate use context)	N/A (Open Label)	N/A	N/A	25

VII. Regulatory Status and Milestones

TrueBinding, Inc. has achieved several key regulatory milestones in the development of TB-006 across its targeted indications.

FDA Investigational New Drug (IND) Clearances:

• Alzheimer's Disease: The initial IND application for TB-006 for the treatment of AD was granted clearance by the U.S. Food and Drug Administration (FDA) on April 23, 2021.[1]
• Acute Ischemic Stroke: An IND for a Phase 2 clinical trial of TB-006 in Acute Ischemic Stroke (NCT05156827) received FDA approval on February 8, 2022.[3]
• Parkinson's Disease: The FDA cleared an IND application for TB-006 for a Phase 2A clinical trial in Parkinson's Disease (NCT06773962) on November 18, 2024.[7]
• Autism Spectrum Disorder: An IND for an Investigator Initiated Phase 2 trial of TB-006 in adult Autism Spectrum Disorder (NCT06500637) was approved by the FDA on July 9, 2024.[7]

FDA End-of-Phase 2 (EOP2) Meeting for AD:

TrueBinding was granted a Type B End-of-Phase 2 meeting with the FDA, which was scheduled to occur in April 2023.1 The purpose of this meeting was to discuss the results of the clinical and non-clinical programs for TB-006 in AD, its readiness for a Biologics License Application (BLA), and to seek guidance on a potential rapid development pathway.1 However, the specific outcomes or detailed guidance resulting from this EOP2 meeting have not been publicly disclosed in the provided 2024-2025 news snippets.7 This lack of information on the FDA's feedback is a significant point of uncertainty regarding the subsequent steps in the AD program.

FDA Expanded Access Program (EAP) / Compassionate Use for AD:

TB-006 has been approved by the FDA for compassionate use under an Expanded Access Program for patients with AD and related dementias (NCT05959239).7 This program was initially approved in May 2023 and received FDA renewal approval in May 2024, allowing continued access for eligible patients.7

Hong Kong Department of Health Named Patient Program (NPP) for AD:

In April 2024, the Hong Kong Department of Health approved a Named Patient Program for the use of TB-006 in treating patients with dementia or Alzheimer's Disease. This program is reported to be actively recruiting patients.7

The rapid succession of IND clearances across four distinct neurological disorders (AD in April 2021, Stroke in February 2022, ASD IIT in July 2024, and PD in November 2024) within a relatively condensed timeframe highlights an assertive and ambitious development strategy by TrueBinding. This approach suggests a strong conviction in the broad therapeutic potential of targeting Galectin-3. Furthermore, the FDA's approval and subsequent renewal of the Expanded Access Program for AD, along with the establishment of a Named Patient Program in Hong Kong, indicate that regulatory authorities have acknowledged a potential unmet need and a preliminary favorable risk-benefit consideration for TB-006 in certain patient populations, even as pivotal clinical trials are presumably being planned or are yet to yield definitive results. Such programs are typically reserved for investigational drugs that show promise for serious conditions lacking adequate alternative therapies.

VIII. Discussion and Future Outlook

TB-006 represents a novel therapeutic approach with its unique mechanism of targeting Galectin-3, a protein implicated in the core pathologies of several neurodegenerative and neuroinflammatory disorders. The clinical development program, spearheaded by TrueBinding, Inc., has shown promising early signals, particularly in Alzheimer's Disease, and is rapidly expanding into other indications.

Synthesis of Findings and Unique Aspects:

The primary innovation of TB-006 lies in its targeting of Galectin-3. This strategy offers a multi-pronged attack on disease pathology by potentially inhibiting the aggregation of multiple pathogenic proteins (Aβ, Tau, alpha-synuclein) and concurrently reducing neuroinflammation.1 This contrasts with many therapies that focus on a single pathological element.

Key differentiating aspects of TB-006 include:

1. Broad Mechanistic Impact: Unlike therapies targeting only amyloid or tau, TB-006's action on Galectin-3 may address a wider array of disease drivers.
2. Potential Efficacy in Diverse AD Populations: Early data suggests TB-006 might be effective in AD patients regardless of their amyloid plaque status and across a spectrum of disease severity (mild, moderate, and severe AD).[4] This could significantly broaden its applicability compared to amyloid-specific treatments that often require PET confirmation of amyloid pathology and are typically indicated for early-stage disease.
3. Favorable Safety Profile (to date): A notable feature of the TB-006 clinical data so far is the reported absence of Amyloid-Related Imaging Abnormalities (ARIA) in AD trials.[5] ARIA is a significant concern with direct amyloid-clearing antibodies, requiring intensive monitoring and sometimes leading to treatment discontinuation. If TB-006 continues to demonstrate a lack of ARIA, it would be a substantial safety advantage.

Unmet Needs Addressed:

TB-006 aims to address the profound unmet need for effective and safe disease-modifying therapies for Alzheimer's Disease, Parkinson's Disease, Autism Spectrum Disorder, and Acute Ischemic Stroke. For AD, particularly, the prospect of a treatment that could benefit patients across various stages of severity and potentially irrespective of amyloid status, with a better safety profile regarding ARIA, is highly significant.

Future Research Directions and Anticipated Milestones:

The future trajectory of TB-006 hinges on several critical factors:

• Pivotal Trial Data for AD: The most immediate and crucial milestone is the initiation and successful completion of a well-designed, adequately powered Phase 2b or Phase 3 trial for Alzheimer's Disease. The design of this trial would ideally incorporate learnings from the FDA EOP2 meeting. Demonstrating statistically significant and clinically meaningful efficacy on primary endpoints in such a trial is paramount for regulatory approval.
• Results from Ongoing Phase 2 Trials: Data from the ongoing or recently initiated Phase 2 trials in Parkinson's Disease (NCT06773962), Autism Spectrum Disorder (NCT06500637), and the Phase 2 trial in Acute Ischemic Stroke (NCT05156827) will be critical in validating the therapeutic hypothesis for Galectin-3 inhibition in these distinct conditions.
• Long-Term OLE Data: Continued long-term follow-up from the AD Open Label Extension study will provide further insights into the durability of any observed effects and the long-term safety profile of TB-006.
• Biomarker Development: Further research into biomarkers that can predict response to TB-006 or track target engagement and downstream effects of Galectin-3 inhibition will be valuable for patient selection and monitoring.
• Elucidation of Galectin-3 Biology: Continued basic and translational research to further unravel the complex roles of Galectin-3 in the CNS under normal and pathological conditions will refine the understanding of TB-006's mechanism and potential.

A significant challenge for TB-006 in Alzheimer's Disease will be to translate the promising, albeit early-phase, clinical signals into robust, statistically significant efficacy in larger, longer, and more rigorously controlled pivotal trials. The Phase 1b/2a AD trial, while showing encouraging trends (e.g., p=0.08 for CDR-SB) and significant MMSE improvement over a very short treatment period, did not meet the conventional threshold for statistical significance on its primary endpoint.[5] The outcome of the End-of-Phase 2 meeting with the FDA, which occurred in April 2023, would have been instrumental in shaping the design, endpoints, and expectations for subsequent later-stage trials. The lack of publicly available detailed outcomes from this FDA meeting represents a critical information gap in assessing the forward path for the AD program.[7]

While the Expanded Access Program (NCT05959239) and Named Patient Program provide early access to TB-006 for patients with AD who have exhausted other options, it is important to recognize their limitations.[7] These programs are primarily designed for compassionate access and safety monitoring; the data collected (mainly AEs/SAEs by the sponsor) is typically uncontrolled and open-label, which limits its utility for definitive efficacy assessment for regulatory approval.[45] Robust evidence from well-controlled pivotal trials remains the cornerstone for full regulatory approval and widespread clinical adoption.

IX. Conclusion

TB-006, a humanized monoclonal antibody targeting Galectin-3, is an innovative therapeutic candidate being developed by TrueBinding, Inc. Its mechanism of action, which involves modulating neuroinflammation and inhibiting the aggregation of multiple pathological proteins, positions it as a potentially first-in-class treatment for a range of challenging neurological disorders.

The most advanced clinical program is in Alzheimer's Disease, where early-phase trials (Phase 1b/2a and an Open Label Extension) have yielded encouraging signals of cognitive and functional improvement, even in patients with moderate to severe disease, and across a patient population not restricted by amyloid status. A particularly noteworthy aspect of its emerging profile is the favorable safety data, especially the reported absence of Amyloid-Related Imaging Abnormalities (ARIA), a common concern with direct amyloid-targeting therapies.

TrueBinding is actively expanding the clinical investigation of TB-006 into Parkinson's Disease (Phase 2A IND cleared), Autism Spectrum Disorder (Phase 2 IIT IND approved), and Acute Ischemic Stroke (Phase 2 IND approved), reflecting a broad therapeutic hypothesis centered on the role of Galectin-3 in these conditions. Preclinical programs for ALS and Glioblastoma also exist.

Despite these promising developments, the path forward requires further validation. The successful translation of early positive signals from AD trials into statistically robust and clinically meaningful outcomes in larger, longer, and well-controlled Phase 2b or Phase 3 trials is a critical next step. The specifics regarding the design and timeline for such pivotal AD trials, and the detailed outcomes of the End-of-Phase 2 meeting with the FDA, remain key pieces of information that will shape the future trajectory of TB-006. Similarly, results from the ongoing and planned Phase 2 trials in PD, ASD, and AIS will be crucial in determining the broader applicability of this Galectin-3 targeting strategy.

In summary, TB-006 holds considerable promise as a novel therapeutic agent with a unique mechanism of action. Its continued development warrants close attention, as it has the potential to address significant unmet medical needs in several debilitating neurological disorders.

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