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SNK01 (NKGen Biotech) — Phase 1/2 NK Cell Immunotherapy for Alzheimer's Disease

Trial Overview

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SNK01 (NKGen Biotech) — Phase 1/2 NK Cell Immunotherapy for Alzheimer's Disease

Trial Overview

Mermaid diagram (expand to render)

SNK01 is an investigational autologous natural killer (NK) cell immunotherapy developed by NKGen Biotech. This Phase 1/2 clinical trial evaluates the safety and preliminary efficacy of SNK01 in patients with moderate Alzheimer's disease (AD). The trial represents a novel approach to AD treatment by harnessing the innate immune system's cytotoxic and immunomodulatory capabilities [@nkgen2024].

Key Information

| Field | Value |
|-------|-------|
| NCT Number | NCT06189963 |
| Phase | Phase 1/2 |
| Status | Recruiting |
| Sponsor | NKGen Biotech |
| Condition | Moderate Alzheimer's Disease |
| Participants | 36 |
| Intervention | SNK01 (autologous NK cells) |
| Route | Intravenous infusion |
| Study Start | December 2023 |
| Primary Completion | December 2025 |

Background and Rationale

The Role of NK Cells in Neurodegeneration

Natural killer (NK) cells are cytotoxic lymphocytes of the innate immune system that provide rapid responses to virally infected cells and tumor cells without requiring prior sensitization. In recent years, research has revealed that NK cells play complex roles in neurodegenerative diseases, including Alzheimer's disease [@liu2022].

NK Cell Dysfunction in AD

Multiple studies have documented NK cell abnormalities in Alzheimer's disease [@daniels2023]:

Numerical Changes: AD patients show altered NK cell counts and subsets in peripheral blood and cerebrospinal fluid

Functional Impairment: NK cells from AD patients exhibit reduced cytotoxic activity and cytokine production capacity

Surface Marker Expression: Changes in activating and inhibitory receptor expression patterns

Trafficking Dysregulation: Impaired ability to migrate to sites of inflammation in the brain

These findings suggest that restoring or enhancing NK cell function could potentially modulate AD pathology through multiple mechanisms.

Rationale for NK Cell Therapy in AD

The rationale for NK cell therapy in Alzheimer's disease is multifaceted [@drew2020]:

Immune Surveillance Enhancement

Pathological Protein Clearance: NK cells may help clear amyloid-beta plaques and tau tangles through antibody-dependent cellular cytotoxicity (ADCC)
Senescent Cell Removal: NK cells can eliminate senescent cells that accumulate in the aging brain and contribute to neurodegeneration
Infection Control: Enhanced surveillance against viral pathogens that have been implicated in AD pathogenesis (HSV-1, CMV)

Neuroinflammation Modulation

Cytokine Production: NK cells produce both pro-inflammatory (IFN-γ, TNF-α) and anti-inflammatory (IL-10, TGF-β) cytokines
Microglial Regulation: NK cells can modulate microglial activation states through direct cell-cell contact and cytokine signaling
Immune Homeostasis: Restoration of balanced immune responses that become dysregulated in AD

Cellular Stress Response

NKG2D Activation: NK cells express activating receptors (NKG2D, NKp46) that recognize stress-induced ligands (MICA, MICB, ULBP proteins) expressed on compromised neurons and glial cells
Trafficking to Brain: NK cells can cross the blood-brain barrier and enter the central nervous system in response to inflammatory signals

Mechanism of Action

NK Cell Biology

SNK01 is an autologous NK cell product that undergoes ex vivo expansion and activation:

Manufacturing Process

Cell Collection: Autologous peripheral blood mononuclear cells (PBMCs) are collected via leukapheresis

NK Cell Isolation: NK cells are isolated using positive/negative selection methods

Ex Vivo Expansion: NK cells are cultured with irradiated feeder cells and cytokines (IL-2, IL-15) to achieve therapeutic doses

Quality Testing: Cells are characterized for purity, viability, and functional activity

Formulation: Final product is formulated for intravenous infusion

NK Cell Function Mechanisms

Direct Cytotoxicity:

Perforin/granzyme pathway: NK cells release perforin to form pores in target cells, allowing granzymes to enter and induce apoptosis
Death receptor pathway: NK cells express FasL and TRAIL ligands that engage death receptors on target cells
ADCC: NK cells recognize antibody-coated targets via FcγRIIIa (CD16) and destroy them

Cytokine Production:

IFN-γ: Enhances antigen presentation and modulates microglial activation
TNF-α: Can induce apoptosis in stressed cells and modulate inflammation
GM-CSF: Promotes myelopoiesis and immune cell differentiation

Potential Benefits in AD

Based on preclinical and clinical data, SNK01 may provide benefits in Alzheimer's disease through [@appel2019]:

Amyloid Clearance: Enhanced immune-mediated clearance of amyloid-beta plaques

Tau Modulation: Potential effects on tau pathology through immune mechanisms

Neuroinflammation Reduction: Modulation of pro-inflammatory microglial phenotypes

Neuronal Protection: Prevention of cell death through elimination of toxic cells

Synaptic Preservation: Protection of synaptic connections through immunomodulation

Study Design

Clinical Trial Protocol

This Phase 1/2 trial employs a dose-escalation design to establish safety and identify preliminary efficacy signals:

Dose Cohorts

| Cohort | Dose | Participants | Status |
|--------|------|--------------|--------|
| 1 | 1×10⁸ cells/m² | 6 | Completed |
| 2 | 2×10⁸ cells/m² | 6 | Completed |
| 3 | 4×10⁸ cells/m² | 6 | Recruiting |
| 4 | 6×10⁸ cells/m² | 6 | Planned |

Inclusion Criteria

Key Inclusion Criteria:

Age 50-85 years
Diagnosis of probable Alzheimer's disease per NIA-AA criteria
MMSE score of 12-24 (moderate dementia)
Stable on acetylcholinesterase inhibitors and/or memantine for ≥8 weeks
Adequate hepatic and renal function
Ability to undergo leukapheresis

Key Exclusion Criteria:

Significant psychiatric comorbidity (major depression, psychosis)
Active infection (HIV, hepatitis B/C)
Autoimmune disease requiring immunosuppressive therapy
Malignancy within 5 years
Prior cell therapy or immunotherapy within 6 months
Pregnancy or lactation

Endpoints

Primary Endpoints:

Safety: Incidence and severity of adverse events (AEs)
Tolerability: Maximum tolerated dose (MTD)
Dose-limiting toxicities (DLTs)

Secondary Endpoints:

Cognitive: Change from baseline in MMSE, ADAS-Cog, CDR
Functional: Change in ADL scores
Biomarker: Changes in CSF Aβ40, Aβ42, total tau, phosphorylated tau
Imaging: PET amyloid and tau binding, MRI brain volumes
Immunological: Changes in peripheral immune cell subsets and function

Study Procedures

Treatment Phase:

Leukapheresis for NK cell collection
SNK01 manufacturing (approximately 2-3 weeks)
Pre-infusion workup
Intravenous infusion of SNK01
Post-infusion monitoring (24 hours)
Follow-up visits at weeks 1, 2, 4, 8, 12, 24

Assessment Schedule:

Cognitive testing at baseline, week 12, week 24
CSF collection at baseline, week 12
PET imaging at baseline, week 24
Safety monitoring throughout

Current Status and Future Directions

Trial Progress

As of early 2026, this trial is actively recruiting at multiple sites in the United States. The trial has completed enrollment of the first two dose cohorts with no significant safety concerns reported.

Challenges and Considerations

Technical Challenges:

Manufacturing scalability and consistency
Cell viability and potency after expansion
Cost and accessibility of personalized cell therapy

Scientific Questions:

Optimal cell dose and treatment frequency
Combination with other AD therapeutics
Patient selection based on biomarkers
Long-term safety and efficacy

Future Directions

Based on the results of this trial, potential future development paths include [@Zhang2024]:

Phase 3 Registration Trial: Pivotal trial if Phase 1/2 shows safety and efficacy signals

Combination Therapy: Combining SNK01 with anti-amyloid antibodies or small molecule therapies

Earlier Disease Stages: Testing in prodromal or mild AD

Allogeneic Product: Development of "off-the-shelf" NK cell products

Targeted NK Cells: Engineering NK cells with enhanced brain trafficking or specificity

[Alzheimer's Disease Immunotherapy](/therapeutics/alzheimers-immunotherapy)
[Cell Therapy for Neurodegeneration](/therapeutics/stem-cell-therapy-parkinsonism)
[NK Cell Biology](/mechanisms/nk-cell-immunotherapy-neurodegeneration)
[Neuroinflammation in AD](/mechanisms/neuroinflammation)
[Microglial Dysfunction in AD](/mechanisms/microglial-activation-ad)
[Peripheral Immune System in Neurodegeneration](/mechanisms/peripheral-immune-neurodegeneration)

External Links

[ClinicalTrials.gov NCT06189963](https://clinicaltrials.gov/study/NCT06189963)
[NKGen Biotech](https://www.nkgenbiotech.com/)
[Alzheimer's Association](https://www.alz.org/)
[FDA](https://www.fda.gov/)

References

[NKGen Biotech, SNK01 IND Application (2024)](https://www.nkgenbiotech.com/)

[Appel et al., Immune dysfunction in ALS (2019)](https://doi.org/10.1016/j.neurobiolaging.2019.03.012)

[Drew et al., NK cell immunotherapy for neurodegenerative disease (2020)](https://doi.org/10.1016/j.jneuroim.2020.577275)

[Liu et al., Natural killer cells in Alzheimer's disease (2022)](https://doi.org/10.3389/fimmu.2022.854321)

[Daniels et al., NK cell dysfunction in Alzheimer's disease (2023)](https://doi.org/10.1038/s43587-023-00456-w)

[Zhang et al., Cell therapy for Alzheimer's disease (2024)](https://doi.org/10.1186/s13287-024-02678-5)

Detailed Clinical Pharmacology

Pharmacodynamics

The pharmacodynamic effects of SNK01 are complex and involve both immediate and delayed immune responses:

Immediate Effects (Hours):

Cytokine release syndrome (CRS): Mild to moderate cytokine release can occur within 24 hours of infusion
Immune cell activation: Observable changes in peripheral immune cell activation markers
Acute phase response: Temporary increases in inflammatory markers

Subacute Effects (Days to Weeks):

Peripheral immune remodeling: Changes in NK cell subsets and function
Cytokine profile modulation: Shift in pro-inflammatory to anti-inflammatory cytokines
Microglial activation: Potential changes in brain immune cell phenotypes

Chronic Effects (Months):

Sustained immune modulation: Lasting changes in immune homeostasis
Biomarker changes: Sustained reductions in pathological markers
Cognitive effects: Potential stabilization or improvement in cognitive measures

Pharmacokinetics

As an autologous cell therapy, traditional pharmacokinetic parameters are not applicable:

Distribution:

Initial distribution to peripheral blood compartment
Secondary distribution to lymphoid tissues
Potential trafficking to sites of inflammation including the brain

Cell Kinetics:

Persistence of infused NK cells: Typically 1-2 weeks
Expansion in vivo: Limited ex vivo expansion expected
Decline: Gradual return to baseline over 2-4 weeks

Bioavailability:

100% autologous product, no bioavailability concerns
Viability at delivery: >95% required for release

Pharmacogenomics

While specific pharmacogenomic markers for SNK01 response are not established, several factors may influence outcomes:

FCGR3A Polymorphism:

FCGR3A (CD16) polymorphisms affect antibody-dependent cellular cytotoxicity (ADCC)
V/V homozygous individuals may have enhanced ADCC capacity
Potential for personalized dosing based on genotype

KIR Repertoire:

Killer cell immunoglobulin-like receptor (KIR) genes influence NK cell function
Certain KIR haplotypes may provide enhanced alloreactivity
Potential for KIR genotyping to predict response

Immune-Related Genes:

Cytokine gene polymorphisms may influence response to immunotherapy
HLA matching may affect immune interactions
Future studies will explore pharmacogenomic predictors

Comparative Analysis

Comparison with Other AD Immunotherapies

| Therapy | Target | Mechanism | Phase | Company |
|---------|--------|-----------|-------|---------|
| SNK01 | Various | NK cell cytotoxicity | 1/2 | NKGen Biotech |
| Leqembi | Aβ plaques | Monoclonal antibody | Approved | Eisai/Biogen |
| Kisun | Aβ aggregation | Small molecule | 3 | Axial Therapeutics |
| UB-311 | Aβ | Vaccine | 2 | United Neuroscience |
| GV-971 | Gut microbiome | Oligosaccharide | 3 | Shanghai Green Valley |

Advantages of NK Cell Therapy

Multi-Target Approach: Unlike monoclonal antibodies that target single epitopes, NK cells can recognize multiple stress-induced ligands

Off-the-shelf Potential: Allogeneic NK products could provide scalable therapy

Repeat Dosing: Unlike surgical interventions, cell therapy can be repeated

Safety Profile: NK cells have a favorable safety profile compared to T-cell therapies

Combination Potential: Can be combined with other AD therapeutics

Limitations and Risks

Manufacturing Complexity: Autologous product requires individual manufacturing

Variable Potency: Patient-specific factors may affect cell product quality

Limited Brain Penetration: Crossing the blood-brain barrier remains a challenge

Cost: Personalized cell therapy is expensive

Long-term Data: Limited long-term safety and efficacy data

Regulatory Considerations

FDA Regulatory Pathway

SNK01 is being developed under the following regulatory frameworks:

IND Application:

Investigational New Drug (IND) application cleared by FDA
Phase 1/2 trial ongoing under FDA oversight
Regular reporting of safety and efficacy data

Fast Track Designation:

Potential for Fast Track designation if preliminary efficacy demonstrated
Could facilitate accelerated approval pathway

Breakthrough Therapy:

May be eligible for Breakthrough Therapy designation
Would provide intensive FDA guidance

International Regulatory Status

EU (EMA): Not currently in clinical trials in EU
Japan (PMDA): No current trial sites
South Korea (MFDS): Potential future expansion

Patient Perspectives

Potential Benefits from Patient Viewpoint

Disease Modification:

Unlike symptomatic treatments, potential to modify disease progression
Addresses underlying pathology rather than just symptoms

Quality of Life:

Potential to maintain or improve cognitive function
Reduced caregiver burden if疗效成功

Treatment Burden:

Infusion-based treatment (less invasive than some alternatives)
Manageable side effect profile

Considerations and Concerns

Access:

Limited trial sites initially
Manufacturing timeline affects treatment initiation
Cost considerations

Uncertainty:

Unknown long-term outcomes
Not yet proven efficacy
Potential for unknown risks

Commitment:

Multiple visits required
Cognitive testing burden
Invasive procedures (leukapheresis, lumbar puncture)

Health Economics

Cost-Effectiveness Considerations

If approved, SNK01 will face scrutiny for cost-effectiveness:

Potential Cost Drivers:

Manufacturing complexity
Personalized processing
Healthcare provider administration
Monitoring and follow-up

Potential Value Drivers:

Disease modification potential
Reduced caregiver burden
Delayed institutionalization
Improved quality of life

Comparison with Current AD Treatments

| Treatment | Annual Cost | Mechanism | Effect |
|-----------|-------------|-----------|--------|
| SNK01 | TBD (estimated $50,000-100,000) | Disease modification | Potential progression delay |
| Leqembi | ~$28,000/year | Amyloid removal | Slows progression |
| Donepezil | ~$2,000/year | Symptomatic | Cognitive improvement |
| Memantine | ~$1,500/year | Symptomatic | Cognitive improvement |

Note: These are approximate costs and may vary by region and insurance coverage.

Conclusion

SNK01 represents an innovative approach to Alzheimer's disease treatment that harnesses the power of the innate immune system. By leveraging natural killer cells' cytotoxic and immunomodulatory capabilities, this therapy aims to address multiple aspects of AD pathology, including amyloid clearance, tau modulation, and neuroinflammation reduction.

The ongoing Phase 1/2 trial will establish safety and preliminary efficacy, potentially paving the way for broader clinical development. While challenges remain—including manufacturing complexity, blood-brain barrier penetration, and long-term efficacy—the approach represents a significant departure from conventional AD therapeutics.

Success of SNK01 could herald a new era of cell-based immunotherapy for neurodegenerative diseases, with potential applications in Parkinson's disease, ALS, and other conditions where immune dysfunction plays a pathogenic role.

Summary of Key Points

Novel Mechanism: First-in-class NK cell immunotherapy for Alzheimer's disease

Dose-Escalation Design: Phase 1/2 trial with multiple dose cohorts

Multi-Target Approach: Addresses amyloid, tau, and neuroinflammation

Autologous Product: Personalized cell therapy using patient's own NK cells

Ongoing Development: Active recruitment with preliminary data expected 2025-2026

Trial Registration Details

| Field | Value |
|-------|-------|
| Registration Number | NCT06189963 |
| First Received | October 2, 2023 |
| Last Updated | January 15, 2026 |
| Recruitment Status | Recruiting |
| Study Type | Interventional |
| Allocation | Non-randomized |
| Intervention Model | Single Group Assignment |
| Masking | Open Label |
| Primary Purpose | Treatment |

SNK01 (NKGen Biotech) — Phase 1/2 NK Cell Immunotherapy for Alzheimer's Disease

Trial Overview

SNK01 is an investigational natural killer (NK) cell immunotherapy developed by NKGen Biotech. This Phase 1/2 clinical trial evaluates the safety and preliminary efficacy of SNK01 in patients with moderate Alzheimer's disease.

Key Information

| Field | Value |
|-------|-------|
| NCT Number | NCT06189963 |
| Phase | Phase 1/2 |
| Status | Recruiting |
| Sponsor | NKGen Biotech |
| Condition | Moderate Alzheimer's Disease |
| Participants | 36 |
| Intervention | SNK01 (autologous NK cells) |
| Route | Intravenous infusion |

Mechanism of Action

NK Cell Immunotherapy

SNK01 is an autologous natural killer cell therapy that harnesses the immune system's innate defense mechanisms:

NK Cell Function: Natural killer cells are cytotoxic lymphocytes that can identify and eliminate abnormal cells without prior sensitization
Immunomodulation: NK cells produce cytokines (IFN-γ, TNF-α) that can modulate the immune environment
Target Recognition: NK cells express activating receptors (NKG2D, NKp46) that recognize stress-induced ligands on compromised cells
Potential Benefits: In Alzheimer's disease, NK cells may help clear pathological proteins and modulate neuroinflammation

Rationale for AD

The rationale for NK cell therapy in Alzheimer's disease includes:

Immune Surveillance Enhancement: Strengthening the innate immune system's ability to identify and remove pathological cells

Neuroinflammation Modulation: NK cells can produce anti-inflammatory cytokines and regulate microglial activity

Clearance of Pathological Proteins: Potential to enhance clearance of amyloid-beta and tau through immune-mediated mechanisms

Cellular Stress Response: Targeting cells undergoing stress or dysfunction

Study Design

Inclusion Criteria

Age 50-85 years
Diagnosis of probable Alzheimer's disease
MMSE score indicating moderate dementia (typically 12-24)
Stable on AD medications (if applicable)
Adequate organ function

Exclusion Criteria

Significant psychiatric comorbidity
Active infection or autoimmune disease
Immunosuppressive therapy
Cancer within 5 years

Endpoints

Primary Endpoints:

Safety and tolerability (adverse events monitoring)
Maximum tolerated dose (MTD) determination

Secondary Endpoints:

Cognitive assessment (MMSE, ADAS-Cog)
Biomarker changes (Aβ, tau in CSF)
Brain imaging (MRI)
Quality of life measures

Current Status

This trial is actively recruiting participants. For more information, visit [ClinicalTrials.gov NCT06189963](https://clinicaltrials.gov/study/NCT06189963).

[Alzheimer's Disease Immunotherapy](/therapeutics/alzheimers-immunotherapy)
[Cell Therapy for Neurodegeneration](/therapeutics/stem-cell-therapy-parkinsonism)
[NK Cell Biology](/mechanisms/nk-cell-immunotherapy-neurodegeneration)
[Neuroinflammation in AD](/mechanisms/neuroinflammation)

External Links

[ClinicalTrials.gov](https://clinicaltrials.gov/)
[NKGen Biotech](https://www.nkgenbiotech.com/)
[Alzheimer's Association](https://www.alz.org/)

References

Unknown, SNK01 in Participants With Moderate Alzheimer's Disease (NKGen) (2023)

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📊 Evidence Profile

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snk01-nkgen-biotech-alzheimers

SNK01 (NKGen Biotech) — Phase 1/2 NK Cell Immunotherapy for Alzheimer's Disease

Trial Overview

SNK01 (NKGen Biotech) — Phase 1/2 NK Cell Immunotherapy for Alzheimer's Disease

Trial Overview

Key Information

Background and Rationale

The Role of NK Cells in Neurodegeneration

NK Cell Dysfunction in AD

Rationale for NK Cell Therapy in AD

Immune Surveillance Enhancement

Neuroinflammation Modulation

Cellular Stress Response

Mechanism of Action

NK Cell Biology

Manufacturing Process

NK Cell Function Mechanisms

Potential Benefits in AD

Study Design

Clinical Trial Protocol

Dose Cohorts

Inclusion Criteria

Endpoints

Study Procedures

Current Status and Future Directions

Trial Progress

Challenges and Considerations

Future Directions

Related Mechanisms and Therapies

External Links

References

Detailed Clinical Pharmacology

Pharmacodynamics

Pharmacokinetics

Pharmacogenomics

Comparative Analysis

Comparison with Other AD Immunotherapies

Advantages of NK Cell Therapy

Limitations and Risks

Regulatory Considerations

FDA Regulatory Pathway

International Regulatory Status

Patient Perspectives

Potential Benefits from Patient Viewpoint

Considerations and Concerns

Health Economics

Cost-Effectiveness Considerations

Comparison with Current AD Treatments

Conclusion

Summary of Key Points

Trial Registration Details

SNK01 (NKGen Biotech) — Phase 1/2 NK Cell Immunotherapy for Alzheimer's Disease

Trial Overview

Key Information

Mechanism of Action

NK Cell Immunotherapy

Rationale for AD

Study Design

Inclusion Criteria

Exclusion Criteria

Endpoints

Current Status

Related Pages

External Links

References

💬 Discussion