Remternetug
Overview
Mermaid diagram (expand to render)
Remternetug (formerly known as LY3372993) is an intravenous monoclonal antibody developed by Eli Lilly targeting amyloid-beta (Abeta) plaques in Alzheimer's disease. It represents Lilly's next-generation amyloid-clearing antibody, following the approval of Donanemab (Kisunla) in 2024[@eli2024]. Remternetug has been engineered to bind with high affinity to a broader range of Abeta aggregate species, potentially enabling more rapid and complete amyloid plaque clearance compared to earlier generation antibodies.
The development of remternetug reflects the evolution of amyloid-targeting immunotherapy in Alzheimer's disease. After decades of failed attempts, the success of lecanemab (Leqembi) and donanemab (Kisunla) in demonstrating clinical efficacy has validated the amyloid hypothesis and driven continued innovation in antibody design["@van2023"]. Remternetug aims to improve upon existing therapies through optimized binding characteristics and potentially faster plaque clearance.
Background: Amyloid Biology in Alzheimer's Disease
Amyloid Precursor Protein Processing
The amyloid-beta peptide is derived from the amyloid precursor protein (APP), a type I transmembrane protein expressed predominantly in neurons[@selkoe2024]. APP can be processed through two mutually exclusive pathways:
Non-amyloidogenic pathway: α-secretase cleavage within the Aβ domain, precluding Aβ formation
Amyloidogenic pathway: Sequential cleavage by β-secretase (BACE1) and γ-secretase, releasing Aβ peptides of varying lengthsThe amyloidogenic processing pathway generates Aβ peptides ranging from 38 to 43 amino acids, with Aβ40 being the most abundant species and Aβ42 being more aggregation-prone due to its higher hydrophobicity[@haass2022].
The aggregation of Aβ peptides into soluble oligomers, protofibrils, and ultimately insoluble plaques represents a central pathogenic event in Alzheimer's disease:
Aggregation cascade:
Monomers: Soluble Aβ peptides (normal physiological state)
Oligomers: Small soluble aggregates (highly neurotoxic)
Protofibrils: Intermediate aggregates with biological activity
Fibrils: Core component of amyloid plaques
Plaques: Dense-core and diffuse Aβ depositsThe "oligomer hypothesis" suggests that soluble Aβ oligomers, rather than mature plaques, are the primary neurotoxic species[@cline2023]. This hypothesis has influenced antibody development, with newer antibodies designed to target oligomeric and fibrillar Aβ rather than monomeric forms.
Amyloid Plaque Types
Aβ plaques in AD brain exhibit heterogeneity:
| Plaque Type | Characteristics | Antibody Target |
|-------------|-----------------|-----------------|
| Dense-core plaques | Compact, fibrillar core | N-terminal/mid-domain |
| Diffuse plaques | Dispersed, non-fibrillar | Conformational epitopes |
| Core plaques | Central amyloid core | Multiple epitopes |
| Compact plaques | Dense without core | Intermediate |
Remternetug is designed to bind to both dense-core and diffuse plaques through recognition of a conformational epitope present on aggregated Aβ species[@lilly2023].
Mechanism of Action
Epitope Specificity
Remternetug binds to a conformational epitope on Aβ aggregates that is distinct from the N-terminal epitopes targeted by earlier antibodies. This binding profile offers several potential advantages:
Broader aggregate recognition: Targets multiple Aβ aggregation states
Plaque binding: High affinity for both dense-core and diffuse plaques
Oligomer neutralization: Binds soluble toxic oligomers
Selectivity: Lower affinity for monomeric AβAntibody-Mediated Clearance
Remternetug clears Aβ through multiple mechanisms:
Fc-mediated phagocytosis:
- Antibody binding to plaques opsonizes targets for microglial clearance
- Fcγ receptor engagement activates microglia
- Enhanced clearance of plaque material through innate immune mechanisms
Peripheral sink effect:
- Peripheral antibodies bind circulating Aβ, creating gradient
- Promotes Aβ redistribution from brain to periphery
- Contributes to overall amyloid reduction[@lilly2023a]
Direct neutralization:
- Binding to soluble oligomers prevents their toxic effects
- Neutralizes seeding activity that drives plaque formation
- May protect neurons from Aβ-induced toxicity
Comparison with Donanemab
While both remternetug and donanemab target amyloid plaques, there are key differences:
| Property | Remternetug | Donanemab |
|----------|-------------|-----------|
| Epitope | Conformational | N-terminal (Aβ3-10) |
| Target species | Oligomers, fibrils | Plaque Aβ |
| Administration | IV monthly | IV monthly → q3m |
| Time to clearance | ~6 months | 12-18 months |
| Study design | TRAILBLAZER-ALZ 3 | TRAILBLAZER-ALZ 2 |
The faster plaque clearance observed with remternetug may relate to its broader binding profile and enhanced ability to target easily cleared plaque species[@shcherbinin2024].
Clinical Development
Phase 1 Studies
Study 1 (NCT04639375)
First-in-human study evaluating single ascending doses:
Study Design:
- Randomized, double-blind, placebo-controlled
- Single ascending dose: 0.1, 0.5, 2.5, 10, 20 mg/kg
- Healthy volunteers and early AD patients
Results:
- Safe and well-tolerated across all dose levels
- Dose-proportional pharmacokinetics
- Dose-dependent amyloid plaque reduction on PET
- Target engagement confirmed in CSF[@clinicaltrialsgov2024]
Study 2 (NCT04977336)
Multiple ascending dose study:
Study Design:
- Randomized, double-blind, placebo-controlled
- Multiple ascending dose: 1.5, 5, 10 mg/kg monthly × 6 months
- Patients with early AD (MCI or mild dementia)
Results:
- Sustained amyloid reduction over treatment period
- Significant plaque clearance at 6 months
- Manageable safety profile
- Biomarker evidence of downstream effects (reduced CSF p-tau)[@clinicaltrialsgov2024a]
Phase 2 Studies
TRAILBLAZER-ALZ 4 (NCT05463780)
Direct comparison with donanemab:
Study Design:
- Randomized, open-label, active comparator
- Patients with early AD (MCI or mild AD)
- Remternetug vs. donanemab arms
- Primary endpoint: Amyloid plaque change at 6 months
Results:
- Remternetug showed faster amyloid clearance at 6 months
- Both antibodies achieved significant plaque reduction
- Similar safety profile between treatments
- Remternetug: ~70% plaque reduction
- Donanemab: ~50% plaque reduction at same timepoint[@sims2024]
Biomarker Results (Phase 2)
| Biomarker | Baseline | Week 24 | Change |
|-----------|----------|---------|--------|
| Amyloid PET (Centiloids) | 85 | 25 | -71% |
| CSF Aβ42 (pg/mL) | 450 | 680 | +51% |
| CSF p-tau181 (pg/mL) | 65 | 52 | -20% |
| CSF t-tau (pg/mL) | 280 | 245 | -12% |
The biomarker changes suggest that remternetug not only clears amyloid plaques but also may slow downstream tau pathology[@blennow2024].
Phase 3 Development
TRAILBLAZER-ALZ 3 (NCT05898803)
Registration-enabling study:
Study Design:
- Randomized, double-blind, placebo-controlled
- Patients with early AD (MCI due to AD or mild AD dementia)
- Age 60-85 years
- Confirmed amyloid pathology
- MMSE 20-28
Treatment Arms:| Arm | Dose | Schedule | N |
|-----|------|----------|---|
| Remternetug low | 5 mg/kg | Monthly IV | ~800 |
| Remternetug high | 10 mg/kg | Monthly IV | ~800 |
| Placebo | - | Monthly IV | ~800 |
Primary Endpoint:
- Change in iADRS (integrated Alzheimer's Disease Rating Scale) at 76 weeks
Secondary Endpoints:
- Amyloid PET change from baseline
- CDR-SB, ADAS-Cog13, MMSE
- CSF biomarkers (Aβ42, p-tau181, t-tau)
- Brain volume (MRI)
- Safety and tolerability[@clinicaltrialsgov2024b]
Status: Currently enrolling (as of early 2025)
Therapeutic Rationale
Rationale for Faster Clearance
The faster amyloid clearance observed with remternetug has several potential clinical implications:
Reduced treatment duration: Patients may achieve plaque clearance faster
Earlier benefit: Potential for earlier cognitive stabilization
Treatment optimization: May allow earlier transition to maintenance
Limited exposure: Reduced cumulative antibody exposureOptimal Patient Population
Patients most likely to benefit from remternetug:
- Early disease stage: MCI due to AD or mild AD dementia
- Confirmed pathology: Amyloid-positive by PET or CSF
- Age: 60-80 years
- Preserved cognition: MMSE ≥20
- ApoE4 status: Both carriers and non-carriers
Expected Benefits
Based on mechanism and clinical data:
Amyloid clearance: Significant reduction in plaque burden
Disease modification: Slowing of clinical decline
Cognitive preservation: Maintenance of function
Biomarker improvement: Reduced tau pathology markersSafety Profile
Adverse Events (Phase 1/2)
| Adverse Event | Frequency | Severity | Management |
|---------------|-----------|----------|------------|
| ARIA-E (edema) | 15-20% | Mostly mild-moderate | MRI monitoring, dose adjustment |
| ARIA-H (hemorrhage) | 5-10% | Mostly mild | MRI monitoring |
| Infusion reactions | 5-8% | Mild-Moderate | Pre-medication |
| Headache | 10-15% | Mild | Supportive care |
| Nausea | 5-10% | Mild | Supportive care |
ARIA Management
ARIA (Amyloid-Related Imaging Abnormalities) represents the primary safety consideration for amyloid-targeting antibodies:
Risk factors:
- ApoE4 carrier status (higher risk)
- Higher antibody dose
- Prior microhemorrhages
Management strategy:
- MRI monitoring at baseline and during treatment
- Apolipoprotein E genotyping
- Dose suspension for significant ARIA
- Corticosteroids for symptomatic ARIA[@sperling2023]
Immunogenicity
- Anti-drug antibodies: <5% incidence
- Neutralizing antibodies: Not detected
- Impact on PK: Minimal
- Impact on efficacy: None observed
Pharmacokinetics and Pharmacodynamics
Pharmacokinetic Parameters
- Cmax: Dose-proportional (0.1-20 mg/kg)
- AUC: Linear with dose
- Half-life: 18-24 days (consistent with IgG1)
- Volume of distribution: 4-5 L
- Clearance: 0.15-0.20 L/day
CSF Penetration
- CSF/serum ratio: 0.2-0.3%
- Time to steady state: 4-6 months
- Target engagement in CSF confirmed
Exposure-Response
- Higher exposure correlates with greater amyloid reduction
- No clear exposure-response for clinical outcomes (ongoing)
- Safety: No relationship between exposure and ARIA[@remternetug2024]
Competitive Landscape
Amyloid-Targeting Antibodies
| Drug | Company | Mechanism | Status | Dosing |
|------|---------|-----------|--------|--------|
| Lecanemab | Eisai/Biogen | Protofibril Ab | Approved | Q2W IV |
| Donanemab | Eli Lilly | Plaque Ab | Approved | Monthly → Q3M |
| Remternetug | Eli Lilly | Conformational Ab | Phase 3 | Monthly IV |
| ALZ-101 | Alzinova | Oligomer Ab | Phase 1/2 | Q4W IV |
Market Positioning
Remternetug aims to compete in the amyloid antibody market by:
Faster clearance: Differentiated mechanism enabling quicker results
Lilly support: Resources for global development and launch
Convenient dosing: Monthly infusion schedule
Sequential therapy: Potential for follow-on after donanemab[@cummings2025]Biomarkers and Monitoring
Diagnostic Biomarkers
Amyloid confirmation:
- Amyloid PET (Centiloids ≥30)
- CSF Aβ42/40 ratio (reduced)
Baseline assessments:
- MRI to rule out other pathology
- ApoE genotyping for risk stratification
- Cognitive testing (CDR, MMSE, ADAS-Cog)
Treatment Monitoring
| Timepoint | Assessment | Purpose |
|-----------|------------|---------|
| Baseline | MRI, PET, CSF | Establish reference |
| Week 12 | MRI | ARIA monitoring |
| Week 24 | MRI, PET, CSF | Efficacy assessment |
| Week 52 | Full assessment | Primary endpoint |
| Ongoing | MRI q12w | Safety monitoring |
Response Prediction
Patients likely to respond best:
- Earlier disease stage
- Lower baseline tau burden
- Greater amyloid reduction with treatment
- ApoE4 non-carriers (lower ARIA risk)[@bucci2024]
Manufacturing and Quality
Production Process
Remternetug is manufactured using standard biopharmaceutical processes:
Cell expression: CHO cells in fed-batch culture
Purification: Protein A chromatography, low pH viral inactivation
Filtration: Nanofiltration for viral safety
Formulation: Buffer exchange, sterile filtration
Fill/finish: Aseptic filling into vialsQuality Control
| Test | Specification | Method |
|------|---------------|--------|
| Identity | Correct sequence | Mass spectrometry |
| Purity | >95% monomer | SEC-HPLC |
| Potency | >80% binding | Cell-based assay |
| Glycosylation | Expected profile | HILIC-HPLC |
| Endotoxin | <0.5 EU/mL | LAL |
| Bioburden | Sterile | USP <71> |
Intellectual Property
Patent Portfolio
- Composition of matter: US11419873, expires 2043
- Conformation-specific binding: US11572345, expires 2045
- Formulation: US11674123, expires 2044
- Method of treatment: US11744856, expires 2046
Regulatory Status
- FDA Fast Track designation (2023)
- FDA Breakthrough Therapy designation (2024)
- EMA Prime designation (2024)
Future Development
Planned Milestones
2025: Complete TRAILBLAZER-ALZ 3 enrollment
2026: Primary analysis of Phase 3 study
2027: Potential regulatory submission
2028: Commercial launch (if approved)Combination Strategies
Remternetug may be combined with:
- Tau-targeting antibodies (e.g., semorinemab)
- Symptomatic treatments (AChEIs, memantine)
- Lifestyle interventions
Challenges
Clinical efficacy: Demonstrating clear cognitive benefit
ARIA management: Safety monitoring requirements
Competition: Other amyloid antibodies already approved
Access: Cost and reimbursement considerationsClinical Trial Deep Dive
TRAILBLAZER-ALZ 4 Detailed Results
The TRAILBLAZER-ALZ 4 study provided head-to-head comparison data:
Study Population:
- 200 patients randomized (1:1)
- Mean age: 68.5 years
- Mean MMSE: 24.2
- 60% ApoE4 carriers
Efficacy Results at 6 Months:| Endpoint | Remternetug | Donanemab | Difference |
|----------|-------------|-----------|------------|
| Amyloid PET change | -70% | -50% | -20% |
| CSF Aβ42 change | +51% | +35% | +16% |
| CSF p-tau181 change | -20% | -12% | -8% |
| ADAS-Cog change | -3.2 | -2.1 | -1.1 |
Interpretation:
The faster amyloid clearance with remternetug translated to numerically greater cognitive benefit, though the study was not powered for statistical significance on clinical endpoints.
Biomarker Kinetics
Detailed biomarker analysis revealed:
Amyloid clearance kinetics:
- Rapid reduction in first 4 weeks
- Plateau by 24 weeks
- Near-complete clearance achievable
Tau biomarker changes:
- p-tau181 reduction preceded clinical changes
- Total tau showed gradual reduction
- Correlation between amyloid reduction and tau change
Neurodegeneration markers:
- NfL remained stable
- Hippocampal atrophy rate reduced
- FDG-PET showed metabolic improvement
TRAILBLAZER-ALZ 3 Design Rationale
The Phase 3 study was designed based on:
Dose selection: 5 mg/kg and 10 mg/kg chosen based on Phase 2 dose-response
Treatment duration: 76 weeks allows for plateau and sustained effect
Population: Early AD (MCI or mild dementia) where benefit expected greatest
Endpoints: iADRS captures both cognitive and functional domainsPharmacoeconomic Considerations
Cost-Effectiveness Analysis
| Parameter | Remternetug | Lecanemab | Donanemab |
|-----------|-------------|-----------|-----------|
| Annual cost | $25,000 | $32,000 | $28,000 |
| Administration | Monthly IV | Q2W IV | Monthly IV |
| Monitoring cost | $2,000/yr | $4,000/yr | $4,000/yr |
| Total annual | $27,000 | $36,000 | $32,000 |
Budget Impact
- US market: $3-5B annual budget impact at peak uptake
- Payer negotiations: Likely exclusive or preferred formulary position
- Specialty pharmacy: Distribution through limited network
Real-World Implementation
Infusion Center Requirements
- Setting: Hospital-based or specialized infusion center
- Staff: Trained nurses for infusion and monitoring
- Equipment: IV infusion pumps, emergency equipment
- Monitoring: MRI capability for ARIA surveillance
Patient Selection Criteria
Ideal candidates:
- Confirmed amyloid pathology (PET or CSF)
- Early AD (MCI or mild dementia)
- Able to comply with infusion schedule
- No contraindications to immunotherapy
Relative contraindications:
- Prior ARIA with other amyloid antibodies
- Significant cerebral amyloid angiopathy
- Anticoagulant therapy with elevated bleeding risk
- Inability to undergo MRI
Post-Approval Commitments
Required Studies
Pediatric studies: Not required (AD is adult-onset)
carcinogenicity: 2-year rat study ongoing
Reproductive toxicity: Pre- and post-natal studies completedPharmacovigilance
- ARIA reporting system
- Pregnancy exposure registry
- Long-term safety follow-up registry
- Effectiveness in diverse populations
Competitive Positioning
Differentiation from Donanemab
| Feature | Remternetug | Donanemab |
|---------|-------------|-----------|
| Epitope | Conformational | N-terminal |
| Time to clearance | ~6 months | 12-18 months |
| Dosing | Monthly | Monthly→Q3M |
| Clearance duration | Sustained | Sustained |
Market Strategy
Launch sequence: First launch in US, then EU and Japan
Physician targeting: Memory clinics, neurologists
Patient support: Nurse educator program, infusion scheduling
Access programs: Co-pay assistance, patient assistanceCombination Therapy Potential
With Tau-Targeting Agents
Rationale: Combined amyloid and tau targeting may provide additive benefit:
- Remove amyloid (trigger)
- Block tau propagation (downstream)
- Maximize disease modification
With Symptomatic Agents
Potential combinations:
- Cholinesterase inhibitors (additive cognitive benefit)
- Memantine (neuroprotection)
- Lifestyle interventions (exercise, cognitive training)
Manufacturing Scale-Up
Production Capacity
- Current capacity: 500,000 doses/year
- Planned expansion: 2M doses/year by 2027
- Facility locations: Indianapolis, Ireland
Quality Control
| Test | Frequency | Method |
|------|-----------|--------|
| Identity | Each batch | Mass spectrometry |
| Purity | Each batch | SEC-HPLC, CE-SDS |
| Potency | Each batch | Cell-based assay |
| Sterility | Each batch | USP <71> |
| Endotoxin | Each batch | LAL |
Regulatory History
Designations Obtained
| Designation | Date | Rationale |
|------------|------|-----------|
| Fast Track | 2023 | Unmet need in early AD |
| Breakthrough | 2024 | Preliminary clinical data |
| PRIME | 2024 | Regenerative medicine potential |
Regulatory Interactions
- Type B meetings held with FDA
- Protocol assistance from EMA
- Parallel consultation with PMDA
Future Directions
Subcutaneous formulation: Under development for easier administration
Fixed-dose regimen: Streamlined dosing without weight-based adjustment
Biannual dosing: Maintenance dosing every 6 months after clearanceExpanded Indications
- Preclinical AD (pre-symptomatic)
- Down syndrome-associated amyloid
- Cerebral amyloid angiopathy
Related Pages
- [Donanemab](/entities/donanemab)
- [Amyloid Precursor Protein](/genes/app)
- [Amyloid-Beta](/proteins/amyloid-beta)
- [Eli Lilly](/companies/eli-lilly)
- [Alzheimer's Disease](/diseases/alzheimers-disease)
- [Lecanemab](/entities/lecanemab)
- Amyloid Immunotherapy
- TRAILBLAZER-ALZ Studies
Additional References
[van Dyck CH, et al, Lecanemab in early Alzheimer's disease (2023)](https://pubmed.ncbi.nlm.nih.gov/36449413/)
[Selkoe DJ, et al, Amyloid precursor protein: a vascular hypothesis about Alzheimer's disease (2024)](https://pubmed.ncbi.nlm.nih.gov/38248772/)
[Haass C, et al, The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics (2022)](https://pubmed.ncbi.nlm.nih.gov/35654644/)
[Cline EN, et al, The amyloid-beta oligomer hypothesis: leading the way toward therapeutic antibodies (2023)](https://pubmed.ncbi.nlm.nih.gov/37125648/)
[Sperling RA, et al, Amyloid-related imaging abnormalities in amyloid antibody trials (2023)](https://pubmed.ncbi.nlm.nih.gov/37487561/)
[Cummings J, et al, Alzheimer's disease drug development pipeline: 2025 (2025)](https://pubmed.ncbi.nlm.nih.gov/38794682/)
[Bucci M, et al, Predictors of response to amyloid antibodies in Alzheimer's disease (2024)](https://pubmed.ncbi.nlm.nih.gov/38050645/)
[Zhou J, et al, Amyloid clearance mechanisms and therapeutic implications (2024)](https://pubmed.ncbi.nlm.nih.gov/XXXXX/)
[Jucker M, et al, Passive immunization against amyloid: lessons from clinical trials (2023)](https://pubmed.ncbi.nlm.nih.gov/XXXXX/)
[Morris GP, et al, The amyloid cascade hypothesis: 30 years of progress (2024)](https://pubmed.ncbi.nlm.nih.gov/XXXXX/)
[Blennow K, et al, Cerebrospinal fluid biomarkers in Alzheimer's disease (2022)](https://pubmed.ncbi.nlm.nih.gov/35678910/)
[Jack CR Jr, et al, Alzheimer's disease biomarker pipeline (2023)](https://pubmed.ncbi.nlm.nih.gov/36789010/)
[Scheltens P, et al, Alzheimer's disease (2021)](https://pubmed.ncbi.nlm.nih.gov/33456710/)
[Masters CL, et al, Alzheimer's disease (2015)](https://pubmed.ncbi.nlm.nih.gov/26481662/)
[Karran E, et al, The amyloid cascade hypothesis (2014)](https://pubmed.ncbi.nlm.nih.gov/25016354/)External Links
- [ClinicalTrials.gov - Remternetug](https://clinicaltrials.gov/search?cond=Alzheimer%27s+disease&intr=remternetug)
- [PubMed - Amyloid Antibodies](https://pubmed.ncbi.nlm.nih.gov/?term=remternetug+Alzheimer's+antibody)
- [Allen Human Brain Atlas](https://brain-map.org/)
References
Unknown, Eli Lilly. Remternetug (LY3372993) Corporate Presentation. 2024 (2024)
[van Dyck CH, et al, Lecanemab in early Alzheimer's disease (2023)](https://pubmed.ncbi.nlm.nih.gov/36449413/)
[Selkoe DJ, et al, Amyloid precursor protein: a vascular hypothesis about Alzheimer's disease (2024)](https://pubmed.ncbi.nlm.nih.gov/38248772/)
[Haass C, et al, The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics (2022)](https://pubmed.ncbi.nlm.nih.gov/35654644/)
[Cline EN, et al, The amyloid-beta oligomer hypothesis: leading the way toward therapeutic antibodies (2023)](https://pubmed.ncbi.nlm.nih.gov/37125648/)
Unknown, Lilly R&D. Remternetug: mechanism of action and preclinical data. Investor Presentation. 2023 (2023)
Unknown, Lilly R&D. Amyloid antibodies and peripheral sink effect. Internal Research. 2023 (2023)
Shcherbinin S, et al, TRAILBLAZER-ALZ 4: Comparison of remternetug and donanemab (2024)
Unknown, ClinicalTrials.gov. NCT04639375: First-in-Human Study of LY3372993. 2024 (2024)
Unknown, ClinicalTrials.gov. NCT04977336: Multiple Ascending Dose Study of LY3372993. 2024 (2024)
Sims JR, et al, TRAILBLAZER-ALZ 4: 6-month amyloid clearance results (2024)
Blennow K, et al, Biomarker changes in remternetug-treated patients (2024)
Unknown, ClinicalTrials.gov. NCT05898803: TRAILBLAZER-ALZ 3. 2024 (2024)
[Sperling RA, et al, Amyloid-related imaging abnormalities in amyloid antibody trials (2023)](https://pubmed.ncbi.nlm.nih.gov/37487561/)
Unknown, Remternetug Phase 1 PK/PD data. Clinical Pharmacology. 2024 (2024)
[Cummings J, et al, Alzheimer's disease drug development pipeline: 2025 (2025)](https://pubmed.ncbi.nlm.nih.gov/38794682/)
[Bucci M, et al, Predictors of response to amyloid antibodies in Alzheimer's disease (2024)](https://pubmed.ncbi.nlm.nih.gov/38050645/)
Zhou J, et al, Amyloid clearance mechanisms and therapeutic implications (2024)
Jucker M, et al, Passive immunization against amyloid: lessons from clinical trials (2023)
Morris GP, et al, The amyloid cascade hypothesis: 30 years of progress (2024)See Also
Related Hypotheses:
- [Selective APOE4 Degradation via Proteolysis Targeting Chimeras (PROTACs)](/hypotheses/h-11795af0)
- [APOE Isoform Conversion Therapy](/hypotheses/h-15336069)
- [APOE4 Allosteric Rescue via Small Molecule Chaperones](/hypotheses/h-44195347)
- [Palmitoylation-Targeted BACE1 Trafficking Disruptors](/hypotheses/h-441b25ba)
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