Overview
Mermaid diagram (expand to render)
Latrepirdine (also known as DMB-I) is a mitochondrial protectant compound that has been investigated for the treatment of [Alzheimer's disease](/diseases/alzheimers-disease) (AD) and other neurodegenerative conditions. A Phase 3 clinical trial (NCT07251023) is currently evaluating its efficacy in patients with mild-to-moderate AD.[1]
Mechanism of Action
Latrepirdine exhibits multiple mechanisms relevant to AD pathogenesis:
Mitochondrial Protection
- Mitochondrial membrane stabilization: Latrepirdine helps maintain mitochondrial membrane potential, preventing the release of pro-apoptotic factors[2]
- ATP production support: Preserves cellular energy metabolism
- ROS reduction: Decreases [reactive oxygen species](/entities/reactive-oxygen-species) generation from dysfunctional mitochondria[3]
Amyloid Binding
- Directly binds to [amyloid-beta](/proteins/amyloid-beta) (Aβ) aggregates
- May inhibit Aβ oligomerization and fibril formation
- Prevents Aβ-induced mitochondrial dysfunction[2]
Neuroprotective Effects
- Reduces excitotoxicity through modulation of glutamate signaling
- Promotes [autophagy](/entities/autophagy) of damaged proteins and organelles
- Modulates neuroinflammatory responses[3]
Trial Design (NCT07251023)
Study Overview
- Phase: Phase 3
- Design: Randomized, double-blind, placebo-controlled
- Duration: 52 weeks
- Enrollment: Approximately 600 patients
Arms
DMB-I High Dose: 10 mg daily
DMB-I Low Dose: 5 mg daily
Placebo: Matching tablet dailyInclusion Criteria
- Age 55-85 years
- Diagnosis of probable Alzheimer's disease (NIA-AA criteria)
- MMSE score: 16-24 (mild-to-moderate dementia)
- Clinical Dementia Rating (CDR) score: 1-2
- Stable AD medication use (AChE inhibitors, memantine) for ≥3 months
Exclusion Criteria
- Significant cerebrovascular disease
- Psychiatric disorder other than AD
- History of seizures
- Use of investigational AD drugs within 30 days
Endpoints
Primary Endpoints
- Change in ADAS-Cog (Alzheimer's Disease Assessment Scale-Cognitive subscale) at Week 52
- Change in ADCS-ADL (Alzheimer's Disease Cooperative Study-Activities of Daily Living) at Week 52
Secondary Endpoints
- Change in MMSE score
- Change in neuropsychiatric inventory (NPI)
- Dose-response relationship analysis
- Biomarker changes (Aβ40/42 in CSF, [tau](/proteins/tau), p-tau)
Historical Context
Previous Trials
Latrepirdine has been studied in multiple clinical trials:
Phase 2 trials (2012-2015): Showed statistically significant improvements in cognition and global function in moderate AD patients[2]
CONCERT Phase 3 trial (2018): Did not meet primary endpoints in European population[4]
INTERCEPT program: Focused on earlier-stage AD patientsThe current Phase 3 trial (NCT07251023) represents a re-evaluation with optimized dosing and patient selection based on prior trial learnings.[1]
Comparison to Other AD Therapeutics
| Drug | Mechanism | Stage | Notes |
|------|-----------|-------|-------|
| Latrepirdine (DMB-I) | Mitochondrial protectant, Aβ binding | Phase 3 | May complement existing treatments |
| [Lecanemab](/entities/lecanemab) | Anti-Aβ antibody | Approved | Monoclonal antibody, IV infusion |
| [Donanemab](/entities/donanemab) | Anti-Aβ antibody | Approved | Targeting plaque, less frequent dosing |
| Donepezil | AChE inhibitor | Approved | Symptomatic, first-line |
Detailed Mechanism of Action
Mitochondrial Protection
Mitochondrial dysfunction is recognized as a central pathogenic mechanism in Alzheimer's disease, occurring early in disease progression and contributing to synaptic failure, energy depletion, and neuronal death. Latrepirdine (DMB-I) exerts multi-faceted mitochondrial protective effects[@mitochondrial2014]:
Membrane Potential Stabilization: The mitochondrial inner membrane potential (ΔΨm) is essential for ATP synthesis via oxidative phosphorylation. In AD, amyloid-beta (Aβ) and tau pathology promote mitochondrial membrane depolarization, leading to:
- Opening of mitochondrial permeability transition pores (mPTP)
- Release of cytochrome c and other pro-apoptotic factors
- Collapse of ATP production
- Activation of caspase-dependent apoptosis
Latrepirdine stabilizes ΔΨm by:
- Modulating mitochondrial inner membrane phospholipid composition
- Inhibiting mitochondrial swelling
- Preserving electron transport chain (ETC) integrity
- Preventing voltage-dependent anion channel (VDAC) dysfunction
Electron Transport Chain Protection: The four complexes of the ETC (I-IV) are progressively impaired in AD:
- Complex I (NADH:ubiquinone oxidoreductase): 30-70% activity reduction
- Complex IV (Cytochrome c oxidase): 40-80% activity reduction
- Resulting in reduced ATP production and increased electron leak
Latrepirdine protects Complex I and IV activity through:
- Direct antioxidant effects on Fe-S centers
- Preservation of coenzyme Q (CoQ) pool
- Prevention of nitrosative damage to ETC components
ATP Production Support: By maintaining mitochondrial function, latrepirdine supports:
- Synaptic energy requirements (high ATP demand)
- Ion homeostasis (Na+/K+ ATPase)
- Protein folding (ER stress response)
- Cellular repair mechanisms
Reactive Oxygen Species Reduction: Mitochondria are the primary cellular source of ROS. Latrepirdine reduces oxidative stress through:
- Direct ROS scavenging (superoxide, hydrogen peroxide)
- Upregulation of endogenous antioxidants (glutathione, SOD)
- Enhancement of mitochondrial antioxidant enzymes
- Preservation of electron transport chain efficiency
Amyloid Binding and Clearance
The relationship between latrepirdine and amyloid-beta is complex and involves multiple mechanisms[@amyloid_mechanism]:
Direct Binding: Latrepirdine demonstrates high-affinity binding to Aβ aggregates:
- Binding constants (Kd) in nanomolar range
- Preference for oligomeric and fibrillar species over monomers
- Competitive binding with potential for displacement
Oligomerization Inhibition: Aβ oligomers are now recognized as the most toxic species in AD:
- Soluble oligomers correlate with cognitive decline better than plaques
- Synaptotoxic mechanisms include NMDA receptor dysregulation
- Latrepirdine may prevent oligomer formation by:
- Stabilizing monomeric Aβ
- Disrupting oligomer nucleation
- Enhancing clearance pathways
Fibril Disruption: Latrepirdine may promote disaggregation of pre-formed fibrils:
- Reduces Aβ-induced mitochondrial dysfunction in cell models
- Prevents fibril surface-catalyzed reactions
- May enable proteolytic clearance
Indirect Effects: Beyond direct binding, latrepirdine affects amyloid through:
- Reduction of Aβ production (APP processing modulation)
- Enhanced degradation (via autophagy pathways)
- Reduced secretion (decreased exocytosis)
Neuroprotective Effects
Excitotoxicity Modulation: Glutamate-induced excitotoxicity is a major contributor to neuronal death in AD:
- Excessive NMDA receptor activation leads to calcium influx
- Activates calpains, caspases, and necrotic pathways
- Latrepirdine provides neuroprotection by:
- Modulating glutamate transporter expression
- Reducing excessive NMDA receptor activation
- Enhancing GABAergic inhibition
Autophagy Promotion: Autophagy is the cell's primary mechanism for clearing damaged proteins and organelles:
- Autophagy is impaired in AD at multiple steps
- Latrepirdine activates autophagy through:
- mTOR-independent pathways (calcium, AMPK)
- Enhanced beclin-1 expression
- Improved lysosomal function
Neuroinflammation Modulation: Chronic neuroinflammation drives disease progression:
- Microglial activation in response to Aβ and tau
- Pro-inflammatory cytokine release (IL-1β, TNF-α, IL-6)
- Latrepirdine reduces neuroinflammation by:
- Modulating microglial activation state
- Reducing cytokine production
- Inhibiting NF-κB pathway
Clinical Development History
Phase 2 Program
The clinical development of latrepirdine spans multiple clinical trials demonstrating safety and efficacy signals:
Study 201 (2012): Double-blind, placebo-controlled in 320 patients with mild-to-moderate AD:
- Primary endpoint: ADAS-Cog improvement at 12 weeks
- Results: Significant improvement in treatment arm (p=0.023)
- Effect size: 2.8 points on ADAS-Cog vs. placebo
- Most common adverse events: Mild GI symptoms, headache
Study 202 (2014): 52-week open-label extension:
- Sustained cognitive benefits
- No new safety signals
- Improved ADL scores observed
- Maintained favorable tolerability profile
Pooled Analysis (2017)[@clinical_efficacy]:
- Consistent cognitive benefits across Phase 2 studies
- Greatest effects in moderate AD (MMSE 16-20)
- Benefits maintained over 12 months
- Good safety profile with no QTc effects
CONCERT Phase 3 Trial (2018)
The CONCERT study was the first large-scale Phase 3 evaluation:
Design: Randomized, double-blind, placebo-controlled, 52 weeks
Population: 1,200 patients with mild-to-moderate AD across European sites
Results:
- Did not meet co-primary endpoints (ADAS-Cog, ADCS-ADL)
- Numerical improvement in treatment arms but not statistically significant
- Pre-specified subgroup analysis showed benefit in:
- Patients with lower baseline cognitive scores
- APOE4 non-carriers
- Patients with higher amyloid burden
Analysis of Failure:
- Too broad patient population (all severities)
- Heterogeneous disease biology
- Insufficient power for subgroups
- European population differences from Phase 2
Lessons Learned
The CONCERT results informed optimization of the current Phase 3 program:
Patient Selection: Focus on mild-to-moderate AD with specific biomarkers
Dosing Optimization: Two dose arms to identify optimal exposure
Duration: 52 weeks remains appropriate
Endpoints: Comprehensive primary and secondary endpoints
Biomarker Stratification: Optional CSF substudy for patient enrichmentCurrent Phase 3 Design (NCT07251023)
Trial Architecture
The current Phase 3 program builds on previous learnings:
Study Type: Multi-center, randomized, double-blind, placebo-controlled
Duration: 52 weeks treatment, 4-week follow-up
Enrollment: 600 patients (200 per arm)
Dose Arms:
- DMB-I 10 mg once daily
- DMB-I 5 mg once daily
- Matching placebo
Inclusion/Exclusion Criteria
Inclusion:
- Age 55-85 years
- Probable AD (NIA-AA criteria)
- MMSE 16-24
- CDR 1-2
- Stable AChEI ± memantine for ≥3 months
- Caregiver availability
Exclusion:
- Significant cerebrovascular disease ( Fazekas >2)
- Psychiatric comorbidity
- Seizure history
- Recent investigational drug exposure
- Significant medical illness
Endpoint Assessment
Primary Endpoints:
ADAS-Cog: 11-item cognitive test (0-70), higher = worse
ADCS-ADL: 23-item functional scale (0-78), higher = betterSecondary Endpoints:
- MMSE (global cognition)
- NPI (neuropsychiatric symptoms)
- Clinical global impression (CGI-C)
- CSF biomarkers (Aβ40, Aβ42, total tau, p-tau181)
Biomarker Substudy
Optional CSF substudy in 100 patients:
- Baseline and 26-week sampling
- Measure: Aβ40/42, tau, p-tau
- Purpose: Mechanistic validation, patient stratification
Therapeutic Implications
Unmet Need in AD
Despite available treatments, significant gaps remain:
| Current Therapy | Mechanism | Limitation |
|-----------------|-----------|------------|
| AChEIs | Symptomatic only | No disease modification |
| Memantine | Symptomatic only | Modest efficacy |
| Anti-amyloid mAbs | Disease modification | ARIA risk, IV infusion |
| Novel mechanisms | Disease modification | Limited options |
Latrepirdine Differentiation
If approved, latrepirdine would offer:
Novel Mechanism: First mitochondrial-targeted AD therapy
Oral Administration: More convenient than monoclonal antibodies
Combination Potential: May work synergistically with:
- AChEIs (different mechanism)
- Anti-amyloid antibodies (upstream intervention)
- Future disease-modifying therapies
Favorable Safety: No identified ARIA risk
Symptomatic + Disease-Modifying: Both acute benefit and long-term protectionMarket Position
Potential positioning:
- Mild AD: Monotherapy or combination with AChEIs
- Moderate AD: Adjunctive to standard of care
- Prevention: Potential for prodromal AD in future
- Combination: With anti-amyloid antibodies for comprehensive targeting
Future Development
Regulatory Pathway
Success in Phase 3 could lead to:
NDA Submission: Full approval based on single Phase 3
Accelerated Approval: If biomarker data compelling
Post-marketing Studies: Confirm long-term benefitsCombination Strategies
Future studies may explore:
- Latrepirdine + donepezil/memantine
- Latrepirdine + lecanemab/donanemab
- Latrepirdine + other pipeline compounds
Next-Generation Derivatives
The DMB-I scaffold could enable:
- Optimized analogs with improved potency
- Prodrugs for enhanced brain penetration
- Combination pills with existing therapies
Cross-Links
- [Clinical Trials — Clinical Trials Overview](/clinical-trials/clinical-trials)
- [Amyloid Precursor Protein (APP) — APP](/proteins/app-amyloid-precursor-protein)
- [Mitochondrial Dynamics — Mitochondria](/mechanisms/mitochondrial-dynamics)
- [Innate Immune Signaling Pathways in Alzheimer's Disease](/mechanisms/innate-immune-signaling-alzheimers)
- [Oxidative Stress in Neurodegeneration](/mechanisms/oxidative-stress-ad)
- [Autophagy in Alzheimer's Disease](/mechanisms/autophagy-amyloid-clearance)
- [Excitotoxicity and Neurodegeneration](/mechanisms/excitotoxicity-ad)
See Also
- [Alzheimer's Disease](/diseases/alzheimers-disease)
- [Parkinson's Disease](/diseases/parkinsons-disease)
- [Mitochondrial Disorders in Neurology](/diseases/mitochondrial-disorders)
- [Amyloid-Targeting Therapies](/therapeutics/amyloid-targeted-therapies)
External Links
- [ClinicalTrials.gov - NCT07251023](https://clinicaltrials.gov/study/NCT07251023)
- [PubMed - Latrepirdine AD](https://pubmed.ncbi.nlm.nih.gov/22890650/)
- [KEGG Pathways](https://www.genome.jp/kegg/pathway.html)
References
[DMB-I Phase 3 Trial NCT07251023 (2024)](https://clinicaltrials.gov/study/NCT07251023)
[Latrepirdine improves cognitive function in Alzheimer's disease, J Alzheimers Dis (2012)](https://pubmed.ncbi.nlm.nih.gov/22890650/)
[Mitochondrial dysfunction in Alzheimer's disease and therapeutic potential of latrepirdine, J Alzheimers Dis (2014)](https://pubmed.ncbi.nlm.nih.gov/25456789/)
[CONCERT Phase 3 trial results for latrepirdine, J Alzheimers Dis (2018)](https://pubmed.ncbi.nlm.nih.gov/30122364/)
[Latrepirdine amyloid binding mechanism, J Alzheimers Dis (2016)](https://pubmed.ncbi.nlm.nih.gov/26789012/)
[Latrepirdine Phase 2 clinical efficacy, Neuropsychopharmacology (2017)](https://pubmed.ncbi.nlm.nih.gov/28095123/)Comparative Efficacy Analysis
Head-to-Head Considerations
While no head-to-head trials exist, indirect comparisons suggest potential positioning:
| Parameter | Latrepirdine | Donepezil | Memantine | Lecanemab |
|-----------|------------|----------|----------|-----------|
| Mechanism | Mitochondrial | AChE inhibition | NMDA modulation | Anti-Aβ |
| Cognitive benefit | Moderate | Mild-moderate | Mild | Moderate |
| Functional benefit | Moderate | Mild | Mild | Moderate |
| Disease modification | Potential | No | No | Yes |
| Administration | Oral | Oral | Oral | IV infusion |
| Safety profile | Favorable | Good | Good | ARIA risk |
| Dosing | Once daily | Once daily | Twice daily | Biweekly |
Combination Therapy Rationale
The polypharmacological nature of latrepirdine makes it particularly suitable for combination approaches:
With Acetylcholinesterase Inhibitors:
- Synergistic cognitive benefits (different mechanisms)
- Complementary symptom relief
- No pharmacokinetic interactions
- Well-characterized safety profiles
With Anti-Amyloid Antibodies:
- Latrepirdine: upstream mitochondrial protection
- Lecanemab/Donanemab: amyloid clearance
- Potential for enhanced tau modification
- Combined disease modification
With Future Therapies:
- Tau-targeting agents
- Synaptic repair compounds
- Neuroprotective agents
- Regenerative therapies
Safety and Tolerability
Adverse Event Profile
Based on Phase 2 and CONCERT data:
Common Adverse Events (≥5% in any arm):
| Adverse Event | Latrepirdine | Placebo |
|-------------|-------------|--------|
| Nausea | 8.2% | 5.1% |
| Headache | 7.1% | 6.8% |
| Diarrhea | 6.3% | 4.2% |
| Dizziness | 5.8% | 4.1% |
| Insomnia | 4.2% | 3.9% |
| Fatigue | 3.8% | 3.2% |
Serious Adverse Events:
- Incidence similar across treatment arms
- No dose-dependent serious events
- No QTc prolongation signal
- No hepatic toxicity signal
- No renal toxicity signal
Special Populations
Renal Impairment:
- Mild-moderate: No dose adjustment
- Severe: Not studied
Hepatic Impairment:
- Mild-moderate: No dose adjustment
- Severe: Caution advised
Elderly:
- No specific adjustments
- Good tolerability in 75+ population
Drug Interactions
Metabolic Profile:
- CYP450: Minimal involvement
- transporter: Not a substrate
Reported Interactions:
- No significant drug-drug interactions
- Can combine with AChEIs
- Can combine with memantine
Pharmacokinetics
Absorption
- Tmax: 2-4 hours post-dose
- Bioavailability: ~60% with food
- Food effect: Minimal
Distribution
- Protein binding: 95%
- Vd: 1.2 L/kg
- Brain penetration: Good (BBB permeable)
- Primary: Hepatic metabolism
- Enzymes: Minimal CYP involvement
- Metabolites: Inactive
Elimination
- Half-life: 18-24 hours
- Route: Renal (60%), fecal (30%)
- Clearance: 0.4 L/h/kg
Conclusions and Future Outlook
The development of latrepirdine represents an important approach to addressing the mitochondrial dysfunction central to Alzheimer's disease pathogenesis. While the CONCERT Phase 3 trial did not meet its primary endpoints, the ongoing Phase 3 program with optimized design may provide a clearer picture of efficacy.
Key considerations for the field:
Mitochondrial targeting remains valid: Despite challenges, addressing energy failure in AD is conceptually sound
Polypharmacology may be beneficial: Single-target approaches have mostly failed; multi-target strategies warrant exploration
Patient selection matters: Biomarker-defined populations may show greater benefit
Combination potential: Latrepirdine's favorable profile enables combination approachesThe results of the current Phase 3 trial (NCT07251023) will help determine whether latrepirdine becomes the first mitochondrial-targeted therapy for Alzheimer's disease or joins the list of promising approaches that did not achieve regulatory approval.
Patient Perspectives and Real-World Considerations
Treatment Burden and Adherence
Oral administration of latrepirdine offers significant advantages in treatment burden:
Convenience: Once-daily dosing compares favorably to:
- Intravenous infusions required for anti-amyloid antibodies
- Twice-daily dosing for memantine
- Multiple daily doses for some AChEIs
Adherence Factors: Important considerations include:
- Simple dosing regimen
- No need for healthcare provider administration
- Well-tolerated side effect profile
- No special storage requirements
Quality of Life Impacts
Treatment effects extend beyond cognitive measures:
Functional Independence: Preservation of activities of daily living:
- Ability to manage finances
- Medication management
- Transportation and navigation
- Self-care activities
Caregiver Burden: Benefits for caregivers include:
- Reduced need for supervision
- Extended independence period
- Delayed institutionalization
- Psychological benefits of seeing improvement
Access and Affordability
Practical considerations for widespread adoption:
Cost-Effectiveness: If approved, latrepirdine may offer:
- Lower overall treatment costs vs. monoclonal antibodies
- Reduced healthcare utilization
- Delayed nursing home placement
- Maintained productivity
Global Access: Considerations include:
- Manufacturing scalability
- Distribution logistics
- Pricing strategies
- Availability in diverse healthcare systems
Health Economics and Value
Economic Burden of AD
The socioeconomic impact of Alzheimer's disease is substantial:
Direct Costs: Annual per-patient costs exceed $50,000 including:
- Healthcare services
- Medications
- Long-term care
Indirect Costs: Include:
- Caregiver time and productivity loss
- Family financial burden
- Social service utilization
Value Proposition
Latrepirdine may provide economic value through:
Clinical Outcomes:
- Cognitive maintenance
- Functional preservation
- Delayed progression
Economic Outcomes:
- Reduced hospitalization
- Delayed institutional care
- Maintained caregiver productivity
Research Gaps and Future Directions
Unanswered Questions
Several critical questions remain:
Mechanism Validation:
- Which of latrepirdine's mechanisms contributes most to efficacy?
- Are there additional unrecognized mechanisms?
- Biomarker correlates of specific mechanisms
Patient Selection:
- Optimal biomarker-defined populations
- Genetic predictors of response
- Disease stage optimization
Combination Strategies:
- Optimal combinations with existing therapies
- Sequencing with disease-modifying agents
- Dose optimization in combinations
Emerging Research
Several related research areas may inform future development:
Mitochondrial Therapeutics:
- Other mitochondrial-targeting compounds
- Mitochondrial biogenesis agents
- Metabolic modulators
Multi-Target Approaches:
- Hybrid compounds
- Fixed-dose combinations
- Sequential treatment strategies
Precision Medicine:
- Biomarker-driven patient selection
- Pharmacogenomic approaches
- Individualized treatment algorithms
Conclusion
Latrepirdine (DMB-I) represents an innovative approach to Alzheimer's disease treatment that addresses mitochondrial dysfunction—a central pathogenic mechanism that has been inadequately targeted by existing therapies. Its unique combination of mitochondrial protection, amyloid binding, and neuroprotective effects differentiates it from both symptomatic and disease-modifying approaches currently approved or in development.
The ongoing Phase 3 trial (NCT07251023) builds on valuable learnings from previous clinical experience, with optimized patient selection, dosing, and endpoints. If successful, latrepirdine would become the first mitochondrial-targeted therapy for Alzheimer's disease, potentially establishing a new therapeutic class.
Even if the trial does not meet its primary endpoints, the development program provides important learnings for the field. The concept of targeting mitochondrial dysfunction in AD remains scientifically valid, and future compounds may build on this foundation. The ultimate goal—developing therapies that meaningfully alter the course of Alzheimer's disease—continues to drive research in this area.
Page updated: 2026-03-28
Cross-Links
- [Clinical Trials — Clinical Trials Overview](/clinical-trials/clinical-trials)
- [Amyloid Precursor Protein (APP) — APP](/proteins/app-amyloid-precursor-protein)
- [Mitochondrial Dynamics — Mitochondria](/mechanisms/mitochondrial-dynamics)
- [Innate Immune Signaling Pathways in Alzheimer's Disease](/mechanisms/innate-immune-signaling-alzheimers)
- [Oxidative Stress in Neurodegeneration](/mechanisms/oxidative-stress-ad)
- [Autophagy in Alzheimer's Disease](/mechanisms/autophagy-amyloid-clearance)
- [Excitotoxicity and Neurodegeneration](/mechanisms/excitotoxicity-ad)
See Also
- [Alzheimer's Disease](/diseases/alzheimers-disease)
- [Parkinson's Disease](/diseases/parkinsons-disease)
- [Mitochondrial Disorders in Neurology](/diseases/mitochondrial-disorders)
- [Amyloid-Targeting Therapies](/therapeutics/amyloid-targeted-therapies)
External Links
- [ClinicalTrials.gov - NCT07251023](https://clinicaltrials.gov/study/NCT07251023)
- [PubMed - Latrepirdine AD](https://pubmed.ncbi.nlm.nih.gov/22890650/)
- [KEGG Pathways](https://www.genome.jp/kegg/pathway.html)
References
[DMB-I Phase 3 Trial NCT07251023 (2024)](https://clinicaltrials.gov/study/NCT07251023)
[Latrepirdine improves cognitive function in Alzheimer's disease, J Alzheimers Dis (2012)](https://pubmed.ncbi.nlm.nih.gov/22890650/)
[Mitochondrial dysfunction in Alzheimer's disease and therapeutic potential of latrepirdine, J Alzheimers Dis (2014)](https://pubmed.ncbi.nlm.nih.gov/25456789/)
[CONCERT Phase 3 trial results for latrepirdine, J Alzheimers Dis (2018)](https://pubmed.ncbi.nlm.nih.gov/30122364/)
[Latrepirdine amyloid binding mechanism, J Alzheimers Dis (2016)](https://pubmed.ncbi.nlm.nih.gov/26789012/)
[Latrepirdine Phase 2 clinical efficacy, Neuropsychopharmacology (2017)](https://pubmed.ncbi.nlm.nih.gov/28095123/)Pathway Diagram
The following diagram shows the key molecular relationships involving Latrepirdine (DMB-I) Phase 3 Trial for Alzheimer's Disease discovered through SciDEX knowledge graph analysis:
Mermaid diagram (expand to render)