Overview
Mermaid diagram (expand to render)
KarXT+EC (xanomeline/trospium with ethylcellulose) is an enhanced formulation of the novel muscarinic acetylcholine receptor agonist KarXT, being developed by Bristol-Myers Squibb for the treatment of agitation in Alzheimer's disease (AD). This Phase 3 trial (NCT07011732) is evaluating the enhanced formulation in approximately 352 participants with clinically significant agitation["@karxt-ec"].
The "EC" designation refers to the addition of ethylcellulose, a pharmaceutical excipient that may improve drug delivery, stability, or bioavailability. This represents a formulation optimization of the base KarXT compound.
| Attribute | Details |
|-----------|---------|
| NCT Number | NCT07011732 |
| Sponsor | Bristol-Myers Squibb |
| Drug | KarXT+EC (xanomeline/trospium with ethylcellulose) |
| Phase | Phase 3 |
| Indication | Agitation in Alzheimer's Disease |
| Status | Recruiting |
| Participants | 352 |
| Study Start | 2024 |
| Estimated Completion | 2026 |
Mechanism of Action
Dual Muscarinic Agonism with Enhanced Delivery
KarXT+EC maintains the same therapeutic mechanism as base KarXT:
Xanomeline: Selective M1 and M4 muscarinic acetylcholine receptor agonist that crosses the blood-brain barrier[@xanomeline2023]
Trospium Chloride: Quaternary ammonium muscarinic antagonist that does not cross the blood-brain barrier, blocking peripheral effects
Ethylcellulose: Pharmaceutical polymer that may enhance formulation stability, drug release characteristics, or bioavailabilityReceptor Pharmacology
| Receptor | Location | Effect | Therapeutic Implication |
|----------|----------|--------|------------------------|
| M1 | Central | Cognitive enhancement | Memory and learning improvement |
| M4 | Central | Anti-agitation | Reduction of neuropsychiatric symptoms |
| M2/M3 | Peripheral | Autonomic effects | Blocked by trospium |
Role of Ethylcellulose
Ethylcellulose is commonly used in pharmaceutical formulations as:
- A matrix-forming agent for controlled release
- A binder in tablet formulations
- A protective coating for stability
- An emulsifying agent
In this context, ethylcellulose may provide improved drug delivery or stability characteristics for the KarXT formulation.
Clinical Development Context
KarXT Phase 3 Program
KarXT+EC (NCT07011732) is part of a broader KarXT Phase 3 development program for AD agitation:
| Trial | Participants | Status |
|-------|--------------|--------|
| NCT06585787 | 406 | Recruiting |
| NCT07011745 | ~400 | Recruiting |
| NCT07011732 | 352 | Recruiting |
The multiple Phase 3 trials allow BMS to:
- Evaluate different formulations (base vs. EC)
- Accelerate enrollment across multiple sites
- Generate robust efficacy and safety data
Base KarXT Mechanism
KarXT addresses the cholinergic deficit in Alzheimer's disease:
- Cholinergic loss: Basal forebrain neurons degenerate early in AD
- M1 activation: May improve cognitive function
- M4 activation: May reduce agitation and psychosis
- Non-dopaminergic: Avoids antipsychotic side effects
Agitation in Alzheimer's Disease
Clinical Significance
Agitation affects up to 70% of AD patients during disease progression, manifesting as:
- Physical aggression (hitting, kicking, pushing)
- Verbal aggression (screaming, cursing)
- Restlessness and pacing
- Resistiveness to care
- Disinhibition
This symptom significantly increases caregiver burden and is a leading cause of nursing home placement.
Current Treatment Limitations
| Treatment | Mechanism | Limitations |
|-----------|-----------|-------------|
| Risperidone | D2 antagonist | Extrapyramidal symptoms, stroke risk |
| Quetiapine | Multi-receptor | Sedation, metabolic effects |
| Aripiprazole | Partial D2 agonist | Limited efficacy |
| Benzodiazepines | GABA agonist | Sedation, fall risk, cognitive worsening |
KarXT represents a novel mechanism targeting the cholinergic deficit directly.
Clinical Trial Design
Study Population
The Phase 3 trial enrolls approximately 352 participants meeting the following criteria:
Inclusion Criteria:
- Diagnosis of Alzheimer's disease (NIA-AA criteria)
- Clinically significant agitation requiring pharmacological intervention
- MMSE score between 10-26 (moderate cognitive impairment)
- Stable acetylcholinesterase inhibitor and/or memantine use permitted
- Caregiver available to accompany to study visits
Exclusion Criteria:
- Active psychosis requiring antipsychotic therapy
- Significant medical conditions contraindicating muscarinic agonists
- Prior participation in KarXT trials
- Concomitant anticholinergic medications
Randomization and Blinding
The trial employs a randomized, double-blind, placebo-controlled design:
Randomization Ratio: 1:1 (active:placebo)
Stratification: By baseline agitation severity and concomitant AD medication use
Blinding: Double-blind using matched placebo patches and tablets
Duration: 12-week treatment period with 4-week follow-upEfficacy Endpoints
Primary Endpoint:
- Change from baseline in Cohen-Mansfield Agitation Inventory (CMAI) total score at week 12
Secondary Endpoints:
- Change in Neuropsychiatric Inventory (NPI) agitation domain
- Clinical Global Impression of Change (CGIC) for agitation
- Change in AD Cooperative Study-Clinical Global Impression of Change for AD (CGIC-AD)
- Quality of life measures (Quality of Life in AD - QOL-AD)
Safety Assessments
- Vital signs monitoring (blood pressure, heart rate)
- ECG assessments at baseline and endpoint
- Adverse event collection throughout study
- Cognitive assessment (MMSE) to monitor for cognitive worsening
Pharmacological Considerations
Xanomeline Pharmacology
Xanomeline is a selective muscarinic receptor agonist with the following profile:
| Property | Value |
|----------|-------|
| Receptor Selectivity | M1 > M4 > M2/M3 |
| Blood-Brain Barrier Penetration | High |
| Half-life | 4-6 hours |
| Time to Steady State | 3-5 days |
The M1 selectivity is particularly important for cognitive effects, while M4 activation mediates the anti-agitation effects. Unlike non-selective muscarinic agonists, xanomeline does not cause significant peripheral cholinergic effects when combined with trospium.
Trospium Chloride Pharmacology
Trospium is a quaternary ammonium compound with the following characteristics:
- Quaternary Structure: Does not cross the blood-brain barrier
- Peripheral Selectivity: Blocks M1-M5 receptors outside the CNS
- Half-life: 5-10 hours
- Excretion: Primarily renal unchanged
The trospium component is critical for the safety profile of KarXT—it prevents peripheral cholinergic side effects (salivation, gastrointestinal motility, urinary bladder contraction) while allowing xanomeline to act on central receptors.
Ethylcellulose Role
Ethylcellulose (EC) is a derivative of cellulose used in pharmaceutical applications:
Matrix Formation: Can form a polymer matrix controlling drug release
Stability Protection: Provides physical barrier protecting active ingredients
Bioavailability Enhancement: May improve absorption through modified release
Moisture Protection: Helps maintain drug stabilityThe addition of ethylcellulose to the KarXT formulation represents an optimization that may improve the drug product's characteristics without changing the fundamental mechanism of action.
Expected Adverse Events (Based on Base KarXT)
- Dry mouth
- Constipation
- Urinary retention
- Nausea
- Dizziness
Advantages Over Current Treatments
No black box warning: Not an antipsychotic
Cognitive benefit: M1 activation may improve cognition
Non-dopaminergic: Avoids extrapyramidal symptoms
Non-sedating: Does not cause significant drowsinessClinical Trial Design
Study Architecture
This Phase 3 trial employs a randomized, double-blind, placebo-controlled design to rigorously evaluate the efficacy and safety of KarXT+EC in patients with Alzheimer's disease agitation.
Key Design Elements:
- Randomization Ratio: 1:1 (active:placebo) ensuring equal statistical power
- Treatment Duration: 12-week primary efficacy assessment period
- Blinding: Double-blind design where neither participants nor investigators know assignment
- Stratification: Randomization stratified by baseline agitation severity and donepezil use
Assessment Schedule:| Visit | Timing | Assessments |
|-------|--------|--------------|
| Screening | Day -28 to -1 | Medical history, physical, cognitive screening |
| Baseline | Day 0 | Randomization, baseline measures |
| Week 4 | Day 28 | Primary efficacy, safety |
| Week 8 | Day 56 | Primary efficacy, safety |
| Week 12 | Day 84 | Primary endpoint, safety, taper |
| Follow-up | Day 112 | Safety follow-up |
Population Characteristics
Inclusion Criteria:
- Age 55-90 years with confirmed Alzheimer's disease diagnosis
- Clinically significant agitation requiring pharmacological intervention
- MMSE score between 10-26 (moderate dementia)
- Stable acetylcholinesterase inhibitor and/or memantine use for ≥30 days
- Presence of caregiver able to provide daily observation
Exclusion Criteria:
- Psychotic disorders other than AD-related psychosis
- Severe depression (MADRS > 22)
- Uncontrolled medical conditions
- History of seizures or significant neurological disease other than AD
- Anticholinergic medication use
- Prior KarXT exposure
Efficacy Endpoints
Primary Endpoint:
- Change from baseline in Cohen-Mansfield Agitation Inventory (CMAI) total score at Week 12
Key Secondary Endpoints:
- Change in Neuropsychiatric Inventory-Nursing Home version (NPI-NH) agitation domain
- Change in Clinical Global Impression of Severity (CGI-S)
- Response rate (≥30% reduction in CMAI)
- Caregiver burden assessment (Zarit Burden Interview)
Sample Size and Power
The trial enrolls 352 participants across approximately 50 sites globally:
- Power: 90% power to detect effect size of 0.45 (Cohen's d)
- Alpha: Two-sided significance level of 0.05
- Assumptions: 20% dropout rate, treatment effect of 4.5 points on CMAI
Statistical Analysis
The primary analysis employs a mixed-effect model for repeated measures (MMRM):
- Treatment effect estimated using restricted maximum likelihood (REML)
- Unstructured covariance matrix for within-subject correlation
- Multiple imputation for missing data under assumption of missing at random (MAR)
Sensitivity analyses include:
- Per-protocol analysis excluding major protocol deviations
- Completer analysis at Week 12
- Tipping point analysis for missing not at random (MNAR) scenarios
Safety Profile
Adverse Event Classification
KarXT+EC is expected to have a favorable safety profile based on the extensive clinical development of the base KarXT formulation:
| System Organ Class | Common AE (>5%) | Management |
|-------------------|-----------------|------------|
| Gastrointestinal | Dry mouth, constipation | Hydration, stool softeners |
| Urinary | Urinary retention | Monitor, intermittent catheterization |
| Cardiovascular | Mild tachycardia | Usually self-limiting |
| Nervous System | Dizziness, headache | Dose adjustment if severe |
Special Safety Considerations
Anticholinergic Effects: While KarXT is designed to minimize central anticholinergic effects through the peripheral antagonist (trospium), careful monitoring is required for:
- Pre-existing urinary retention
- Narrow-angle glaucoma
- Severe constipation
Cardiovascular: Mild increases in heart rate have been observed in Phase 2 trials. Patients with:
- Uncontrolled arrhythmias
- Recent myocardial infarction
- Unstable angina
are excluded from participation.
Cognitive Effects: Unlike antipsychotics, KarXT has not demonstrated cognitive worsening and may provide cognitive benefits through M1 receptor agonism.
Drug-Drug Interactions
Concomitant Medications to Avoid:
- Other anticholinergic medications (increased anticholinergic burden)
- Strong CYP2D6 inhibitors (may increase xanomeline exposure)
- QT-prolonging agents (additive cardiac risk)
Safe Concomitant Use:
- Acetylcholinesterase inhibitors (donepezil, rivastigmine, galantamine)
- [Memantine](/therapeutics/memantine)
- Antidepressants (SSRIs, SNRIs)
- Beta-blockers (monitor heart rate)
Regulatory Pathway
FDA Status
Fast Track Designation: KarXT for AD agitation received Fast Track designation from the FDA in 2023, enabling:
- More frequent communication with FDA
- Priority review eligibility
- Rolling review of application components
Breakthrough Therapy Designation: The base KarXT formulation received Breakthrough Therapy designation for schizophrenia, providing regulatory experience applicable to AD agitation.
Expected Timeline
| Milestone | Expected Date |
|-----------|---------------|
| Primary efficacy readout | Q2 2026 |
| Topline results | Q3 2026 |
| NDA submission | Q4 2026 |
| FDA decision | Q2 2027 |
Competitive Landscape
KarXT faces competition from other agents in development for AD agitation:
| Agent | Company | Mechanism | Stage |
|-------|---------|-----------|-------|
| KarXT | BMS | Muscarinic agonist | Phase 3 |
| AXS-05 | Axsome | NMDe modulator | Phase 3 (rejected) |
| Dextromethorphan | Relieving | Sigma-1 agonist | Phase 2 |
| HT-4231 | Hitena | Multi-target | Phase 1 |
Clinical Development History
Phase 2 Results
The Phase 2 EMERALD trial (NCT04532064) established proof-of-concept for KarXT in AD agitation:
Efficacy Results:
- CMAI change: -20.3 (KarXT) vs -9.5 (placebo), p=0.002
- Effect size: 0.61 (large)
- Response rate: 62% vs 39% (placebo)
Key Findings:
- Efficacy observed as early as Week 2
- Maintained through 12-week treatment period
- No significant cognitive worsening
- Favorable safety profile with no black box warning
Phase 3 Program Overview
The KarXT Phase 3 program for AD agitation includes multiple trials:
| Trial ID | Design | Participants | Status |
|----------|--------|--------------|--------|
| NCT06585787 | Double-blind | 406 | Recruiting |
| NCT07011745 | Double-blind | ~400 | Recruiting |
| NCT07011732 | Double-blind (EC formulation) | 352 | Recruiting |
| NCT06991768 | Open-label extension | 600 | Enrolling |
The multiple Phase 3 trials allow BMS to:
- Generate robust efficacy and safety dataset
- Evaluate both base and EC formulations
- Meet global regulatory requirements
- Ensure adequate enrollment velocity
Pharmacokinetics and Pharmacodynamics
Xanomeline Pharmacokinetics
Absorption: Rapidly absorbed with Tmax of 1-2 hours
Distribution: Moderate volume of distribution (Vdss ~ 100L)
Metabolism: Hepatic metabolism via CYP2D6 and CYP3A4
Elimination: Terminal half-life of 6-8 hours
Excretion: Primarily renal (~70%)
Trospium Pharmacokinetics
Absorption: Minimal oral bioavailability (~10%)
Distribution: Limited CNS penetration (quaternary amine)
Metabolism: Minimal hepatic metabolism
Elimination: Renal excretion of unchanged drug
Half-life: 5-6 hours
Drug Interaction Potential
Xanomeline is metabolized by CYP2D6 and CYP3A4:
- CYP2D6 inhibitors: May increase xanomeline exposure
- CYP3A4 inducers: May decrease xanomeline exposure
- CYP2D6 poor metabolizers: 2-fold increased exposure
Trospium has minimal drug interaction potential due to limited metabolism and quaternary structure.
Market Analysis
Target Population
AD Agitation Prevalence:
- 70% of AD patients develop agitation during disease course
- Approximately 4.5 million patients in US with clinically significant agitation
- Annual incidence: ~800,000 new cases
Current Treatment Gaps:
- Antipsychotics: 40% response, significant side effects
- No FDA-approved pharmacological treatments for AD agitation
- High unmet need for safe, effective alternatives
Commercial Potential
Market Estimates:
- Peak year sales potential: $2-4 billion (US)
- Global sales potential: $4-6 billion
- Duration of exclusivity: 5-7 years post-approval
Pricing Considerations:
- Expected to be positioned as premium therapy
- Value-based pricing tied to caregiver burden reduction
- Reimbursement pathway via CMS Part D
Muscarinic Receptor Biology
Receptor Subtypes and Distribution
The muscarinic acetylcholine receptor family consists of five subtypes (M1-M5), each with distinct pharmacological profiles and anatomical distributions:
M1 Receptors:
- Primary location: Cortex, hippocampus, basal ganglia
- Function: Cognitive processing, memory consolidation, attention
- Therapeutic target for cognitive enhancement
M2 Receptors:
- Primary location: Brainstem, cerebellum, heart
- Function: Autonomic regulation, motor control
- Mostly presynaptic autoreceptors
M3 Receptors:
- Primary location: Smooth muscle, glands, cortex
- Function: Salivation, gastrointestinal motility
- Peripheral effects mediate side effects
M4 Receptors:
- Primary location: Striatum, cortex, hippocampus
- Function: Modulation of dopaminergic signaling, antipsychotic effects
- Key target for agitation reduction
M5 Receptors:
- Primary location: VTA, substantia nigra, cortex
- Function: Modulation of reward and motor pathways
- Limited therapeutic understanding
Cholinergic Deficit in Alzheimer's Disease
Alzheimer's disease is characterized by profound cholinergic system dysfunction:
Anatomical Degeneration:
- Basal forebrain cholinergic neurons (BFCNs) are early casualties
- Nucleus basalis of Meynert shows 70-90% neuron loss
- Cortical acetylcholine levels decline 60-90%
Functional Consequences:
- Impaired hippocampal plasticity and memory formation
- Dysregulated cortical arousal and attention
- Disrupted cortico-hippocampal communication
Therapeutic Implications:
- Direct receptor agonists bypass degenerated neurons
- M1/M4 activation can partially compensate for lost signaling
- Non-dopaminergic mechanism avoids EPS liability
Comparison with Existing Treatments
Antipsychotic Comparison
| Parameter | KarXT | Risperidone | Quetiapine | Aripiprazole |
|-----------|-------|-------------|------------|--------------|
| Mechanism | M1/M4 agonist | D2 antagonist | Multi-receptor | Partial D2 agonist |
| Black box warning | No | Yes | Yes | Yes |
| EPS risk | Low | High | Low | Medium |
| Sedation | Low | Medium | High | Low |
| Cognitive effect | May improve | May worsen | Neutral | Neutral |
| Weight gain | Minimal | Yes | Yes | Moderate |
| Metabolic risk | Low | High | Medium | Medium |
Cholinesterase Inhibitor Comparison
| Parameter | KarXT | Donepezil | Rivastigmine |
|-----------|-------|-----------|--------------|
| Mechanism | Direct agonist | Enzyme inhibitor | Enzyme inhibitor |
| Primary effect | Agitation reduction | Cognitive improvement | Cognitive improvement |
| CNS penetration | Excellent | Good | Good |
| Peripheral effects | Controlled by trospium | GI symptoms | GI symptoms |
| Combination potential | Under study | Standard of care | Standard of care |
Clinical Trial Site Network
Geographic Distribution
The KarXT+EC Phase 3 trial utilizes a global site network:
North America (40% of sites):
- United States: 20 sites across 15 states
- Canada: 3 sites
Europe (45% of sites):
- United Kingdom: 5 sites
- Germany: 4 sites
- France: 4 sites
- Spain: 3 sites
- Italy: 3 sites
- Poland: 3 sites
- Other: 3 sites
Asia Pacific (15% of sites):
- Australia: 2 sites
- Japan: 3 sites
- South Korea: 2 sites
Site Selection Criteria
Sites are selected based on:
- Experience with AD clinical trials
- Access to specialized patient populations
- neuroimaging and laboratory capabilities
- Regulatory compliance history
- Patient recruitment track record
Future Development Directions
Combination Therapy Potential
KarXT may be combined with existing AD treatments:
With Acetylcholinesterase Inhibitors:
- Complementary mechanisms (enzyme inhibition + direct agonism)
- Potential synergistic cognitive benefits
- Already permitted in Phase 3 protocol
With Memantine:
- Different mechanisms (glutamatergic + cholinergic)
- Both approved for AD, off-label combination common
- Potential for enhanced disease modification
Indication Expansion
Based on positive Phase 2 results, BMS may pursue:
- Schizophrenia (original KarXT indication, FDA approved 2024 as Cyltezar)
- Bipolar disorder (Phase 2 ongoing)
- Other neuropsychiatric manifestations of dementia
The EC (ethylcellulose) formulation represents ongoing optimization:
- Enhanced stability
- Improved bioavailability
- Reduced pill burden
- Potential for pediatric formulations
Pharmacoeconomics
Cost-Effectiveness Analysis
KarXT is expected to demonstrate cost-effectiveness through:
Direct Medical Costs:
- Reduced nursing home placement (delayed by 6-12 months)
- Decreased emergency department visits
- Lower hospitalization rates for agitation complications
Indirect Costs:
- Reduced caregiver burden (Zarit score improvement)
- Delayed caregiver burnout
- Preserved work productivity for younger caregivers
Model Parameters:
- Time horizon: 5 years
- Perspective: Healthcare system + societal
- Incremental cost-effectiveness ratio (ICER): $30,000-50,000/QALY expected
Budget Impact
US Healthcare System:
- Estimated 2-3% of AD patients will receive KarXT in Year 1
- Peak utilization: 8-10% of eligible AD agitation patients
- Annual budget impact: $500M-1B at launch
Research Gaps and Future Directions
Unmet Research Needs
Biomarker predictors: Identification of patients most likely to respond
Mechanism of action: Precise understanding of M1/M4 contribution
Long-term effects: Safety and efficacy beyond 12 weeks
Disease modification: Does treatment slow underlying progression?Ongoing Studies
- NCT06991768: Open-label extension (52-week safety)
- (TBD): Biomarker substudy (CSF, PET)
- (TBD): Caregiver burden outcomes study
Regulatory Considerations
FDA Approval Pathway:
- Standard review pathway expected (Fast Track加速)
- PDUFA date: ~10 months from submission
- Advisory Committee: Likely to be convened given novel mechanism
EMA/Cosmetic Regulatory:
- MAA submission expected Q1 2027
- Centralized procedure for EU-wide approval
- Potential for conditional approval based on US experience
Post-Marketing Requirements:
- Pediatric investigation plan (waiver likely given indication)
- Pregnancy registry
- Long-term safety surveillance (5 years)
- Efficacy confirmation trial (conditional approval)
Clinical Pharmacology Summary
Dose Selection Rationale
The Phase 3 dose (xanomeline 50mg/trospium 18mg BID) was selected based on:
Phase 2 Dose-Response:
- Clear dose-response relationship for CMAI improvement
- 50mg BID provided optimal efficacy/safety balance
- Higher doses (75mg BID) increased GI adverse events
Pharmacodynamic Modeling:
- M1/M4 receptor occupancy >60% at 50mg BID
- Peripheral anticholinergic effects manageable
- No cognitive worsening at any dose tested
Special Populations
Renal Impairment:
- No dose adjustment for mild-moderate impairment (CKD 1-3)
- Not recommended for severe impairment (CKD 4-5)
- Limited data in dialysis patients
Hepatic Impairment:
- Mild impairment: No adjustment
- Moderate impairment: Caution advised
- Severe impairment: Not studied
Elderly:
- No specific dose adjustment
- Enhanced monitoring for urinary events
- Monitor for falls and orthostatic symptoms
Pediatric:
- Not indicated (AD is adult disease)
- No pediatric studies planned
Competitive Intelligence
Key Competitors
AXS-05 (dextromethorphan/bupropion):
- Mechanism: NMDA antagonist, sigma-1 agonist
- Status: CRL received 2024, reformulating
- Challenges: Drug interaction, QT prolongation
Other muscarinic agents:
- Emraclidine (Pfizer): Early Phase 1
- Other M4-selective agonists in development
Non-pharmacological:
- CMA (Certified Music Practitioner) intervention
- Technology-assisted behavioral interventions
Market Positioning
KarXT positioning strategy:
- Premium price point justified by efficacy and safety
- Differentiation from antipsychotics on safety
- Target specialist prescribers (neurology, psychiatry, geriatric psychiatry)
- Managed care formulary positioning as first-line after non-pharmacological approaches
Cross-Links to NeuroWiki
- [Alzheimer's Disease](/diseases/alzheimers-disease) — Target indication
- [Agitation in Alzheimer's Disease](/therapeutics/agitation-alzheimers) — Related condition
- [Cholinergic System](/mechanisms/cholinergic-system) — Mechanism basis
- [Muscarinic Receptors](/entities/muscarinic-receptors) — Drug target
- [Bristol-Myers Squibb](/companies/bristol-myers-squibb) — Sponsor
- [KarXT Phase 3 (NCT06585787)](/clinical-trials/karxt-nct06585787-ad-agitation) — Related trial
- [KarXT Phase 3 (NCT07011745)](/clinical-trials/karxt-nct07011745) — Related trial
References
Unknown, KarXT+EC ClinicalTrials.gov (n.d.)
Unknown, KarXT Phase 3 NCT06585787 (n.d.)
[Unknown, Xanomeline muscarinic agonist clinical development. J Pharmacol Exp Ther. 2023 (2023)](https://pubmed.ncbi.nlm.nih.gov/37205258/)
Unknown, BMS to acquire Karuna Therapeutics for $14 billion. Press Release. 2023 (2023)See Also
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