LEQEMBI® (lecanemab-irmb) logo

LEQEMBI® (lecanemab-irmb) logo
Lance and Liz
Lance and Liz

LEQEMBI®
clinical results

Lance is a real LEQEMBI patient and Liz is his care partner.
People shown were compensated for their time, and information is accurate as of August 2025.

With LEQEMBI, early and continuous treatment can slow progression1,2

Study description

Clarity AD Core placebo-controlled period1,3⁣:

An 18-month, global, placebo-controlled, double-blind, parallel-group, randomized clinical trial of 1795 patients with mild cognitive impairment (MCI) due to Alzheimer's disease (AD) or mild AD dementia with confirmed amyloid beta (Aβ) pathology. Patients were randomized 1:1 to receive infusions of LEQEMBI 10 mg/kg (n=898) or placebo (n=897) once every 2 weeks. The primary objective was to evaluate the effect of LEQEMBI as measured by CDR-SB.

Clarity AD long-term extension (LTE)4-6⁣:

A global, open-label, single-arm study evaluating LEQEMBI in patients with early AD for up to 48 months. Patients enrolled in the Clarity AD Core period (0-18 months) were given the option to participate in Clarity AD LTE (18-48 months); some remained on infusion while others were on different subcutaneous maintenance doses. The primary objective was to evaluate the long-term safety and whether the effect of LEQEMBI, as measured by CDR-SB at the end of the Clarity AD Core period, is maintained over time.

Alzheimer’s Disease Neuroimaging Initiative (ADNI):

ADNI is a global (US and Canada) research study that follows the natural progression of AD, including imaging, biomarkers, genetics, and neurocognitive tests, and that actively evaluates the investigation and development of treatments for AD. ADNI is an untreated observational cohort (n=436 at baseline, followed for 48 months) that was a prespecified matched ADNI cohort used to design the Clarity AD study, based on demographics and clinical characteristics.4,5

LEQEMBI met the primary endpoint1

In the Core placebo-controlled period (0-18 months), LEQEMBI achieved statistical significance, slowing progression by 27% vs placebo (P<0.0001).

Ongoing treatment showed continued benefit out to 4 years5,7-9

Data at 4 years show continued separation in CDR-SB scores vs Alzheimer's Disease Neuroimaging Initiative (ADNI). About 94% of patients in the LEQEMBI arm who completed the Core period opted to continue in the LTE after 18 months.

CDR-SB: Change from baseline in cognition and function1,5

Chart showing the cognition and functional decline of LEQEMBI® patients compared to the untreated cohort.

Cutoff: March 31, 2025.10

The LTE study is ongoing.11

LTE data limitations: Patients were enrolled in the LTE after completion of the controlled period and are subject to continued dropout. These data included patients on a range of subcutaneous doses, all within the FDA bioequivalence acceptance criteria (PK/PD)."4,6

ADNI data limitations: This retrospective analysis for ADNI should be interpreted carefully to determine a difference with LEQEMBI because of the potential selection bias and attrition.⁣

AD, Alzheimer’s disease; ADNI, Alzheimer’s Disease Neuroimaging Initiative; CDR, Clinical Dementia Rating; CDR-SB, Clinical Dementia Rating-Sum of Boxes; LTE, long-term extension; PD, pharmacodynamics; PK, pharmacokinetics; SE, standard error.

In a prespecified analysis of delayed risk of progression, 4 of 5 patients treated with LEQEMBI remained in the early AD stages through 4 years5,12

Patient progression over time5

In a prespecified analysis, graph visualizing patient dementia stage progression over 48 months. In a prespecified analysis, graph visualizing patient dementia stage progression over 48 months.

81%

of patients remained in the MCI due to AD or mild AD stages through 4 years of treatment5,12

Silhouette of person surrounded by icons representing hobbies

Moderate to severe AD dementia stages are associated with loss of independence and difficulty with daily activities13

Limitations: Patients were enrolled in the LTE after completion of the controlled period and are subject to continued dropout. After 18 months, data included patients on a range of subcutaneous doses, all within the FDA bioequivalence acceptance criteria (PK/PD).4,6

ADNI data limitations: This retrospective analysis for ADNI should be interpreted carefully to determine a difference with LEQEMBI because of the potential selection bias and attrition.

Early AD and low tau data

In a post hoc analysis, LEQEMBI was evaluated in patients with early AD and low tau5,14

At 4 years, 69% of patients with early AD and low tau levels showed no worsening in CDR-SB scores compared with baseline*5

A post-hoc analysis showing the percentage of LEQEMBI® patients with early AD and low tau with no worsening symptoms at 4 years. A post-hoc analysis showing the percentage of LEQEMBI® patients with early AD and low tau with no worsening symptoms at 4 years.

LEQEMBI patients with early AD and low tau showed improvement in CDR-SB scores vs baseline*5

At 18 months:

60%

improved

(placebo 28%)

At 4 years:

56%

improved

  • An increase in CDR-SB score=worsening and a decrease in score=improvement14

*No placebo post 18 months during the LTE.5

Limitations: These are post hoc exploratory analyses data from the tau PET subgroup of the Clarity AD study. These analyses were limited by small sample size and no conclusions can be drawn. After 18 months, data included patients on a range of subcutaneous doses, all within
the FDA bioequivalence acceptance criteria (PK/PD).6,14

Clarity AD: Post hoc analyses of CDR-SB scores in a low tau patient population14

Study description: The predefined optional tau PET substudy looked at outcomes of CDR-SB results across tau levels stratified by the participants’ level of the brain tau aggregates (tau PET), using the Cerveau database, as well as correlations of tau data to clinical outcomes (n=342).

Results of post hoc analysis:

  • Overall tau PET substudy (placebo, 167; LEQEMBI, 175): Adjusted mean difference vs placebo: -0.52 (95% CI: -1.01, -0.04)14,15

  • Low tau PET (<1.06): (placebo, 71; LEQEMBI, 70): Adjusted mean difference vs placebo: -0.59 (95% CI: -1.09, -0.09)14,15

  • Intermediate tau levels (n=191; SUVR ≥1.06-≤2.91) and high tau levels (n=10: SUVR >2.91): (placebo, 96; LEQEMBI, 105): Adjusted mean difference vs placebo: -0.49 (95% CI: -1.19, 0.21)14,15

  • As shown, further analyses were conducted in the low tau group to measure the change from baseline on the CDR-SB14

Magnifying glass exclamation icon

Diagnose with urgency and treat early:

Lower levels of tau accumulation, as identified by SUVR, were found to be indicative of a patient with earlier stages of disease.13,14

No testing for tau is required to start LEQEMBI.1

CI, confidence interval; PET, positron emission tomography; SUVR, standardized uptake value ratio.

Diagnosis to Treatment Brochure

An overview of the steps involved from diagnosis through treatment with LEQEMBI (for eligible patients)

Download brochure

Biomarker endpoint: Plaque negativity

More than half of LEQEMBI patients achieved plaque negativity at 12 months1,3

Key secondary endpoint: Change in Aβ PET Centiloid1

  • -59.1 Centiloid (CL) difference vs placebo at 18 months (P<0.00001)3

Prespecified biomarker endpoint percentage of patients achieving plaque negativity: Measured by conversion to PET amyloid negative (<30 CL)3

3 MONTHS

24%
OF PATIENTS

Placebo: 15%

LEQEMBI n=296

Placebo n=303

6 MONTHS

36%
OF PATIENTS

Placebo: 14%

LEQEMBI n=275

Placebo n=286

12 MONTHS

54%
OF PATIENTS

Placebo: 15%

LEQEMBI n=276

Placebo n=259

18 MONTHS

68%
OF PATIENTS

Placebo: 16%

LEQEMBI n=210*

Placebo n=205*

Limitations: Prespecified biomarker endpoint was not adjusted for multiplicity, therefore, no conclusions or comparisons can be drawn.

*73 subjects were not included at 18 months (per the statistical analysis plan) since their PET assessments were performed after receiving LEQEMBI in the extension phase.3

Abstract ab peptide icon

LEQEMBI can help you treat beyond plaque:

Continuous administration of LEQEMBI works in 2 ways to remove insoluble and soluble Aβ1,3

Explore the MOA

Frequently asked questions

In Clarity AD, in which stage of AD were most of the patients?

The majority of patients were in the earliest symptomatic stage—MCI due to AD.1,2

{{buttontext}}

Were the LTE data inclusive of both IV and subcutaneously treated patients?

Yes, patients receiving both IV and different subcutaneous maintenance doses were included in the LTE data.5
{{buttontext}}

What patient population do the low tau data represent?

This cohort represents patients with early AD and low tau levels.13,14

{{buttontext}}

Safety matters
See the safety results from the Clarity AD study, including long-term ARIA rates

Get the results
Top

INDICATION & IMPORTANT SAFETY INFORMATION

INDICATION

LEQEMBI® is indicated for the treatment of Alzheimer's disease (AD). Treatment with LEQEMBI should be initiated in patients with mild cognitive impairment (MCI) or mild dementia stage of disease, the population in which treatment was initiated in clinical trials.

CONTRAINDICATION

Contraindicated in patients with serious hypersensitivity to lecanemab-irmb or to any of the excipients. Reactions have included angioedema and anaphylaxis.

WARNINGS AND PRECAUTIONS

AMYLOID-RELATED IMAGING ABNORMALITIES

Medications in this class, including LEQEMBI, can cause ARIA-E, which can be observed on MRI as brain edema or sulcal effusions, and ARIA-H, which includes microhemorrhage and superficial siderosis. ARIA can occur spontaneously in patients with AD, particularly in patients with MRI findings suggestive of cerebral amyloid angiopathy (CAA), such as pretreatment microhemorrhage or superficial siderosis. ARIA-H generally occurs with ARIA-E. Reported ARIA symptoms may include headache, confusion, visual changes, dizziness, nausea, and gait difficulty. Focal neurologic deficits may also occur. Symptoms usually resolve over time.

Incidence of ARIA

Symptomatic ARIA occurred in 3% and serious ARIA symptoms in 0.7% with LEQEMBI. Clinical ARIA symptoms resolved in 79% of patients during the period of observation. ARIA, including asymptomatic radiographic events, was observed: LEQEMBI, 21%; placebo, 9%. ARIA-E was observed: LEQEMBI, 13%; placebo, 2%. ARIA-H was observed: LEQEMBI, 17%; placebo, 9%. No increase in isolated ARIA-H was observed for LEQEMBI vs placebo.

Incidence of ICH

ICH >1 cm in diameter was reported in 0.7% with LEQEMBI vs 0.1% with placebo. Fatal events of ICH in patients taking LEQEMBI have been observed.

WARNING: AMYLOID-RELATED IMAGING ABNORMALITIES (ARIA)

  • Monoclonal antibodies directed against aggregated forms of beta amyloid, including LEQEMBI, can cause ARIA, characterized as ARIA with edema (ARIA-E) and ARIA with hemosiderin deposition (ARIA-H). Incidence and timing of ARIA vary among treatments. ARIA usually occurs early in treatment and is usually asymptomatic, although serious and life-threatening events, including seizure and status epilepticus, can occur. ARIA can be fatal. Serious intracerebral hemorrhages (ICH) >1 cm, some of which have been fatal, have been observed with this class of medications. Because ARIA-E can cause focal neurologic deficits that can mimic an ischemic stroke, consider whether such symptoms could be due to ARIA-E before giving thrombolytic therapy to a patient being treated with LEQEMBI.

    _Apolipoprotein E ε4 (ApoE ε4) Homozygotes: Patients who are ApoE ε4 homozygotes (~15% of patients with AD) treated with this class of medications have a higher incidence of ARIA, including symptomatic, serious, and severe radiographic ARIA, compared to heterozygotes and noncarriers. Testing for ApoE ε4 status should be performed prior to initiation of treatment to inform the risk of developing ARIA. Prior to testing, prescribers should discuss with patients the risk of ARIA across genotypes and the implications of genetic testing results. Prescribers should inform patients that if genotype testing is not performed, they can still be treated with LEQEMBI; however, it cannot be determined if they are ApoE ε4 homozygotes and at higher risk for ARIA.

  • Consider the benefit of LEQEMBI for the treatment of AD and the potential risk of serious ARIA events when deciding to initiate treatment with LEQEMBI.

IMPORTANT SAFETY INFORMATION

WARNING: AMYLOID-RELATED IMAGING ABNORMALITIES (ARIA)

  • Monoclonal antibodies directed against aggregated forms of beta amyloid, including LEQEMBI, can cause ARIA, characterized as ARIA with edema (ARIA-E) and ARIA with hemosiderin deposition (ARIA-H). Incidence and timing of ARIA vary among treatments. ARIA usually occurs early in treatment and is usually asymptomatic, although serious and life-threatening events, including seizure and status epilepticus, can occur. ARIA can be fatal. Serious intracerebral hemorrhages (ICH) >1 cm, some of which have been fatal, have been observed with this class of medications. Because ARIA-E can cause focal neurologic deficits that can mimic an ischemic stroke, consider whether such symptoms could be due to ARIA-E before giving thrombolytic therapy to a patient being treated with LEQEMBI.

    _Apolipoprotein E ε4 (ApoE ε4) Homozygotes: Patients who are ApoE ε4 homozygotes (~15% of patients with AD) treated with this class of medications have a higher incidence of ARIA, including symptomatic, serious, and severe radiographic ARIA, compared to heterozygotes and noncarriers. Testing for ApoE ε4 status should be performed prior to initiation of treatment to inform the risk of developing ARIA. Prior to testing, prescribers should discuss with patients the risk of ARIA across genotypes and the implications of genetic testing results. Prescribers should inform patients that if genotype testing is not performed, they can still be treated with LEQEMBI; however, it cannot be determined if they are ApoE ε4 homozygotes and at higher risk for ARIA.

  • Consider the benefit of LEQEMBI for the treatment of AD and the potential risk of serious ARIA events when deciding to initiate treatment with LEQEMBI.

CONTRAINDICATION

Contraindicated in patients with serious hypersensitivity to lecanemab-irmb or to any of the excipients. Reactions have included angioedema and anaphylaxis.

WARNINGS AND PRECAUTIONS

AMYLOID-RELATED IMAGING ABNORMALITIES

Medications in this class, including LEQEMBI, can cause ARIA-E, which can be observed on MRI as brain edema or sulcal effusions, and ARIA-H, which includes microhemorrhage and superficial siderosis. ARIA can occur spontaneously in patients with AD, particularly in patients with MRI findings suggestive of cerebral amyloid angiopathy (CAA), such as pretreatment microhemorrhage or superficial siderosis. ARIA-H generally occurs with ARIA-E. Reported ARIA symptoms may include headache, confusion, visual changes, dizziness, nausea, and gait difficulty. Focal neurologic deficits may also occur. Symptoms usually resolve over time.

Incidence of ARIA

Symptomatic ARIA occurred in 3% and serious ARIA symptoms in 0.7% with LEQEMBI. Clinical ARIA symptoms resolved in 79% of patients during the period of observation. ARIA, including asymptomatic radiographic events, was observed: LEQEMBI, 21%; placebo, 9%. ARIA-E was observed: LEQEMBI, 13%; placebo, 2%. ARIA-H was observed: LEQEMBI, 17%; placebo, 9%. No increase in isolated ARIA-H was observed for LEQEMBI vs placebo.

Incidence of ICH

ICH >1 cm in diameter was reported in 0.7% with LEQEMBI vs 0.1% with placebo. Fatal events of ICH in patients taking LEQEMBI have been observed.

Risk Factors of ARIA and ICH

ApoE ε4 Carrier Status

Of the patients taking LEQEMBI, 16% were ApoE ε4 homozygotes, 53% were heterozygotes, and 31% were noncarriers. With LEQEMBI, ARIA was higher in ApoE ε4 homozygotes (LEQEMBI: 45%; placebo: 22%) than in heterozygotes (LEQEMBI: 19%; placebo: 9%) and noncarriers (LEQEMBI: 13%; placebo: 4%). Symptomatic ARIA-E occurred in 9% of ApoE ε4 homozygotes vs 2% of heterozygotes and 1% of noncarriers. Serious ARIA events occurred in 3% of ApoE ε4 homozygotes and in ~1% of heterozygotes and noncarriers. The recommendations on management of ARIA do not differ between ApoE ε4 carriers and noncarriers.

Radiographic Findings of CAA

  • Neuroimaging findings that may indicate CAA include evidence of prior ICH, cerebral microhemorrhage, and cortical superficial siderosis. CAA has an increased risk for ICH. The presence of an ApoE ε4 allele is also associated with CAA.

  • The baseline presence of at least 2 microhemorrhages or the presence of at least 1 area of superficial siderosis on MRI, which may be suggestive of CAA, have been identified as risk factors for ARIA. Patients were excluded from Clarity AD for the presence of >4 microhemorrhages and additional findings suggestive of CAA (prior cerebral hemorrhage >1 cm in greatest diameter, superficial siderosis, vasogenic edema) or other lesions (aneurysm, vascular malformation) that could potentially increase the risk of ICH.

Concomitant Antithrombotic or Thrombolytic Medication

  • In Clarity AD, baseline use of antithrombotic medication (aspirin, other antiplatelets, or anticoagulants) was allowed if the patient was on a stable dose. Most exposures were to aspirin. Antithrombotic medications did not increase the risk of ARIA with LEQEMBI. The incidence of ICH: 0.9% in patients taking LEQEMBI with a concomitant antithrombotic medication vs 0.6% with no antithrombotic and 2.5% in patients taking LEQEMBI with an anticoagulant alone or with antiplatelet medication such as aspirin vs none in patients receiving placebo.

  • Fatal cerebral hemorrhage has occurred in 1 patient taking an anti-amyloid monoclonal antibody in the setting of focal neurologic symptoms of ARIA and the use of a thrombolytic agent.

  • Additional caution should be exercised when considering the administration of antithrombotics or a thrombolytic agent (e.g., tissue plasminogen activator) to a patient already being treated with LEQEMBI. Because ARIA-E can cause focal neurologic deficits that can mimic an ischemic stroke, treating clinicians should consider whether such symptoms could be due to ARIA-E before giving thrombolytic therapy in a patient being treated with LEQEMBI.

  • Caution should be exercised when considering the use of LEQEMBI in patients with factors that indicate an increased risk for ICH and, in particular, patients who need to be on anticoagulant therapy or patients with findings on MRI that are suggestive of CAA.

Radiographic Severity With LEQEMBI

Most ARIA-E radiographic events occurred within the first 7 doses, although ARIA can occur at any time, and patients can have >1 episode. Maximum radiographic severity of ARIA-E with LEQEMBI was mild in 4%, moderate in 7%, and severe in 1% of patients. Resolution on MRI occurred in 52% of ARIA-E patients by 12 weeks, 81% by 17 weeks, and 100% overall after detection. Maximum radiographic severity of ARIA-H microhemorrhage with LEQEMBI was mild in 9%, moderate in 2%, and severe in 3% of patients; superficial siderosis was mild in 4%, moderate in 1%, and severe in 0.4% of patients. With LEQEMBI, the rate of severe radiographic ARIA-E was highest in ApoE ε4 homozygotes (5%) vs heterozygotes (0.4%) or noncarriers (0%). With LEQEMBI, the rate of severe radiographic ARIA-H was highest in ApoE ε4 homozygotes (13.5%) vs heterozygotes (2.1%) or noncarriers (1.1%).

Monitoring and Dose Management Guidelines

Baseline brain MRI and periodic monitoring with MRI are recommended. Enhanced clinical vigilance for ARIA is recommended during the first 14 weeks of treatment. Depending on ARIA-E and ARIA-H clinical symptoms and radiographic severity, use clinical judgment when considering whether to continue dosing or to temporarily or permanently discontinue LEQEMBI. If a patient experiences ARIA symptoms, clinical evaluation should be performed, including MRI if indicated. If ARIA is observed on MRI, careful clinical evaluation should be performed prior to continuing treatment.

HYPERSENSITIVITY REACTIONS

Hypersensitivity reactions, including angioedema, bronchospasm, and anaphylaxis, have occurred with LEQEMBI. Promptly discontinue the infusion upon the first observation of any signs or symptoms consistent with a hypersensitivity reaction and initiate appropriate therapy.

INFUSION-RELATED REACTIONS (IRRs)

  • IRRs were observed—LEQEMBI: 26%; placebo: 7%—and most cases with LEQEMBI (75%) occurred with the first infusion. IRRs were mostly mild (69%) or moderate (28%). Symptoms included fever and flu-like symptoms (chills, generalized aches, feeling shaky, and joint pain), nausea, vomiting, hypotension, hypertension, and oxygen desaturation.

  • IRRs can occur during or after the completion of infusion. In the event of an IRR during the infusion, the infusion rate may be reduced or discontinued, and appropriate therapy initiated as clinically indicated. Consider prophylactic treatment prior to future infusions with antihistamines, acetaminophen, nonsteroidal anti-inflammatory drugs, or corticosteroids.

ADVERSE REACTIONS

  • The most common adverse reactions reported in ≥5% with LEQEMBI infusion every 2 weeks and ≥2% higher than placebo were IRRs (LEQEMBI: 26%; placebo: 7%), ARIA-H (LEQEMBI: 14%; placebo: 8%), ARIA-E (LEQEMBI: 13%; placebo: 2%), headache (LEQEMBI: 11%; placebo: 8%), superficial siderosis of central nervous system (LEQEMBI: 6%; placebo: 3%), rash (LEQEMBI: 6%; placebo: 4%), and nausea/vomiting (LEQEMBI: 6%; placebo: 4%)

  • Safety profile of LEQEMBI IQLIK for maintenance treatment was similar to LEQEMBI infusion. Patients who received LEQEMBI IQLIK experienced localized and systemic (less frequent) injection-related reactions (mild to moderate in severity)

LEQEMBI (lecanemab-irmb) is available

  • Intravenous infusion: 100 mg/mL

  • Subcutaneous injection: 200 mg/mL

Please see full Prescribing Information for LEQEMBI, including Boxed WARNING.

INDICATION & IMPORTANT SAFETY INFORMATION

INDICATION

LEQEMBI® is indicated for the treatment of Alzheimer's disease (AD). Treatment with LEQEMBI should be initiated in patients with mild cognitive impairment (MCI) or mild dementia stage of disease, the population in which treatment was initiated in clinical trials.

CONTRAINDICATION

Contraindicated in patients with serious hypersensitivity to lecanemab-irmb or to any of the excipients. Reactions have included angioedema and anaphylaxis.

WARNINGS AND PRECAUTIONS

AMYLOID-RELATED IMAGING ABNORMALITIES

Medications in this class, including LEQEMBI, can cause ARIA-E, which can be observed on MRI as brain edema or sulcal effusions, and ARIA-H, which includes microhemorrhage and superficial siderosis. ARIA can occur spontaneously in patients with AD, particularly in patients with MRI findings suggestive of cerebral amyloid angiopathy (CAA), such as pretreatment microhemorrhage or superficial siderosis. ARIA-H generally occurs with ARIA-E. Reported ARIA symptoms may include headache, confusion, visual changes, dizziness, nausea, and gait difficulty. Focal neurologic deficits may also occur. Symptoms usually resolve over time.

Incidence of ARIA

Symptomatic ARIA occurred in 3% and serious ARIA symptoms in 0.7% with LEQEMBI. Clinical ARIA symptoms resolved in 79% of patients during the period of observation. ARIA, including asymptomatic radiographic events, was observed: LEQEMBI, 21%; placebo, 9%. ARIA-E was observed: LEQEMBI, 13%; placebo, 2%. ARIA-H was observed: LEQEMBI, 17%; placebo, 9%. No increase in isolated ARIA-H was observed for LEQEMBI vs placebo.

Incidence of ICH

ICH >1 cm in diameter was reported in 0.7% with LEQEMBI vs 0.1% with placebo. Fatal events of ICH in patients taking LEQEMBI have been observed.

WARNING: AMYLOID-RELATED IMAGING ABNORMALITIES (ARIA)

  • Monoclonal antibodies directed against aggregated forms of beta amyloid, including LEQEMBI, can cause ARIA, characterized as ARIA with edema (ARIA-E) and ARIA with hemosiderin deposition (ARIA-H). Incidence and timing of ARIA vary among treatments. ARIA usually occurs early in treatment and is usually asymptomatic, although serious and life-threatening events, including seizure and status epilepticus, can occur. ARIA can be fatal. Serious intracerebral hemorrhages (ICH) >1 cm, some of which have been fatal, have been observed with this class of medications. Because ARIA-E can cause focal neurologic deficits that can mimic an ischemic stroke, consider whether such symptoms could be due to ARIA-E before giving thrombolytic therapy to a patient being treated with LEQEMBI.

    _Apolipoprotein E ε4 (ApoE ε4) Homozygotes: Patients who are ApoE ε4 homozygotes (~15% of patients with AD) treated with this class of medications have a higher incidence of ARIA, including symptomatic, serious, and severe radiographic ARIA, compared to heterozygotes and noncarriers. Testing for ApoE ε4 status should be performed prior to initiation of treatment to inform the risk of developing ARIA. Prior to testing, prescribers should discuss with patients the risk of ARIA across genotypes and the implications of genetic testing results. Prescribers should inform patients that if genotype testing is not performed, they can still be treated with LEQEMBI; however, it cannot be determined if they are ApoE ε4 homozygotes and at higher risk for ARIA.

  • Consider the benefit of LEQEMBI for the treatment of AD and the potential risk of serious ARIA events when deciding to initiate treatment with LEQEMBI.

EXPAND COLLAPSE

INDICATION & IMPORTANT SAFETY INFORMATION

INDICATION

LEQEMBI® is indicated for the treatment of Alzheimer's disease (AD). Treatment with LEQEMBI should be initiated in patients with mild cognitive impairment (MCI) or mild dementia stage of disease, the population in which treatment was initiated in clinical trials.

CONTRAINDICATION

Contraindicated in patients with serious hypersensitivity to lecanemab-irmb or to any of the excipients. Reactions have included angioedema and anaphylaxis.

WARNINGS AND PRECAUTIONS

AMYLOID-RELATED IMAGING ABNORMALITIES

Medications in this class, including LEQEMBI, can cause ARIA-E, which can be observed on MRI as brain edema or sulcal effusions, and ARIA-H, which includes microhemorrhage and superficial siderosis. ARIA can occur spontaneously in patients with AD, particularly in patients with MRI findings suggestive of cerebral amyloid angiopathy (CAA), such as pretreatment microhemorrhage or superficial siderosis. ARIA-H generally occurs with ARIA-E. Reported ARIA symptoms may include headache, confusion, visual changes, dizziness, nausea, and gait difficulty. Focal neurologic deficits may also occur. Symptoms usually resolve over time.

Incidence of ARIA

Symptomatic ARIA occurred in 3% and serious ARIA symptoms in 0.7% with LEQEMBI. Clinical ARIA symptoms resolved in 79% of patients during the period of observation. ARIA, including asymptomatic radiographic events, was observed: LEQEMBI, 21%; placebo, 9%. ARIA-E was observed: LEQEMBI, 13%; placebo, 2%. ARIA-H was observed: LEQEMBI, 17%; placebo, 9%. No increase in isolated ARIA-H was observed for LEQEMBI vs placebo.

Incidence of ICH

ICH >1 cm in diameter was reported in 0.7% with LEQEMBI vs 0.1% with placebo. Fatal events of ICH in patients taking LEQEMBI have been observed.

WARNING: AMYLOID-RELATED IMAGING ABNORMALITIES (ARIA)

  • Monoclonal antibodies directed against aggregated forms of beta amyloid, including LEQEMBI, can cause ARIA, characterized as ARIA with edema (ARIA-E) and ARIA with hemosiderin deposition (ARIA-H). Incidence and timing of ARIA vary among treatments. ARIA usually occurs early in treatment and is usually asymptomatic, although serious and life-threatening events, including seizure and status epilepticus, can occur. ARIA can be fatal. Serious intracerebral hemorrhages (ICH) >1 cm, some of which have been fatal, have been observed with this class of medications. Because ARIA-E can cause focal neurologic deficits that can mimic an ischemic stroke, consider whether such symptoms could be due to ARIA-E before giving thrombolytic therapy to a patient being treated with LEQEMBI.

    _Apolipoprotein E ε4 (ApoE ε4) Homozygotes: Patients who are ApoE ε4 homozygotes (~15% of patients with AD) treated with this class of medications have a higher incidence of ARIA, including symptomatic, serious, and severe radiographic ARIA, compared to heterozygotes and noncarriers. Testing for ApoE ε4 status should be performed prior to initiation of treatment to inform the risk of developing ARIA. Prior to testing, prescribers should discuss with patients the risk of ARIA across genotypes and the implications of genetic testing results. Prescribers should inform patients that if genotype testing is not performed, they can still be treated with LEQEMBI; however, it cannot be determined if they are ApoE ε4 homozygotes and at higher risk for ARIA.

  • Consider the benefit of LEQEMBI for the treatment of AD and the potential risk of serious ARIA events when deciding to initiate treatment with LEQEMBI.

IMPORTANT SAFETY INFORMATION

WARNING: AMYLOID-RELATED IMAGING ABNORMALITIES (ARIA)

  • Monoclonal antibodies directed against aggregated forms of beta amyloid, including LEQEMBI, can cause ARIA, characterized as ARIA with edema (ARIA-E) and ARIA with hemosiderin deposition (ARIA-H). Incidence and timing of ARIA vary among treatments. ARIA usually occurs early in treatment and is usually asymptomatic, although serious and life-threatening events, including seizure and status epilepticus, can occur. ARIA can be fatal. Serious intracerebral hemorrhages (ICH) >1 cm, some of which have been fatal, have been observed with this class of medications. Because ARIA-E can cause focal neurologic deficits that can mimic an ischemic stroke, consider whether such symptoms could be due to ARIA-E before giving thrombolytic therapy to a patient being treated with LEQEMBI.

    _Apolipoprotein E ε4 (ApoE ε4) Homozygotes: Patients who are ApoE ε4 homozygotes (~15% of patients with AD) treated with this class of medications have a higher incidence of ARIA, including symptomatic, serious, and severe radiographic ARIA, compared to heterozygotes and noncarriers. Testing for ApoE ε4 status should be performed prior to initiation of treatment to inform the risk of developing ARIA. Prior to testing, prescribers should discuss with patients the risk of ARIA across genotypes and the implications of genetic testing results. Prescribers should inform patients that if genotype testing is not performed, they can still be treated with LEQEMBI; however, it cannot be determined if they are ApoE ε4 homozygotes and at higher risk for ARIA.

  • Consider the benefit of LEQEMBI for the treatment of AD and the potential risk of serious ARIA events when deciding to initiate treatment with LEQEMBI.

CONTRAINDICATION

Contraindicated in patients with serious hypersensitivity to lecanemab-irmb or to any of the excipients. Reactions have included angioedema and anaphylaxis.

WARNINGS AND PRECAUTIONS

AMYLOID-RELATED IMAGING ABNORMALITIES

Medications in this class, including LEQEMBI, can cause ARIA-E, which can be observed on MRI as brain edema or sulcal effusions, and ARIA-H, which includes microhemorrhage and superficial siderosis. ARIA can occur spontaneously in patients with AD, particularly in patients with MRI findings suggestive of cerebral amyloid angiopathy (CAA), such as pretreatment microhemorrhage or superficial siderosis. ARIA-H generally occurs with ARIA-E. Reported ARIA symptoms may include headache, confusion, visual changes, dizziness, nausea, and gait difficulty. Focal neurologic deficits may also occur. Symptoms usually resolve over time.

Incidence of ARIA

Symptomatic ARIA occurred in 3% and serious ARIA symptoms in 0.7% with LEQEMBI. Clinical ARIA symptoms resolved in 79% of patients during the period of observation. ARIA, including asymptomatic radiographic events, was observed: LEQEMBI, 21%; placebo, 9%. ARIA-E was observed: LEQEMBI, 13%; placebo, 2%. ARIA-H was observed: LEQEMBI, 17%; placebo, 9%. No increase in isolated ARIA-H was observed for LEQEMBI vs placebo.

Incidence of ICH

ICH >1 cm in diameter was reported in 0.7% with LEQEMBI vs 0.1% with placebo. Fatal events of ICH in patients taking LEQEMBI have been observed.

Risk Factors of ARIA and ICH

ApoE ε4 Carrier Status

Of the patients taking LEQEMBI, 16% were ApoE ε4 homozygotes, 53% were heterozygotes, and 31% were noncarriers. With LEQEMBI, ARIA was higher in ApoE ε4 homozygotes (LEQEMBI: 45%; placebo: 22%) than in heterozygotes (LEQEMBI: 19%; placebo: 9%) and noncarriers (LEQEMBI: 13%; placebo: 4%). Symptomatic ARIA-E occurred in 9% of ApoE ε4 homozygotes vs 2% of heterozygotes and 1% of noncarriers. Serious ARIA events occurred in 3% of ApoE ε4 homozygotes and in ~1% of heterozygotes and noncarriers. The recommendations on management of ARIA do not differ between ApoE ε4 carriers and noncarriers.

Radiographic Findings of CAA

  • Neuroimaging findings that may indicate CAA include evidence of prior ICH, cerebral microhemorrhage, and cortical superficial siderosis. CAA has an increased risk for ICH. The presence of an ApoE ε4 allele is also associated with CAA.

  • The baseline presence of at least 2 microhemorrhages or the presence of at least 1 area of superficial siderosis on MRI, which may be suggestive of CAA, have been identified as risk factors for ARIA. Patients were excluded from Clarity AD for the presence of >4 microhemorrhages and additional findings suggestive of CAA (prior cerebral hemorrhage >1 cm in greatest diameter, superficial siderosis, vasogenic edema) or other lesions (aneurysm, vascular malformation) that could potentially increase the risk of ICH.

Concomitant Antithrombotic or Thrombolytic Medication

  • In Clarity AD, baseline use of antithrombotic medication (aspirin, other antiplatelets, or anticoagulants) was allowed if the patient was on a stable dose. Most exposures were to aspirin. Antithrombotic medications did not increase the risk of ARIA with LEQEMBI. The incidence of ICH: 0.9% in patients taking LEQEMBI with a concomitant antithrombotic medication vs 0.6% with no antithrombotic and 2.5% in patients taking LEQEMBI with an anticoagulant alone or with antiplatelet medication such as aspirin vs none in patients receiving placebo.

  • Fatal cerebral hemorrhage has occurred in 1 patient taking an anti-amyloid monoclonal antibody in the setting of focal neurologic symptoms of ARIA and the use of a thrombolytic agent.

  • Additional caution should be exercised when considering the administration of antithrombotics or a thrombolytic agent (e.g., tissue plasminogen activator) to a patient already being treated with LEQEMBI. Because ARIA-E can cause focal neurologic deficits that can mimic an ischemic stroke, treating clinicians should consider whether such symptoms could be due to ARIA-E before giving thrombolytic therapy in a patient being treated with LEQEMBI.

  • Caution should be exercised when considering the use of LEQEMBI in patients with factors that indicate an increased risk for ICH and, in particular, patients who need to be on anticoagulant therapy or patients with findings on MRI that are suggestive of CAA.

Radiographic Severity With LEQEMBI

Most ARIA-E radiographic events occurred within the first 7 doses, although ARIA can occur at any time, and patients can have >1 episode. Maximum radiographic severity of ARIA-E with LEQEMBI was mild in 4%, moderate in 7%, and severe in 1% of patients. Resolution on MRI occurred in 52% of ARIA-E patients by 12 weeks, 81% by 17 weeks, and 100% overall after detection. Maximum radiographic severity of ARIA-H microhemorrhage with LEQEMBI was mild in 9%, moderate in 2%, and severe in 3% of patients; superficial siderosis was mild in 4%, moderate in 1%, and severe in 0.4% of patients. With LEQEMBI, the rate of severe radiographic ARIA-E was highest in ApoE ε4 homozygotes (5%) vs heterozygotes (0.4%) or noncarriers (0%). With LEQEMBI, the rate of severe radiographic ARIA-H was highest in ApoE ε4 homozygotes (13.5%) vs heterozygotes (2.1%) or noncarriers (1.1%).

Monitoring and Dose Management Guidelines

Baseline brain MRI and periodic monitoring with MRI are recommended. Enhanced clinical vigilance for ARIA is recommended during the first 14 weeks of treatment. Depending on ARIA-E and ARIA-H clinical symptoms and radiographic severity, use clinical judgment when considering whether to continue dosing or to temporarily or permanently discontinue LEQEMBI. If a patient experiences ARIA symptoms, clinical evaluation should be performed, including MRI if indicated. If ARIA is observed on MRI, careful clinical evaluation should be performed prior to continuing treatment.

HYPERSENSITIVITY REACTIONS

Hypersensitivity reactions, including angioedema, bronchospasm, and anaphylaxis, have occurred with LEQEMBI. Promptly discontinue the infusion upon the first observation of any signs or symptoms consistent with a hypersensitivity reaction and initiate appropriate therapy.

INFUSION-RELATED REACTIONS (IRRs)

  • IRRs were observed—LEQEMBI: 26%; placebo: 7%—and most cases with LEQEMBI (75%) occurred with the first infusion. IRRs were mostly mild (69%) or moderate (28%). Symptoms included fever and flu-like symptoms (chills, generalized aches, feeling shaky, and joint pain), nausea, vomiting, hypotension, hypertension, and oxygen desaturation.

  • IRRs can occur during or after the completion of infusion. In the event of an IRR during the infusion, the infusion rate may be reduced or discontinued, and appropriate therapy initiated as clinically indicated. Consider prophylactic treatment prior to future infusions with antihistamines, acetaminophen, nonsteroidal anti-inflammatory drugs, or corticosteroids.

ADVERSE REACTIONS

  • The most common adverse reactions reported in ≥5% with LEQEMBI infusion every 2 weeks and ≥2% higher than placebo were IRRs (LEQEMBI: 26%; placebo: 7%), ARIA-H (LEQEMBI: 14%; placebo: 8%), ARIA-E (LEQEMBI: 13%; placebo: 2%), headache (LEQEMBI: 11%; placebo: 8%), superficial siderosis of central nervous system (LEQEMBI: 6%; placebo: 3%), rash (LEQEMBI: 6%; placebo: 4%), and nausea/vomiting (LEQEMBI: 6%; placebo: 4%)

  • Safety profile of LEQEMBI IQLIK for maintenance treatment was similar to LEQEMBI infusion. Patients who received LEQEMBI IQLIK experienced localized and systemic (less frequent) injection-related reactions (mild to moderate in severity)

LEQEMBI (lecanemab-irmb) is available

  • Intravenous infusion: 100 mg/mL

  • Subcutaneous injection: 200 mg/mL

Please see full Prescribing Information for LEQEMBI, including Boxed WARNING.

References:

1. LEQEMBI (lecanemab-irmb) [package insert]. Nutley, NJ: Eisai Inc. 2. van Dyck CH, Swanson CJ, Aisen P, et al. Lecanemab in early Alzheimer’s disease. N Engl J Med. 2023;388(1):9-21. 3. Iwatsubo T, Irizarry M, van Dyck C, Sabbagh M, Bateman R, Cohen S. 2022 Clarity AD CTAD Presentations. Clarity AD: a Phase 3 placebo-controlled, double-blind, parallel-group, 18-month study evaluating lecanemab in early Alzheimer’s disease. Paper presented at: Clinical Trials on Alzheimer’s Disease; November 29-December 2, 2022; San Francisco, CA. 4. Data on file. 40 years plus 1. Eisai Inc., Nutley, NJ. 5. van Dyck C, Sperling R, Li D, et al. The lecanemab Clarity AD open-label extension in early Alzheimer’s disease: initial findings from the 48-month analysis. Paper presented at: Alzheimer’s Association International Conference; July 27-31, 2025; Toronto, Canada. 6. Data on file. Clarity AD 48-month data IV+SC. Eisai Inc., Nutley, NJ. 7. Data on file. Eisai protocol No. BAN 2401-G000-301 Core. Eisai Inc., Nutley, NJ. 8. Data on file. Eisai protocol No. BAN 2401-G000-301 CSR 5. Eisai Inc., Nutley, NJ. 9. Data on file. Eisai protocol No. BAN 2401-G000-301 CSR 6. Eisai Inc., Nutley, NJ. 10. Data on file. Clarity AD 48-month cut-off. Eisai Inc., Nutley, NJ. 11. Data on file. Clarity AD OLE extension. Eisai Inc., Nutley, NJ. 12. Data on file. Delayed progression to dementia through 48 months. Eisai Inc., Nutley, NJ. 13. Jack CR Jr, Andrews JS, Beach TG, et al. Revised criteria for diagnosis and staging of Alzheimer's disease: Alzheimer's Association Workgroup. Alzheimers Dement. 2024;20(8):5143-5169. 14. Johnson K. Biomarker assessments from Clarity AD: downstream implications of targeting protofibrils and tau as a
predictive biomarker. Presented at: Clinical Trials on Alzheimer’s Disease; October 24-27, 2023; Boston, MA. 15. Data on file. LEQEMBI low tau. Eisai Inc., Nutley, NJ.

Eisai logo Eisai logo Biogen® logo Biogen® logo

LEQEMBI® is a registered trademark of Eisai R&D Management Co., Ltd. LEQEMBI® IQLIK™ and LEQEMBI® Companion™ are trademarks of Eisai R&D Management Co., Ltd. © 2025 Eisai Inc. and Biogen. All trademarks and company names are the property of their respective owners. All rights reserved. LEQE-US4691 12/2025

You are now leaving LEQEMBIHCP.com

Eisai does not control the content or privacy policies of these third-party sites. Click "Continue" to proceed or "Cancel" to stay on LEQEMBIhcp.com

You are now leaving LEQEMBIHCP.com

By clicking "Continue", you are connecting your patient with an independent telehealth specialist who can help with medical evaluations. The resulting care decision may or may not include medication. Eisai does not endorse any specialists or their medical opinions. The providers listed are not exhaustive, and other providers may be available for your patients.

Eisai does not control the content or privacy policies of these third-party sites. Click "Continue" to proceed or "Cancel" to stay on LEQEMBIhcp.com