Version July 2025
Monoclonal antibodies directed against aggregated forms of beta amyloid, including lecanemab, can cause amyloid-related imaging abnormalities (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 can occur. ARIA can be fatal. Serious intracerebral hemorrhages >1 cm, some of which have been fatal, have been observed in patients treated with this class of medications. 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 to a patient being treated with lecanemab.
ApoE ε4 homozygotes: Patients who are apolipoprotein E ε4 (ApoE ε4) homozygotes (approximately 15% of Alzheimer disease patients) treated with this class of medications, including lecanemab, 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 lecanemab; however, it cannot be determined if they are ApoE ε4 homozygotes and at higher risk for ARIA.
Consider the benefit of lecanemab for the treatment of Alzheimer disease and potential risk of serious adverse events associated with ARIA when deciding to initiate treatment with lecanemab.
Note: Confirm the presence of amyloid beta pathology prior to treatment initiation. Testing for apolipoprotein E ε4 status prior to treatment initiation is recommended to inform on the risk of amyloid-related imaging abnormalities (ARIA), which can be life-threatening..
Alzheimer disease: IV: Dosing based on actual body weight:
Initial dosing: 10 mg/kg once every 2 weeks for 18 months.
Maintenance dosing: After 18 months, may continue 10 mg/kg once every 2 weeks or switch to 10 mg/kg once every 4 weeks.
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
There are no dosage adjustments provided in the manufacturer's labeling; however, lecanemab is not expected to undergo renal elimination.
There are no dosage adjustments provided in the manufacturer's labeling; however, lecanemab is not expected to undergo hepatic metabolism.
Amyloid-related imaging abnormalities (ARIA), symptoms: Perform clinical evaluation, including MRI if indicated.
Amyloid-related imaging abnormalities – edema (ARIA-E): See table below:
|
Severity of clinical symptomsa |
ARIA-E severity on MRI | |
|---|---|---|
|
Mild |
Moderate or severe | |
|
a For patients experiencing symptoms associated with ARIA, perform clinical evaluation, including MRI if indicated. | ||
|
Asymptomatic |
Continue current lecanemab dosing. |
Withhold lecanemab until MRI shows radiographic resolution. Consider follow-up MRI to assess for resolution (eg, 2 to 4 months following initial ARIA-E identification); resume dosing based on clinical judgment. |
|
Milda (eg, discomfort but no disruption of normal daily activity) |
Continue lecanemab dosing based on clinical judgment. |
Withhold lecanemab until MRI shows radiographic resolution and symptoms resolve. Consider follow-up MRI to assess for resolution (eg, 2 to 4 months following initial ARIA-E identification); resume dosing based on clinical judgment. |
|
Moderate or severea (eg, symptoms ranging from discomfort that impacts normal daily activity to incapacitation and inability to perform normal daily activity or work) |
Withhold lecanemab until MRI shows radiographic resolution and symptoms resolve. Consider follow up MRI to assess for resolution (eg, 2 to 4 months following initial ARIA-E identification); resume dosing based on clinical judgment. | |
Amyloid-related imaging abnormalities – hemosiderin (ARIA-H): See table below:
|
Severity of clinical symptomsa |
ARIA-H Severity on MRI | ||
|---|---|---|---|
|
Mild |
Moderate |
Severe | |
|
a For patients experiencing symptoms associated with ARIA, perform clinical evaluation, including MRI if indicated. | |||
|
Asymptomatic |
Continue current lecanemab dosing. |
Withhold lecanemab until MRI shows radiographic stabilization. Consider follow up MRI to assess for resolution (eg, 2 to 4 months following initial ARIA-H identification); resume dosing based on clinical judgment. |
Withhold lecanemab until MRI shows radiographic stabilization. Use clinical judgment to determine whether to continue treatment or permanently discontinue lecanemab. |
|
Symptomatica |
Withhold lecanemab until MRI shows radiographic stabilization and symptoms resolve. Consider follow up MRI to assess for resolution (eg, 2 to 4 months following initial ARIA-H identification); resume dosing based on clinical judgment. |
Withhold lecanemab until MRI shows radiographic stabilization and symptoms resolve. Use clinical judgment to determine whether to continue treatment or permanently discontinue lecanemab. | |
Intracerebral hemorrhage >1 cm in diameter: Withhold lecanemab until MRI shows radiographic stabilization and symptoms (if present) resolve. Use clinical judgment to determine whether to continue treatment or permanently discontinue lecanemab.
Hypersensitivity reaction signs/symptoms (eg, angioedema, bronchospasm, anaphylaxis ): Promptly discontinue infusion at first sign/symptom of hypersensitivity and initiate appropriate treatment.
Infusion reaction signs/symptoms (eg, fever, flu-like symptoms, nausea, vomiting, BP changes): Consider reducing rate of administration, discontinuing the infusion, and/or initiating supportive therapy as clinically appropriate. Consider premedication with antihistamines, acetaminophen, nonsteroidal anti-inflammatory drugs, or corticosteroids prior to future infusions.
Refer to adult dosing.
Amyloid-related imaging abnormalities (ARIA), including ARIA consistent with vasogenic edema and/or sulcal effusions (ARIA-E) (Ref) and ARIA with hemosiderin deposition (ARIA-H) characterized by superficial siderosis, microhemorrhages, and macrohemorrhages (Ref) have been reported with lecanemab therapy. Patients may develop ARIA-H with concomitant ARIA-E. In patients who developed ARIA during lecanemab clinical trials, most cases were asymptomatic with mild to moderate radiographic severity; however, serious and/or fatal symptoms have been reported (Ref). Recurrent episodes of ARIA-E have also been described (Ref). Clinical symptoms suggesting ARIA may include abnormal gait, confusion, dizziness, focal neurologic deficits, headache, nausea, visual disturbance, and seizures. Focal neurologic deficits caused by ARIA-E can mimic an ischemic stroke. Resolution of ARIA (-E and/or -H) occurred within 4 months in the majority of cases in clinical trials (Ref).
Mechanism: Not clearly established; speculated that increased clearance of amyloid from parenchymal plaques into perivascular space may result in excess fluid shifts. This movement of amyloid into cerebral vessel walls may also increase vascular friability and permeability, thus impairing vessel wall integrity to permit small amounts of blood passage. Increased vascular permeability at which both fluid and red blood cells cross the vessel wall may suggest a common pathophysiologic mechanism for both ARIA-E and ARIA-H (Ref).
ARIA-E: Dose-related; related to the pharmacologic action. Increased cerebrovascular permeability due to antibody binding to deposited amyloid-beta results in an increase in extracellular fluid volume and vasogenic edema (Ref).
ARIA-H: Dose-related; related to the pharmacologic action. Leakage of blood from a vessel into adjacent tissue parenchyma or subarachnoid space/periadventitial compartments leaves residual deposits of iron in the form of hemosiderin, resulting in superficial siderosis and/or radiographic evidence of hemorrhage (Ref).
Onset: Varied; ARIA may occur at any time during treatment, but most events occur within the first 3 months (Ref).
Risk factors:
ARIA-E:
• Apolipoprotein E ε4 (ApoE ε4) carriers; specifically ApoE ε4 homozygotes
• Dose; risk increases with higher doses (Ref)
ARIA-H: Microhemorrhages:
• Apolipoprotein E ε4 carriers; specifically ApoE ε4 homozygotes
• Increasing age (Ref)
• Greater number of microhemorrhages at baseline (Ref)
• Older adults with cardiovascular risk factors and/or evidence of prior cerebrovascular event (Ref)
• Concomitant risk factors for intracerebral hemorrhages (cerebral amyloid angiopathy, prior cerebral hemorrhage >1 cm, ≥2 microhemorrhages, ≥1 area of superficial siderosis, vasogenic edema, aneurysm, vascular malformation)
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. Adverse reactions reported in adults.
>10%:
Hematologic & oncologic: Hemosiderosis (ARIA-H, including microhemorrhage, superficial siderosis: 6% to 17%)
Hypersensitivity: Infusion-related reaction (20% to 26%)
Nervous system: Brain edema (ARIA-E, including sulcal effusion: 10% to 13%), headache (11% to 14%) (table 1)
|
Drug (Lecanemab) |
Placebo |
Dose |
Number of Patients (Lecanemab) |
Number of Patients (Placebo) |
|---|---|---|---|---|
|
14% |
10% |
10 mg/kg every 2 weeks |
161 |
245 |
|
11% |
8% |
10 mg/kg every 2 weeks |
898 |
897 |
1% to 10%:
Cardiovascular: Atrial fibrillation (3%)
Dermatologic: Skin rash (6%)
Gastrointestinal: Diarrhea (8%), nausea and vomiting (6%)
Hematologic & oncologic: Lymphocytopenia (4%)
Respiratory: Cough (9%)
<1%: Nervous system: Cerebral hemorrhage
Frequency not defined:
Hematologic & oncologic: Increased neutrophils
Hypersensitivity: Hypersensitivity reaction (including anaphylaxis, angioedema)
Serious hypersensitivity (eg, anaphylaxis, angioedema) to lecanemab or any component of the formulation.
Concerns related to adverse effects:
• Infusion reaction: Lecanemab may cause infusion reactions; symptoms include fever, flu-like symptoms (chills, generalized aches, shakiness, joint pain), nausea, vomiting, hypotension, hypertension, and oxygen desaturation. The highest incidence of infusion reactions occurs with the first infusion.
Dosage form specific issues:
• Polysorbate 80: Some dosage forms may contain polysorbate 80 (also known as Tweens). Hypersensitivity reactions, usually a delayed reaction, have been reported following exposure to pharmaceutical products containing polysorbate 80 in certain individuals (Isaksson 2002; Lucente 2000; Shelley 1995). Thrombocytopenia, ascites, pulmonary deterioration, and renal and hepatic failure have been reported in premature neonates after receiving parenteral products containing polysorbate 80 (Alade 1986; CDC 1984). See manufacturer's labeling.
Other warnings and precautions:
• Alzheimer disease registry: Health care providers are encouraged to have patients participate in real world data collection (eg, registry) to help further understand Alzheimer disease and the impact of treatment; health care providers may contact the manufacturer at 888-274-2378 for a list of current programs.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Solution, Intravenous [preservative free]:
Leqembi: Lecanemab-irmb 200 mg/2 mL (2 mL); Lecanemab-irmb 500 mg/5 mL (5 mL) [contains polysorbate 80]
No
Solution (Leqembi Intravenous)
200 mg/2 mL (per mL): $155.19
500 mg/5 mL (per mL): $155.19
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IV: Dilution required prior to administration. Administer by IV infusion over 1 hour through an IV line containing a terminal low-protein binding 0.2 micron in-line filter. Flush IV line following infusion.
An FDA-approved patient medication guide, which is available with the product information and as follows, must be dispensed with this medication:
Leqembi: https://www.accessdata.fda.gov/drugsatfda_docs/label/2025/761269s005lbl.pdf#page=22
Alzheimer disease: Treatment of Alzheimer disease; to be initiated in patients with mild cognitive impairment or mild dementia stage of disease.
None known.
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program by clicking on the “Launch drug interactions program” link above.
Anticoagulants: Lecanemab may increase adverse/toxic effects of Anticoagulants. Specifically, the risk of hemorrhage may be increased. Management: Avoid use of lecanemab in patients who are being treated with an anticoagulant when possible. If concurrent use is necessary, monitor closely for evidence of intracerebral hemorrhage or other bleeding. Risk D: Consider Therapy Modification
Efgartigimod Alfa: May decrease therapeutic effects of Fc Receptor-Binding Agents. Risk C: Monitor
Nipocalimab: May decrease therapeutic effects of Fc Receptor-Binding Agents. Risk C: Monitor
Rozanolixizumab: May decrease therapeutic effects of Fc Receptor-Binding Agents. Risk C: Monitor
Therapeutic Antiplatelets: Lecanemab may increase antiplatelet effects of Therapeutic Antiplatelets. Risk C: Monitor
Thrombolytic Agents: Lecanemab may increase adverse/toxic effects of Thrombolytic Agents. Specifically, the risk of hemorrhage may be increased. Management: Avoid use of thrombolytic agents in patients being treated with lecanemab when possible. If concurrent use is necessary, monitor closely for evidence of intracerebral hemorrhage or other bleeding. Risk D: Consider Therapy Modification
Animal reproduction studies have not been conducted.
Lecanemab is a humanized monoclonal antibody (IgG1). Human IgG crosses the placenta. Fetal exposure is dependent upon the IgG subclass, maternal serum concentrations, placental integrity, newborn birth weight, and GA, generally increasing as pregnancy progresses. The lowest exposure would be expected during the period of organogenesis and the highest during the third trimester (Clements 2020; Palmeira 2012; Pentsuk 2009).
It is not known if lecanemab is present in breast milk.
Lecanemab is a humanized monoclonal antibody (IgG1). Human IgG is present in breast milk; concentrations are dependent upon IgG subclass and postpartum age (Anderson 2021).
According to the manufacturer, the decision to breastfeed during therapy should consider the risk of infant exposure, the benefits of breastfeeding to the infant, and the benefits of treatment to the mother.
PET or lumbar puncture to confirm presence of amyloid beta pathology (prior to initiation) (van Dyck 2023); apolipoprotein E ε4 (ApoE ε4) status testing (prior to initiation); brain MRI (prior to initiation [within 1 year]; prior to 5th, 7th, 14th infusions; periodically as appropriate in the setting of amyloid-related imaging abnormalities (ARIA) [eg, 2 to 4 months following identification of ARIA]); monitor closely for clinical and MRI changes; monitor for symptoms suggestive of ARIA (eg, headache, altered mental status, visual changes, dizziness, nausea, gait difficulty, focal neurologic deficits, seizure).
Lecanemab is a humanized monoclonal antibody directed against aggregated soluble and insoluble forms of amyloid beta. Lecanemab reduces amyloid beta plaques, the accumulation of which is a defining pathophysiological feature of Alzheimer disease.
Distribution: Vdss: 3.24 L.
Metabolism: Degradation by proteolytic enzymes.
Half-life elimination: 5 to 7 days.
