Currently Enrolling Trials
Leqembi (lecanemab-irmb) injection is an amyloid beta-directed antibody.
Leqembi is specifically indicated for the treatment of Alzheimer’s disease. Treatment with Leqembi should be initiated in patients with mild cognitive impairment or mild dementia stage of disease, the population in which treatment was initiated in clinical trials. There are no safety or effectiveness data on initiating treatment at earlier or later stages of the disease than were studied.
Leqembi is supplied as a solution for intravenous infusion. The recommended dosage of Leqembi is 10 mg/kg that must be diluted then administered as an intravenous infusion over approximately one hour, once every two weeks. If an infusion is missed, administer the next dose as soon as possible.
Mechanism of Action
Leqembi (lecanemab-irmb) is a humanized immunoglobulin gamma 1 (IgG1) monoclonal antibody directed against aggregated soluble and insoluble forms of amyloid beta. The accumulation of amyloid beta plaques in the brain is a defining pathophysiological feature of Alzheimer’s disease. Leqembi reduces these amyloid beta plaques.
Adverse effects associated with the use of Leqembi may include, but are not limited to, the following:
- infusion-related reactions
Clinical Trial Results
Leqembi is approved under accelerated approval based on reduction in amyloid beta plaques observed in clinical studies. Continued approval for this indication may be contingent upon verification of clinical benefit in a confirmatory trial.
Accelerated approval was based on a double-blind, placebo-controlled, parallel-group, dose-finding study of 856 patients with Alzheimer’s disease. Treatment was initiated in patients with mild cognitive impairment or mild dementia stage of disease and confirmed presence of amyloid beta pathology. Patients receiving the treatment had significant dose- and time-dependent reduction of amyloid beta plaque, with patients receiving the approved dose of lecanemab, 10 milligram/kilogram every two weeks, having a statistically significant reduction in brain amyloid plaque from baseline to Week 79 compared to the placebo arm, which had no reduction of amyloid beta plaque.