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Leqembi and Kisunla are FDA-approved antibodies that target different forms of beta-amyloid in people with early Alzheimer’s disease. Clinical trials found modestly slower cognitive and functional decline, but the size of the everyday benefit, long-term effects and risks remain under discussion.
Leqembi (lecanemab) and Kisunla (donanemab), the two anti-amyloid monoclonal antibodies approved in the United States for Alzheimer’s disease, bind to different forms of beta-amyloid and help the immune system clear it from the brain. Clinical trials found that the drugs modestly slowed decline in people with early Alzheimer’s, but they do not cure the disease or restore lost memory, and experts continue to debate how meaningful the measured benefit is for patients’ daily lives.
Monoclonal antibodies are laboratory-made proteins designed to recognize a particular target. In Alzheimer’s treatment, Leqembi and Kisunla target beta-amyloid, a protein that can accumulate in the brain and form plaques. The antibodies bind to amyloid and help the body’s immune system remove it. The two drugs do not bind to precisely the same forms: Leqembi targets plaques and smaller aggregates called protofibrils, while Kisunla primarily targets a modified form of beta-amyloid found in established plaques.
In its phase 3 trial, Leqembi was associated with decline about 27% more slowly over 18 months than placebo. In Kisunla’s phase 3 trial, participants had a 37% lower risk of progressing to the next clinical stage over 76 weeks than those who received placebo. These figures come from different trials and measures, so they should not be read as a direct comparison between the medicines. Both drugs reduced brain amyloid in trials, but removal of more amyloid does not necessarily translate into proportionally greater slowing of symptoms.
The drugs are intended for people in the earliest symptomatic stages of Alzheimer’s, not for reversing established memory loss. A 2026 Cochrane review, as described in the report, pooled 17 trials involving more than 20,000 participants and concluded that average cognitive and functional benefits of anti-amyloid antibodies were too small to be clinically meaningful; it also found increased risks of brain swelling and bleeding. Some Alzheimer’s specialists disputed the review’s conclusions, including its grouping of newer drugs with older antibodies that did not substantially clear amyloid.
What Amyloid Removal Can—and Cannot—Do
These treatments mark a shift from medicines that mainly address symptoms toward drugs intended to affect underlying Alzheimer’s biology. For eligible patients and families, a slower rate of decline could matter, but trial results do not establish that every patient will experience a noticeable change in everyday functioning. The findings also do not mean that lost abilities return: neither medicine is a cure.
The balance of benefit and risk matters because treatment involves exposure to possible brain swelling and bleeding, as well as the burden of determining eligibility and monitoring care. The evidence summarized in the report supports a measured conclusion: the drugs can clear amyloid and slow decline on average in trials, while the size and practical meaning of that effect remain contested.
Alzheimer's monoclonal antibody treatment
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Two Drugs, Different Amyloid Targets
Beta-amyloid buildup is one of the biological features associated with Alzheimer’s, but scientists are still working to understand how different forms of the protein contribute to cognitive decline. The U.S. Food and Drug Administration approved Leqembi in July 2023 and Kisunla about a year later, according to the report. Both approvals concern treatment of early Alzheimer’s, and both drugs are considered disease-modifying because they act on disease-related biology rather than only treating symptoms.
Evidence beyond clinical trials is emerging, but it has limits. An Eisai-funded study of 177 people who had taken Leqembi for a year reported that 77% had not progressed to the next disease stage and 7% had moved from early Alzheimer’s to mild cognitive impairment. Because that study had no placebo group, it cannot show how much of the reported stability resulted from the drug. The report also notes that short follow-up is a challenge when disease progression is gradual and treatment effects are modest.
“Existing approved drugs offer some benefit for some patients, but there remains a high unmet need for more effective treatments.”
— Edo Richard, professor of neurology at Radboud University Medical Centre and senior author of the Cochrane review
How Much Benefit Patients Notice
It remains unclear how reliably the trial-measured slowing translates into a meaningful difference in a person’s daily life. The Cochrane review’s pooled assessment and the more favorable view expressed by some Alzheimer’s specialists reflect different interpretations of the evidence; the report says critics objected in part to combining newer drugs with older antibodies that did not substantially clear amyloid.
Longer-term effects are also uncertain. Available real-world observations do not settle how much stability is caused by treatment, particularly when studies lack a placebo group and follow people for only a year or two. The report does not provide a head-to-head trial comparing Leqembi with Kisunla, so their separate trial results cannot establish which is more effective. Individual eligibility and treatment decisions also depend on clinical assessment.
Longer Follow-Up and Patient Selection
Researchers will need longer follow-up and stronger real-world comparisons to clarify how durable the effects are and how they relate to cognition and daily function. Continued study may also help explain the relationship between the amount of amyloid cleared and the degree of clinical benefit.
For now, treatment consideration centers on identifying people while Alzheimer’s is at an early symptomatic stage and weighing potential benefit against risks. The report does not specify a new regulatory decision or upcoming milestone. Patients should discuss diagnosis, eligibility, monitoring and treatment choices with a qualified health professional.
Key Questions
How do Leqembi and Kisunla work?
Both are monoclonal antibodies that bind to forms of beta-amyloid and help the immune system clear it from the brain. Leqembi binds to plaques and smaller aggregates called protofibrils; Kisunla primarily targets a modified form found in established plaques.
Do these medicines cure Alzheimer’s or restore lost memory?
No. The report says neither medicine is a cure or restores memory already lost. In trials, both were associated with slower cognitive and functional decline in people with early Alzheimer’s.
How large was the benefit in clinical trials?
Leqembi’s phase 3 trial found decline about 27% more slowly over 18 months than placebo. Kisunla’s trial found a 37% lower risk of progression to the next clinical stage over 76 weeks. These are results from different trials and measures, not a direct comparison.
What risks and uncertainties are reported?
The 2026 Cochrane review described in the report found increased risks of brain swelling and bleeding alongside benefits it judged too small to be clinically meaningful on average. Some specialists disputed its conclusions. The real-world impact and longer-term effects remain uncertain.
Who were the drugs studied and approved for?
The report says Leqembi and Kisunla were studied and approved for people in the earliest symptomatic stages of Alzheimer’s. A qualified health professional can assess an individual’s diagnosis and whether treatment may be appropriate.
Source: rss
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