Monoclonal Antibodies For Alzheimer’s: How Leqembi And Kisunla Work

TL;DR

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Leqembi and Kisunla are FDA-approved anti-amyloid antibodies for people with early symptomatic Alzheimer’s in the United States. Clinical trials found that both reduce brain amyloid and modestly slow decline, but neither restores lost memory or cures the disease; the scale of everyday benefit and longer-term effects remain under study.

Leqembi and Kisunla, the two anti-amyloid antibodies approved by the U.S. Food and Drug Administration for Alzheimer’s treatment, bind to different forms of beta-amyloid and help the immune system clear it from the brain. Clinical trials found that both drugs modestly slowed cognitive and functional decline in people with early Alzheimer’s, but neither is a cure or restores memory already lost.

Monoclonal antibodies are laboratory-made proteins designed to bind to a particular target. In Alzheimer’s, lecanemab, sold as Leqembi, binds to amyloid plaques and smaller clusters called protofibrils. Donanemab, sold as Kisunla, primarily targets a modified form of beta-amyloid found in established plaques. After binding, the antibodies help the immune system clear amyloid from the brain.

Beta-amyloid can clump into aggregates and plaques between brain cells. Plaques are a hallmark of Alzheimer’s, though researchers are still studying how different forms of amyloid contribute to cognitive decline. In clinical trials, both medicines substantially reduced brain amyloid, while also producing more modest effects on clinical progression.

In Leqembi’s phase 3 trial, participants taking the drug declined about 27% more slowly over 18 months than those receiving placebo. In Kisunla’s phase 3 trial, participants across the overall study population had a 37% lower risk of progressing to the next clinical stage over 76 weeks than placebo recipients. These are trial-specific comparisons, not a guarantee of an individual patient’s experience.

What Amyloid Removal Can Change

The medicines are described as disease-modifying treatments because they target an underlying feature of Alzheimer’s biology rather than only treating symptoms. For eligible people with early symptomatic disease, slowing progression could affect how quickly cognitive and functional abilities change. The size of the benefit, however, does not mean that symptoms stop or that lost abilities return.

Whether trial-scale differences amount to a meaningful change in daily life remains disputed. An April 2026 Cochrane review, which pooled 17 trials involving more than 20,000 participants, concluded that average cognitive and functional benefits from anti-amyloid antibodies were too small to be clinically meaningful, while finding increased risks of brain swelling and bleeding. The report also notes that some Alzheimer’s specialists objected that the review grouped newer drugs with older antibodies that did not substantially clear amyloid.

The disagreement matters for patients and families weighing a modest potential slowing against treatment risks and the demands of care. It also highlights an unresolved scientific question: how much amyloid removal translates into clinical benefit. Clearing more amyloid does not necessarily produce a proportionally greater slowing of decline, according to research discussed in the report.

How the Two Drugs Differ

Leqembi was approved in July 2023, followed by Kisunla about a year later. Both were studied and approved for people in the earliest symptomatic stages of Alzheimer’s, making timely identification of eligible patients part of the treatment process. The source report does not provide a full list of eligibility criteria, so patients should discuss suitability with a qualified clinician.

Real-world findings are adding to trial evidence, but they need careful interpretation. In an Eisai-funded study of 177 people who had taken Leqembi for one year, 77% had not advanced to the next disease stage and 7% had moved from early Alzheimer’s to mild cognitive impairment. Because the study had no placebo group, it cannot show how much of that stability resulted from treatment rather than other factors or the disease’s course.

Researchers are also studying antibodies directed at other targets involved in Alzheimer’s, including proteins on brain immune cells. Those investigations are distinct from the evidence for the two currently approved anti-amyloid medicines.

“Existing approved drugs offer some benefit for some patients, but there remains a high unmet need for more effective treatments.”

— Edo Richard, senior author of the April 2026 Cochrane review and professor of neurology at Radboud University Medical Centre

Benefits, Risks and Long-Term Evidence

The practical size of the benefit remains unsettled. Trial results report average outcomes over defined periods, and experts disagree over whether those differences are meaningful in daily life. The reported real-world Leqembi study lacked a comparison group, while follow-up of a year or two may be too short to establish long-term effects for a slowly progressing disease.

Risks also matter: the Cochrane review reported increased brain swelling and bleeding with anti-amyloid antibodies. The source material does not provide individual risk estimates or a complete account of monitoring and treatment protocols. It is also unclear exactly how amyloid removal produces the observed clinical effects, or whether greater removal reliably means greater slowing.

More Follow-Up and Patient Selection

Researchers are expected to keep tracking longer-term outcomes and gathering real-world evidence as more patients receive treatment. Further evidence may help clarify how durable the effects are, which patients are most likely to benefit, and how the potential slowing compares with treatment risks.

For now, Leqembi and Kisunla remain treatments studied for early symptomatic Alzheimer’s, not cures. Decisions about evaluation or treatment should be made with a qualified health professional who can consider a person’s circumstances and explain the relevant benefits and risks.

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 protofibrils; Kisunla primarily targets a modified form of amyloid in established plaques.

Do the drugs cure Alzheimer’s or restore memory?

No. Neither drug is a cure, and neither restores memory already lost. Trial evidence indicates that they can modestly slow cognitive and functional decline in people with early Alzheimer’s.

How much did the clinical trials find progression slowed?

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, the overall study population had a 37% lower risk of progressing to the next clinical stage over 76 weeks than the placebo group. These results use different measures and time periods.

Are the benefits considered meaningful?

Experts disagree. The April 2026 Cochrane review judged the average benefits too small to be clinically meaningful, while some specialists argued that newer antibodies provide a modest but meaningful benefit. The effect on an individual’s daily life is not settled by these competing assessments.

What risks have been reported?

The Cochrane review reported increased risks of brain swelling and bleeding with anti-amyloid antibodies. The source report does not give individual risk estimates. Patients should discuss treatment risks and suitability with a qualified clinician.

Source: rss