The companies have announced data on the drug candidate lecanemab (BAN2401).
The presentations included findings suggesting that lecanemab could be of potential benefit for adults with Down’s syndrome with signs of functional or cognitive deterioration. Preliminary results presented from the ongoing open-label extension of the Phase 2b study in early Alzheimer’s disease continue to support the effect of lecanemab on brain amyloid levels, the company states in a press release.
“The latest data further support the effects of lecanemab, and I’m encouraged to see the continued progress of both Eisai’s broad ongoing clinical trial programs in Alzheimer’s disease, as well as our own research related to Down’s syndrome. We look forward to the continued development of lecanemab as a potential disease-modifying treatment,” says BioArctic’s CEO Gunilla Osswald.
Read more: Interview – Gunilla Osswald, CEO, BioArctic
Down’s syndrome
BioArctic presented data that confirmed that similar to adults with Alzheimer’s disease, individuals with Down’s syndrome with dementia show significantly elevated levels of soluble amyloid-beta (Aβ) aggregates, so called protofibrils, compared to control groups. The presentation also demonstrated for the first time that lecanemab binds to these Aβ aggregates and Aβ plaques in this Down’s syndrome population with dementia. These combined findings suggest that targeting toxic soluble Aβ aggregates with lecanemab could help preserve brain function in adults with Down’s syndrome with dementia.
Lecanemab
Eisai presented updated results from subjects who participated in the amyloid imaging sub studies in both the Core and the ongoing open-label extension of the Phase 2b study of lecanemab in early Alzheimer’s disease. The results showed that the effects of lecanemab on reducing amyloid in the brain on average persist for at least two years following discontinuation of lecanemab dosing. In participants who were treated with placebo in the core study and started on 10 mg/kg biweekly lecanemab in the open label extension, showed rapid reduction in brain amyloid levels as early as three months of lecanemab treatment, with continued reduction over 12 months of treatment. Lecanemab, dosed at 10 mg/kg biweekly, was also shown to reduce brain amyloid to negative levels1 in more than 80 percent of patients who participated in the core and open-label extension study, as early as 12 months into treatment.
Photo of Gunilla Osswald: BioArctic
