STOCKHOLM, Nov. 21, 2022 /PRNewswire/ — BioArctic AB’s (publ) (Nasdaq Stockholm: BIOA B) partner Eisai will present the efficacy, safety and biomarker results from the Phase 3 confirmatory Clarity AD clinical trial for lecanemab[1] (development code: BAN2401), at the 15th Clinical Trials on Alzheimer’s Disease (CTAD) conference, held in San Francisco, CA and virtually from November 29 to December 2. The data will be presented by Eisai and distinguished faculty members in a scientific session on the first day of the meeting (November 29 at 4:50 p.m. PT). Additionally, BioArctic will present a poster on Aß protofibrils and binding properties of lecanemab and Eisai will present other important research from the lecanemab clinical development program in several oral and poster presentations.
Topline results from Clarity AD were announced in late September and showed that lecanemab met the primary endpoint and all key secondary endpoints with highly statistically significant results, and the profile of Amyloid-Related Imaging Abnormalities (ARIA) incidence was within expectations.
Key lecanemab CTAD presentations
Clarity AD: Results from the Phase 3 confirmatory Clarity AD clinical trial of lecanemab in patients with early AD will be presented in a scientific session on November 29 at 4:50 p.m. PT. Eisai will host a live webcast of presentations in the session and can be viewed live on the investors section of the Eisai Co., Ltd. website.
Aß protofibrils and lecanemab ninding properties: Research studying the characterization of Aß protofibrils and the unique binding properties and mechanisms of Aß clearance of lecanemab (Poster #P029)
AHEAD 3-45 Study:
An evaluation of tau PET screening data from the Phase 3 AHEAD 3-45 study of lecanemab for associations with plasma p-tau217 and cognitive testing (Late Breaker Oral #LB1)
A study exploring increased accuracy of amyloid PET prediction in preclinical AD using plasma levels for Aß42/40 and p-tau217 ratios from screening data from the Phase 3 study AHEAD 3-45 (Late Breaker Oral #LB2)
Eisai aims to file for traditional approval in the U.S., and to submit marketing authorization applications in Japan and Europe by the end of the first quarter 2023. In July 2022, the U.S. Food and Drug Administration (FDA) accepted Eisai’s Biologics License Application (BLA) for lecanemab under the Accelerated Approval Pathway and granted Priority Review. The Prescription Drugs User Fee Act action date (PDUFA) is set for January 6, 2023. The FDA has agreed that the results of Clarity AD can serve as the confirmatory study to verify the clinical benefit of lecanemab. In an effort to secure traditional FDA approval for lecanemab as soon as possible, Eisai submitted the BLA through the FDA’s Accelerated Approval Pathway so that the agency could complete its review of all lecanemab data with the exception of the data from the confirmatory Clarity AD study. In March 2022, Eisai began submitting application data, with the exception of Clarity AD data, to Japan’s Pharmaceuticals and Medical Devices Agency (PMDA) under the prior assessment consultation system with the aim of obtaining early approval for lecanemab so that people living with early AD may have access to the therapy as soon as possible.
CTAD 2022 presentations relating to lecanemab
Scientific Session:
Oral presentations
Poster presentations
This release discusses investigational uses of agents in development and is not intended to convey conclusions about efficacy or safety. There is no guarantee that such investigational agents will successfully complete clinical development or gain health authority approval.
The information was released for public disclosure, through the agency of the contact persons below, on November 21, 2022, at 08:00 a.m. CET.
For further information, please contact:
Gunilla Osswald, CEO
-E-mail: gunilla.osswald@bioarctic.se
Phone: +46 8 695 69 30
Oskar Bosson, VP Communications and IR
-E-mail: oskar.bosson@bioarctic.se
Phone: +46 70 410 71 80
About Clarity AD
About lecanemab (BAN2401)
Lecanemab is an investigational humanized monoclonal antibody for Alzheimer’s disease (AD) that is the result of a strategic research alliance between BioArctic and Eisai. Lecanemab selectively binds to neutralize and eliminate soluble toxic Aß aggregates (protofibrils) that are thought to contribute to the neurodegenerative process in AD. As such, lecanemab may have the potential to have an effect on disease pathology and to slow down the progression of the disease. Currently, lecanemab is being developed as the only late-stage anti-Aß antibody that can be used for the treatment of early AD without the need for titration, enabling full treatment effect from day one.
In the global Phase 3 confirmatory Clarity AD study, lecanemab treatment met the primary endpoint and reduced clinical decline on the global cognitive and functional scale, CDR-SB, compared with placebo at 18 months by 27%, which represents a treatment difference in the score change of -0.45 (p=0.00005) in the analysis of Intent-to-treat (ITT) population. Starting as early as six months, across all time points, the treatment showed highly statistically significant changes in CDR-SB from baseline compared to placebo (all p-values are less than 0.01). All key secondary endpoints were also met with highly statistically significant results compared with placebo (p0.01). Key secondary endpoints were the change from baseline at 18 months compared with placebo of treatment in amyloid levels in the brain measured by amyloid positron emission tomography (PET), the AD Assessment Scale-cognitive subscale14 (ADAS-cog14), AD Composite Score (ADCOMS) and the AD Cooperative Study-Activities of Daily Living Scale for Mild Cognitive Impairment (ADCS MCI-ADL). The incidence of amyloid-related imaging abnormalities-edema/effusion (ARIA-E), an adverse event associated with anti-amyloid antibodies, was 12.5% in the lecanemab group and 1.7% in the placebo group. The incidence of symptomatic ARIA-E was 2.8% in the lecanemab group and 0.0% in the placebo group. The ARIA-H (ARIA cerebral microhemorrhages, cerebral macrohemorrhages, and superficial siderosis) rate was 17.0% in the lecanemab group and 8.7% in the placebo group. The incidence of symptomatic ARIA-H was 0.7% in the lecanemab group and 0.2% in the placebo group. There was no imbalance in isolated ARIA-H (i.e., ARIA-H in patients who did not also experience ARIA-E) between lecanemab (8.8%) and placebo (7.6%). The total incidence of ARIA (ARIA-E and/or ARIA-H) was 21.3% in the lecanemab group and 9.3% in the placebo group. Overall, lecanemab’s ARIA incidence profile was within expectations.
(CONTINUA)