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Long-Term Anti-Amyloid Treatment May Delay Alzheimer's Symptom Onset, Study Suggests

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3D illustration showing amyloid plaques in Alzheimer's disease

PHILADELPHIA – Long-term treatment with Roche's beta-amyloid-targeting drug gantenerumab has shown signs of delaying the symptoms of Alzheimer's disease in patients with genetic mutations known to cause an inherited form of the illness, but who haven't exhibited symptoms yet, researchers reported Sunday at the Alzheimer's Association International Conference.

Roche had been advancing gantenerumab as a monoclonal antibody treatment for early Alzheimer's but ceased most clinicals trials of the therapeutic candidate in 2022, after it failed to slow the decline of patients' symptoms in the Phase III GRADUATE I and GRADUATE II trials and removed beta-amyloid at lower levels than expected.

However, investigators at Washington University School of Medicine in St. Louis continued to study the drug through mid-2023 within the open-label extension portion of the Phase II/III DIAN-TU-001 trial, involving patients who would likely develop dominantly inherited Alzheimer's disease (DIAD) because they carried a mutated form of the PSEN1, PSEN2, or APP genes, but did not have symptoms of disease.

Researchers at the time said it was worth continuing to study the drug, since they were testing it at a higher dose in DIAD and at an earlier stage of the disease, and not in sporadic Alzheimer's, as in the GRADUATE trials.

Tackling Alzheimer's before symptoms emerge is an area of interest for many drugmakers in this space. Eisai and Biogen, for example, are studying their anti-amyloid Alzheimer's treatment Leqembi (lecanemab) in patients who haven't displayed disease symptoms but have elevated levels of beta-amyloid in the Phase III AHEAD 3-45 trial. Eli Lilly is also testing its recently approved anti-amyloid drug Kisunla (donanemab) for this indication within the Phase III TRAILBLAZER-ALZ 3 trial.

For the DIAN-TU-001 study, investigators recruited nearly 200 patients from WashU's Dominantly Inherited Alzheimer Network (DIAN), an international, observational study of patients and family members of those who have a genetic mutation linked to DIAD. Patients in the study received either placebo, gantenerumab, or solanezumab, a failed anti-amyloid drug that Lilly stopped developing last year. For the analysis presented Sunday, investigators homed in on 52 patients who received gantenerumab subcutaneously every other week at escalating doses for at least four and up to seven years.

Seventy-three patients with genetically confirmed DIAD enrolled in the subsequent open-label extension portion, in which they received gantenerumab even if they had originally received solanezumab in the randomized portion. That extension study, which launched in 2020, was discontinued last summer after an interim efficacy analysis, according to information on ClinicalTrials.gov.

Investigators did not observe an improvement on the Clinical Dementia Rating (CDR) Global or the CDR-Sum of Boxes scales among patients who received gantenerumab for four to seven years during the initial study period when they compared patients' outcomes to the placebo group or DIAN observational study. There were no trends suggesting that gantenerumab slowed disease progression when researchers focused on just the patients in the open-label extension portion, either. However, the subset of patients who were on gantenerumab for the longest, for an average of around eight years, from the initial study period through the open-label extension portion exhibited signs of delayed symptom onset. The patient who had taken gantenerumab the longest in this subset had received the drug for a decade.

That suggests anti-amyloid therapies may need to be administered not only at an early stage of intervention, but also for a long time, to successfully delay onset of Alzheimer's symptoms in asymptomatic patients, said Randall Bateman, a professor of neurology at WashU and director of the DIAN and DIAN Trials Unit (DIAN-TU), during a presentation Sunday. "The DIAN-TU trial of gantenerumab may provide the first proof of principle that removing amyloid plaques may prevent the onset of Alzheimer's disease dementia," Bateman said.

The data suggest, according to Bateman, that removing beta-amyloid plaque for an average of eight years could lead to a 50 percent decrease in the risk of asymptomatic DIAD patients developing Alzheimer's symptoms. He further noted that the trends observed in the longest-treated patients suggest gantenerumab may delay symptoms by between five years and 15 years compared to natural progression.

Gantenerumab also substantially reduced levels of beta-amyloid plaque in patients' brains. Higher doses of the drug were associated with greater removal, according to an analysis comparing patients' baseline beta-amyloid plaque in the open-label extension portion to their levels three years later. Thirty percent of patients in the study sustained normal levels of beta-amyloid or converted to normal levels during the study.

"While the clinical development program for gantenerumab has been discontinued, Roche and Genentech remain committed to advancing the understanding of Alzheimer's disease, one of the most complex neurological disorders and a major public health challenge," a Roche spokesperson said in an email. "We continue to develop and deliver diagnostic tests for the disease, and have a pipeline of investigational medicines for different targets, types, and stages of the disease."

Bateman acknowledged some limitations of the analysis, such as the small study size and limited follow-up data after the expected age of symptom onset. "Because this study design included an [open-label extension] and external controls, firm conclusions are limited," study authors noted in a preprint paper on the clinical trial results.

The study was funded by the US National Institutes of Health's National Institute on Aging, the Alzheimer's Association, the GHR Foundation, and Roche.

During a discussion on the results after Bateman's presentation, Alzheimer's Association CSO Maria Carrillo said these findings provide "hope" for Alzheimer's patients and their families, as researchers continue to try to better understand what preventive steps people can take to reduce the likelihood of disease onset while also prioritizing safety.

While these results suggest the potential benefit of early intervention during the asymptomatic phase of Alzheimer's, this is harder to identify in the sporadic Alzheimer's population, noted Janice Smith, who was previously the global development lead for the gantenerumab program at Roche and currently leads the trontinemab program.

Although Roche is no longer advancing gantenerumab, it continues to develop a formulation of the monoclonal antibody, called trontinemab, which uses a different mechanism to try to increase its uptake in the brain. Roche is testing trontinemab in a Phase Ib/IIa trial of patients with prodromal or mild-to-moderate Alzheimer's and beta-amyloid pathology.

"The data that we've seen today [on gantenerumab] are really interesting and intriguing," Smith said during the discussion. "It really encourages us to go early."

Researchers at WashU are continuing to study long-term treatment with beta-amyloid-targeting drugs in this patient population. The DIAN-TU last month launched a new study, the open-label DIAN-TU-003 Amyloid Removal Trial (ART), in which patients who had been receiving gantenerumab through the open-label extension study will receive Eisai and Biogen's Leqembi for at least five years. The US Food and Drug Administration approved Leqembi last year for patients with early Alzheimer's and beta-amyloid pathology.

In DIAN-TU-003 ART, researchers hope to improve the understanding of anti-amyloid therapies and their ability to delay dementia onset, as well as the effect of long-term treatment on biomarker and safety outcomes, according to Jorge Llibre-Guerra, an assistant professor of neurology at WashU and associate medical director of the DIAN-TU. The study will also provide insights into the safety of switching between different anti-amyloid therapies, he added.