Takeda, AC Immune ink Alzheimer’s licensing deal
License out/inPhase 3ImmunotherapyPhase 2
Takeda has signed a worldwide licensing agreement with Swiss biotech AC Immune to develop and commercialize ACI-24.060, an immunotherapy aimed at treating Alzheimer's disease by targeting amyloid beta plaques.
Under the terms of the agreement, AC Immune will receive an upfront payment of $100 million upon the closing of the deal. Additionally, the company is eligible for an option exercise fee, along with potential milestones that could total approximately $2.1 billion if all targets are met. Upon commercialization, AC Immune will also receive tiered double-digit royalties on worldwide net sales.
ACI-24.060 is currently under investigation in the ABATE phase 1b/2 trial, which is a randomized, double-blind, placebo-controlled study evaluating the safety, tolerability, immunogenicity, and pharmacodynamic effects of the immunotherapy in individuals with prodromal Alzheimer's disease and adults with Down syndrome.
The partnership aims to leverage Takeda’s global presence and experience in drug development and commercialization while AC Immune continues to oversee the ongoing phase 1b/2 trial. Takeda will take responsibility for further clinical development, global regulatory activities, and worldwide commercialization upon exercise of the option.
AC Immune has faced significant setbacks in its pursuit of an effective Alzheimer’s treatment. In 2019, Roche and AC discontinued a phase 3 trial of crenezumab, an early Alzheimer’s treatment, after it was found ineffective. Despite the setback to the hypothesis that blocking amyloid plaques could slow cognitive decline, Roche decided to continue a study of crenezumab on healthy individuals with a genetic predisposition to Alzheimer’s.
Then in 2020, Roche and AC Immune faced another setback when their experimental Alzheimer's treatment, semorinemab, failed to enhance cognitive function in a phase 2 trial with early-stage patients. Unlike many treatments that target amyloid beta peptides, semorinemab aimed at "tau" proteins but did not prove more effective.
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