AlzeCure shares soar over 300% after Eli Lilly strikes Alzheimer’s deal worth over $1bn

The agreement centres on ACD680, a preclinical small-molecule candidate from Alzecure’s platform. The candidate modulates gamma-secretase, an enzyme involved in the production of amyloid-beta peptides, which have long been implicated in Alzheimer’s. According to the press release, Eli Lilly will assume responsibility for the further development and commercialisation of the programme.

As the Swedish biotech company found a major pharmaceutical partner in Eli Lilly for one of its lead neurology programmes, its shares went up from SEK1,38 the day before the announcement to SEK5,70 at some point during the day of the announcement, marking a 313% jump in stock price. On the Eli Lilly side, the company adds another Alzheimer’s disease asset to its growing neurodegeneration pipeline.

Lilly bets on a new take on the amyloid hypothesis

Lilly’s interest in ACD680 comes as the company is already active in Alzheimer’s through Kisunla, its approved amyloid-targeting antibody. But instead of clearing amyloid plaques that have already formed, ACD680 is acting earlier in the amyloid pathway by changing how amyloid-beta peptides are produced.

ACD680 is a gamma-secretase modulator (GSM), and according to AlzeCure, the candidate is intended to reduce production of Aβ42, the amyloid-beta form most associated with plaque formation, while increasing shorter variants such as Aβ37 and Aβ38, which are considered less prone to aggregation.

Gamma-secretase has a difficult history in Alzheimer’s disease. Earlier attempts to block the enzyme, including Lilly’s semagacestat, failed in clinical trials after showing an unfavourable risk-benefit profile. The problem was that gamma-secretase does more than produce amyloid-beta. The enzyme is involved in processing several proteins, including the Notch receptor, which helps regulate cell development and tissue maintenance. By blocking gamma-secretase broadly, drugs such as semagacestat interfere with these normal biological functions.

The class had not disappeared, but it remains early today. Eisai previously advanced GSMs E2012, later improved and renamed E2212, before terminating its development in 2011, while more recent work has included Roche’s second-generation GSM programme. 

For now, however, ACD680 remains preclinical. AlzeCure says the programme has shown a favourable preclinical safety and pharmacological profile, leaving Eli Lilly to test whether this upstream amyloid approach can translate into clinical benefit.

Eli Lilly’s Alzheimer’s pipeline is thickening

Kisunla and Leqembi slow disease progression but do not stop it, and both are associated with amyloid-related imaging abnormalities (ARIA). The burden of both these treatments is also significant. It is too early to know whether ACD680 can overcome any of these limitations, but the deal suggests companies are still looking to improve on amyloid biology.

For Eli Lilly specifically, the AlzeCure deal adds a third amyloid approach to an Alzheimer’s portfolio that is already anchored by Kisunla and remternetug. While both of those therapies are designed to remove amyloid plaques from the brain, ACD680 targets an earlier step in the process by influencing how amyloid-beta peptides are produced.

Lilly is not treating the approval of Kisunla as the end of its amyloid strategy. Instead, the company is exploring multiple ways of intervening in the same biological pathway. Remternetug, currently in phase 3 development, represents a next generation of plaque-clearing antibodies, while ACD680 revives interest in modifying amyloid production itself through a small-molecule approach.

At the same time, Lilly’s Alzheimer’s strategy is not limited to amyloid. The company is also developing LY3954068, a MAPT-targeting siRNA that aims to reduce tau expression and is currently being evaluated in a phase 1 study. 

A 2026 Alzheimer’s disease drug development review identified that 158 therapies are currently in clinical development. According to that review, the field is becoming more diverse with amyloid based approaches representing only 20% of the drugs being evaluated versus 33% only 10 years ago. It is still an important share of the candidates and it means that despite the arrival of plaque-clearing antibodies on the market, companies are still searching for the most effective way to target amyloid biology. 

Amyloid approaches remain an important part of the pipeline, but they now face growing competition from other strategies. The review noted that tau-targeting therapies and candidates aimed at inflammation or immune dysfunction each account for around 20% of drugs currently in development, up from roughly 6% 10 years ago. 

The field might be becoming more diverse, but Lilly’s Alzheimer’s pipeline remains strongly anchored in amyloid biology compared to its historic competition, Biogen and Eisai, which have brought leqembi to market and now both have phase 2 tau targeting assets in their pipelines. Eisai shared positive phase 2 data for E2814 in December, while Biogen announced last month that the study evaluating BIIB080 did not meet its endpoint but it still plans of pursuing registrational development.