
Eisai and SEED Therapeutics have entered into a strategic research collaboration aimed at developing molecular glue degraders (MGDs) for multiple undisclosed neurodegeneration and oncology targets, with the deal worth up to $1.5bn.
MGDs are a new class of drugs that can be directed at targets that have previously been considered ‘undruggable’ by other approaches.
The partnership will see SEED lead preclinical discovery activities for the selected targets, including E3 ligase selection and identification of appropriate MGDs. Eisai will then have exclusive rights to develop and commercialise any resulting compounds.
In exchange, SEED will be entitled to receive as much as $1.5bn in upfront and preclinical, clinical, regulatory and sales milestone payments, plus tiered royalties on potential future sales.
Takashi Owa, Eisai’s chief scientific officer, said: “SEED has a cutting-edge technology platform to discover a class of molecular-glue target protein degraders, one of the most highlighted modalities in modern drug discovery… Our collaboration with SEED is unique and clearly differentiated, and I look forward to learning of the important progress being made by both companies to achieve social good.”
Lan Huang, SEED’s co-founder, chairman and chief executive officer, added that the company is “honoured to collaborate with Eisai… to discover impactful medicines for undruggable targets”.
Eisai has also led a series A-3 financing with a first close of $24m for SEED, which is planning to use the money to “further accelerate” the clinical development of its internal proprietary programmes in oncology and neurodegeneration, as well as to expand its targeted protein degradation platform and pipeline.
The alliance comes just days after Eisai presented positive three-year data for its Biogen-partnered Alzheimer’s drug Leqembi (lecanemab-irmb), which holds approvals to treat patients with mild cognitive impairment and early stages of the neurodegenerative disease.
The latest data showed that more than 50% of patients receiving continuous Leqembi treatment showed ongoing improvement over three years, with a -0.95 decline on the CDR-SB cognition rating scale.
Additionally, no new safety findings were observed with continued Leqembi treatment over three years, with the majority of amyloid-related imaging abnormalities occurring in the first six months of treatment.




