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Takeda exits co-development of Denali's dementia drug

DNL593, a progranulin replacement biologic engineered with Denali Therapeutics' (NASDAQ: DNLI) TransportVehicle technology, will advance under sole Denali...

Denali Therapeutics (NASDAQ: DNLI) issued a press release revealing that Takeda (NYSE: TAK) has decided to terminate their co-development and co-commercialization agreement in relation to DNL593, a progranulin replacement biologic engineered with Denali's TransportVehicle technology. The molecule will subsequently advance under sole Denali control. Takeda attributed the exit to internal strategic considerations, stating explicitly that the decision was unrelated to efficacy or safety. DNL593 is the subject of an ongoing Phase I/II study in frontotemporal dementia driven by GRN mutations (FTD-GRN), with data expected by year-end 2026.

DNL593 is a biologic fusion protein that pairs a progranulin payload with an antibody-based moiety targeting transferrin receptor 1 (TfR1) on brain endothelial cells. Loss-of-function mutations in the GRN gene reduce progranulin levels in the brain, disrupting lysosomal homeostasis and driving neurodegeneration in FTD-GRN. By binding TfR1, DNL593 is designed to exploit receptor-mediated transcytosis to ferry progranulin across the blood-brain barrier — a delivery route that Denali describes as yielding more than 10- to 30-fold greater brain exposure compared with unmodified biologics. Interim data from Part A of the Phase I/II study in healthy volunteers showed dose-dependent increases in cerebrospinal fluid progranulin levels, and no significant safety signals have emerged. Enrollment in the patient cohort is complete at 40 participants with FTD-GRN.

Deal context

The original collaboration dates to January 2018, when Takeda paid USD 150 million in cash and equity to access options on up to three Denali programs targeting genetically validated neurodegeneration mechanisms. Takeda exercised its option on DNL593 in November 2021, converting that program into a full co-development and co-commercialization arrangement. With Takeda's exit, Denali regains the full DNL593 intellectual property portfolio and assumes sole financial responsibility for continued development.

Takeda also previously exercised its option on DNL919, an anti-TREM2 antibody engineered with Denali's ATV sub-platform for Alzheimer's disease, but that program was subsequently discontinued following Phase I findings of a narrow therapeutic window. The termination of the DNL593 collaboration leaves the broader 2018 partnership effectively wound down.

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Denali's TransportVehicle platform secured a first US FDA approval for the company in March 2026, when Avlayah (tividenofusp alfa-eknm; DNL310) was cleared to treat Hunter syndrome (mucopolysaccharidosis type II, or MPS II). Another four TV-enabled programs are currently in clinical development across the portfolio. Tividenofusp alfa is an enzyme replacement therapy developed on Denali's ETV sub-platform. DNL593 represents the platform's application to a protein replacement context in a genetically defined neurodegenerative disease, a mechanistically distinct use case from the enzyme replacement programs.

FTD is the most common form of dementia in people under 60, and no approved therapy exists to slow its progression. The GRN mutation subtype represents one of the most common genetic causes of the disease. Full Phase I/II results, including data from the FTD-GRN patient cohort, are expected before the end of 2026 and will be the primary near-term value inflection for the asset.


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