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Roche licenses Parkinson’s therapy for up to $1.27 billion

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Swiss drugmaker Roche will pay up to $1.27 billion to license Alector’s experimental treatment for ​Parkinson’s disease, the US biotech said ‌on Monday, sending its shares surging 72% in premarket trading.

Genentech, a unit of Roche, will ​pay Alector $100 million upfront and up ​to $1.17 billion more if the treatment reaches development, regulatory ⁠and sales targets. Alector is also ​eligible for royalties.

Genentech has been granted exclusive worldwide rights to develop, manufacture and sell AL050, an experimental treatment aimed at addressing an enzyme deficiency linked to Parkinson’s disease.

Under the agreement, Genentech will lead all development, regulatory submissions, manufacturing and commercialization activities for the therapy.

AL050 is an enzyme replacement therapy designed to correct a deficiency of the GCase enzyme. A lack of GCase can lead to the buildup of certain fats in cells, which is associated with a higher risk of developing Parkinson’s disease.

The therapy is intended to restore normal enzyme levels and potentially slow disease progression.
The deal marks the latest in a series of licensing agreements by Roche as it looks to expand its drug pipeline. In June,

Roche also signed a licensing and collaboration deal with Nurix Therapeutics worth up to $2.3 billion for a blood cancer drug, underscoring its push into new therapeutic areas through external partnerships.

AL050 features an engineered glucocerebrosidase (GCase) with improved activity and stability, which can be effectively delivered to the brain using ABC technology. The technology leverages the transferrin receptor, which is expressed by cells that line blood vessels, allowing substances to cross the BBB through the cells, rather than between them. This allows therapeutic agents to reach the brain at effective levels, contributing to reducing treatment dosage and minimizing side effects.

Preclinical studies showed AL050 increased GCase activity and reduced toxic substrate accumulation in animal models of GBA disease, supporting its potential as a therapy for Parkinson’s disease and Lewy body dementia associated with loss-of-function mutations in the GBA gene.



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