Roche pays €70M upfront for Tusk’s preclinical Treg depleter

The Roche Tower. (Roche)

Roche has paid €70 million ($81 million) upfront to buy Tusk Therapeutics. The takeover gives Roche control of an anti-CD25 antibody that depleted levels of regulatory T cells (Tregs) in preclinical tests.

U.K.-based Tusk in licensed the anti-CD25 antibody from UCL and Cancer Research UK, and went on to work with their researchers to generate preclinical proof-of-concept data on the antibody as a monotherapy and in combination with PD-1/L1 checkpoint inhibitors. The early-stage data suggests Tusk’s antibody depletes Tregs that suppress the activity of other immune cells—without inhibiting effector cell responses—and thereby supports the control of solid tumors. 

Tusk was gearing up to test that idea in a phase 1 trial next year but has instead opted to sell up to Roche. The Big Pharma is acquiring the preclinical antibody for €70 million upfront and up to €585 million in milestones. As a result of the deal, Tusk is spinning out its remaining, earlier-stage assets into a new biotech, Black Belt Therapeutics. 


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Roche will now take responsibility for getting the antibody into humans around the end of next year. That puts Roche, once again, at the fore of efforts to deplete the Tregs of cancer patients by targeting CD25.  

Researchers have been depleting Tregs in animal models using anti-CD25 antibodies for decades and Roche won approval for a now-withdrawn drug against the target in 1997. Roche’s drug, daclizumab, was used to treat multiple sclerosis and prevent rejection of kidney transplants. Researchers trialed the drug in cancers including leukemia, too, but the anti-tumor potential of CD25 remains unrealized. 

Roche’s belief that Tusk’s antibody may be the drug to realize that potential rests, in part, on data suggesting it doesn’t block IL2 signaling. Tusk and its collaborators at UCL set out to develop a drug that targeted CD25 without interfering with IL2 signaling after generating evidence that the efficacy of existing antibodies was limited by their effect on the latter pathway.

Understanding of the nature of Tregs and related pathways is still evolving. But, backed by evidence that the antibody depletes regulatory cells while allowing effector T cells to proliferate, Tusk thinks it may be on to a winner.  

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