Boehringer Ingelheim and Tessellate Bio tackle hard-to-treat cancers in €500m deal

Cancer continues to be one of the leading challenges in medicine and treatment options for many cancers remain limited.

Tessellate Bio is entitled to receive near-term payments including an upfront licence fee, research funding and technical milestone payments - as well as downstream success-based milestones - with an overall deal value in excess of €500 million. This is its first deal in the field of pharma.

German business Boehringer Ingelheim is committed to changing the current impasse in a challenging field of medicine.

The new collaboration with Tessellate Bio, a Dutch company with a base at Stevenage Bioscience Catalyst, aims to develop treatments targeting tumours dependent on alternative lengthening of telomeres (ALT) for their growth. This feature is present in 10-15 per cent of all cancers and associated with poor prognosis and a lack of targeted therapies.

“We look forward to working with Tessellate Bio’s team of scientists to develop innovative cancer treatments based on their synthetic lethality approach targeting ALT positive tumours," said Lamine Mbow, Global Head of Discovery Research at Boehringer Ingelheim.

"This new collaboration complements our oncology research portfolio and further reinforces our commitment to transforming the lives of people living with cancer."

Andree Blaukat, CEO, Tessellate Bio added: “This is our first pharma collaboration and we believe that Boehringer Ingelheim is the ideal partner to advance this innovative program to benefit patients with ALT positive cancers.

“The company has a proven commitment to oncology and the agreement aligns with our collaborative strategy for bringing new targeted treatment options based on the concept of synthetic lethality to patients across a wider range of cancers.”

Tessellate Bio has developed inhibitors of an undisclosed target that plays a key role in enabling the uncontrolled growth of ALT positive cancer cells. Blocking this target has been shown to lead to increased DNA damage, replication stress and ultimately tumour cell death, specifically in ALT positive tumour cells. A clear benefit is that healthy cells are not affected because they have no dependency on this mechanism.