Roche ends Relay Therapeutics SHP2 inhibitor deal

Roche has withdrawn from its partnership with Relay Therapeutics to develop the SHP2 inhibitor RLY-1971, marking another instance of a major pharmaceutical company stepping back from this particular area of cancer research. Relay Therapeutics revealed this development in a filing with the US Securities and Exchange Commission (SEC), indicating that Roche terminated the agreement "without cause."

The agreement between the two companies was initially signed in 2020. Under the terms of this deal, Roche’s Genentech unit made an upfront payment of $75 million to acquire the rights to RLY-1971, also known as migoprotafib or GDC-1971. At the time, the Swiss pharmaceutical giant announced plans to explore the oral cancer drug in conjunction with its KRAS G12C inhibitor, GDC-6036.

The SEC filing from Relay Therapeutics disclosed that, including the initial payment, the company received a total of $121.8 million from Genentech. This sum comprises $45 million in milestone payments and the reimbursement of specific research and development costs.

This isn't the first instance of a major pharmaceutical company retracting its involvement in SHP2 inhibitor development. Last year, AbbVie concluded its collaboration with Jacobio Pharmaceuticals, which was focused on SHP2 inhibitors. Similarly, Sanofi previously terminated its partnership with Revolution Medicines, which aimed at developing cancer treatments targeting SHP2.

The trend of major pharmaceutical companies pulling away from SHP2 inhibitor collaborations suggests a reassessment of the viability or strategic importance of this approach in cancer treatment. Each of these partnerships showed initial promise but ultimately did not lead to sustained collaborations.

In summary, Roche's exit from the agreement with Relay Therapeutics underscores a broader pattern within the industry. The termination, though officially "without cause," aligns with similar moves by other pharma giants such as AbbVie and Sanofi, reflecting the evolving landscape of cancer drug development and the challenges inherent in targeting SHP2.