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The companies are entering into a license and collaboration agreement for the development and commercialization of Relay’s investigational cancer treatment, RLY-1971, a potent inhibitor of SHP2, a molecule that plays a role in cancer cell survival.
Genentech, a member of the Roche Group, and Relay Therapeutics, a clinical-stage precision medicine company located in the US, announced they are entering into a license and collaboration agreement for the development and commercialization of Relay’s RLY-1971, a potent inhibitor of Src homology region 2 domain-containing phosphatase-2 (SHP2), found to be a critical signaling node and regulator that promotes cancer cell survival and growth and that plays a key role in therapy resistance by cancer cells.
Under the terms of the agreement, Relay will receive an upfront payment of $75 million and will be eligible to receive $25 million in additional near-term payments, Relay said in a company press release. Genentech will develop RLY-1971 with the hope of expanding it into multiple combination studies, including with Genentech’s investigational inhibitor of KRAS G12C, GDC-6036.
“RLY-1971 has the potential to serve as a backbone for combination therapy across numerous solid tumors and therefore represents an encouraging approach for cancer patients,” said Sanjiv Patel, MD, president and CEO of Relay Therapeutics, in the press release. “Roche and Genentech’s global footprint and deep expertise in oncology makes them the perfect partner for us to execute the broad development and commercialization of RLY-1971.”
“Genentech has a longstanding commitment to understanding the underlying biology of KRAS, the most commonly mutated oncogene and an important driver of cancer growth,” added James Sabry, MD, PhD, global head of pharma partnering, Roche, in the press release. “We are excited to partner with Relay Therapeutics, and we believe that the combination of KRAS G12C and SHP2 inhibitors together represents a promising approach that we hope could become a new treatment option for patients with KRAS G12C mutant tumors.”