Catenaa, Friday, October 24, 2025- Scientists from the Francis Crick Institute and Vividion Therapeutics have developed compounds that selectively block the interaction between the cancer-driving RAS gene and the PI3K enzyme, halting tumor growth without harming healthy cells. The discovery has advanced to its first human clinical trial.
RAS mutations, found in roughly one in five cancers, lock the protein in an active state, triggering uncontrolled cell growth.
Directly inhibiting RAS or PI3K has previously caused side effects, including hyperglycemia, because of their essential roles in normal cell function.
The new compounds, however, prevent RAS and PI3K from binding while leaving other PI3K functions intact.
Preclinical studies in mice with RAS-mutated lung tumors showed that the compound halted tumor growth without adverse metabolic effects.
Testing in combination with other RAS-pathway inhibitors produced stronger and longer-lasting tumor suppression.
Experiments on HER2-mutated tumors, common in breast cancer, also showed growth inhibition, suggesting the approach could target multiple cancer types.
The first human trials will assess safety, side effects, and efficacy, including combination therapy potential. Julian Downward, principal group leader at the Crick, highlighted that targeting the RAS–PI3K interaction could overcome years of therapeutic challenges.
Vividion’s Chief Scientific Officer, Matt Patricelli, emphasized that the approach selectively blocks a key cancer growth signal while preserving healthy cell processes.
