To combat resistance to drugs like Osimertinib, Blossom Hill designed a molecule potent against the C797S resistance mutation and equally potent against original mutations. This dual efficacy, preventing cancer evolution, is central to their promising clinical results and is a key design principle for durable cancer therapies.
CEO Jean Cui is not just a manager but the company's scientific engine. Drawing on her experience designing three previously FDA-approved drugs, she personally created Blossom Hill's clinical assets. This model of a proven Scientific Founder leading both drug design and corporate strategy provides deep, integrated expertise from the top.
Blossom Hill is developing a 'switch two' allosteric pan-KRAS inhibitor. Unlike tri-complex molecules that block protein interaction but may not fully stop signaling, their approach 'rigidifies' the KRAS protein. This completely shuts down the signaling cycle, potentially offering superior durability and preventing the evolution of resistance.
Faced with the 'undruggable' switch two pocket in KRAS, Blossom Hill modifies the drug's properties rather than the protein target. By engineering a molecule with 'pseudo irreversible' characteristics, they create a long-lasting effect that compensates for the challenging binding pocket, thereby enhancing in-vivo efficacy.