ARX788, a site-specific next-generation anti-HER2 ADC, employs an unnatural amino acid to conjugate cytotoxic drug with a highly stable oxime bond, resulting in superior stability and an extended half-life of 12.5 days in mice. In xenograft and PDX animal models, ARX788 demonstrates strong activity in breast and gastric tumors with both high HER2 and low HER2 expression levels. ARX788 is also highly effective in T-DM1 resistant PDX models. The encouraging preclinical data warrant further investigation of ARX788, which is currently in multi-regional clinical trials.

HRAS is exclusively dependent on farnesylation, a post-translational modification that is required for inserting the protein into the cell membrane and for aspects of signaling. Therefore, Gilardi and colleagues investigated the use of a farnesyltransferase inhibitor, tipifarnib, in restricting HRAS mutant cancer cells. Tipifarnib reduced MAPK signaling and generated cytostatic or cytotoxic responses in six HRAS mutant xenografts. Based on their findings, tipifarnib represents a candidate...

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