The tri-complex inhibitors can effectively stimulate GTP hydrolysis in RAS mutants, thereby enhancing therapeutic effects specifically for certain mutation types within oncogenic RAS.
Our findings indicate that by modulating the switch II motif of RAS, these inhibitors not only block downstream signaling but also restore GTPase activity.
The targeted therapies using tri-complex inhibitors represent a significant advance due to their dual mechanism of action—both inhibiting RAS-associated signaling and restoring enzyme function.
The data reveals that RAS mutants, which respond to enhanced GTPase activity, show significantly improved therapeutic outcomes with this new class of drugs.
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