Targeting the RAS-PI3Kα Interaction as an Efficacious & Tolerated Means of Inhibiting the PI3K/AKT Pathway in RAS-Diven Cancers
Time: 4:15 pm
day: Day Two
Details:
• Identification and functionalization of C242, unique to p110α, to disrupt RAS-driven activation of PI3Kα
• Pre-clinical models identify disruption of the RAS-PI3Kα interaction as an efficacious and well tolerated means of targeting the PI3K/AKT pathway
• Detailed mechanistic exploration identifies the PI3K/AKT pathway as critical signaling node that drives resistance to direct targeting of KRAS-G12C. In both CDX and PDX models, addition of VVD’s RAS-PI3K disruptors to a KRAS-G12C inhibitor dosing schedule provide more profound and durable responses
