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This research aims to evaluate the efficacy of a PROTAC pan-KRAS degrader against traditional inhibitors in mutant KRAS models.

Abstract PR008: Preclinical activity of an orally bioavailable PROTAC pan-KRAS degrader versus inhibitors in mutant KRAS models

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This research aims to evaluate the efficacy of a PROTAC pan-KRAS degrader against traditional inhibitors in mutant KRAS models.
Identified and characterized a PROTAC pan-KRAS degrader targeting various KRAS mutations.
Conducted degradation assays in mutant KRAS cell lines.
Evaluated the impact on MAPK pathway and apoptosis in spheroid models.
Performed in vivo efficacy tests in xenograft models of various cancers.
Analyzed protein modulation through proteomic analysis.
The PROTAC induced potent degradation across multiple KRAS mutations with minimal off-target effects.
In xenograft models, the PROTAC displayed significant tumor regressions and MAPK pathway inhibition.
Superior apoptosis induction was observed compared to clinical pan-KRAS inhibitors.
In CRCA models, tumor growth inhibition was higher for the PROTAC than for a pan-RAS(ON) inhibitor.
PROTAC treatment showed enhanced immunological memory in syngeneic models.

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Preclinical activity reveals that PROTAC KRAS degraders induce tumor regression in mutant KRAS models, suggesting a new therapeutic approach.

Lopez-Arroyo et al. (2026) studied this question.

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Preclinical activity reveals that PROTAC KRAS degraders induce tumor regression in mutant KRAS models, suggesting a new therapeutic approach.