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Selective Inhibition of Oncogenic KRAS Output with Small Molecules Targeting the Inactive State.

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Cancer Discov2016PMID 26739882stubpubmedProvenance
Source
PubMed
Retrieved
Sep 8, 2026
Layer
normalized (units and labels harmonized; values unchanged)
Run
ING-CIVIC-20260908-000001
Published

Abstract

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Linked entities

Linked entities (5)

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Validated 5

Curated evidence

Evidence citing this paper (1)

civicProvenance
Source
CIViC — Clinical Interpretation of Variants in Cancer
Dataset
CIViC evidence items
Version
civic-2026-09-08
Retrieved
Sep 8, 2026
Layer
normalized (units and labels harmonized; values unchanged)
Evidence
expert curation
License
CC0 1.0
PMID
26739882
Run
ING-CIVIC-20260908-000001
Open at source
CuratedShowing 1–1 of 1 evidence items · levels, directions and significance as curated at the source; each row links to its CIViC record.
TherapyCancerTypeLevelDirection · significanceRating (1–5)StatusEvidenceSource
KRAS G12C1
ARS-853 + Epidermal Growth Factor Receptor Tyrosine Kinase InhibitorCombinationMalignant NeoplasmALIASPredictiveDSupports Sensitivity Response3accepted
EID1173

Preclinical study to investigate mechanisms of KRAS G12C activity and inhibition with ARS-853, a covalent (irreversible) inhibitor which binds KRAS G12C in the GDP-bound state to prevent activation. R… (full text at CIViC)

PMID 26739882 · Patricelli et al., 2016 · Open in CIViC

civic