Back to discover

Protein / target

GTPase KRas

Encoded byKRASP01116Homo sapiensSwiss-Prot
Clinically validated
Therapeutic maturity
2
Approved medicines
Open Targets target-level
View by indication →
30
Clinical trials
Small-molecule tractable
Druggability
Approved Drug

Protein at a glance

Biological role

Protein-containing complex binding

Strongest disease association

Noonan syndrome 3

Via encoding gene KRAS · Genetic evidence · score 0.94

Therapeutic position

Established drug target

Small molecules

Derived from structured UniProt, Open Targets and literature data on this page.

Protein profile

UniProt 2026_02

Canonical identity and biological annotation from UniProt.

Function overview

Signal transducer in the Ras-MAPK signaling pathway that regulates cell proliferation and survival.

View complete UniProt function annotation

Signal transducer in the Ras-MAPK signaling pathway that regulates cell proliferation and survival (PubMed:22711838, PubMed:23698361). Ras proteins bind GDP/GTP and possess intrinsic GTPase activity (PubMed:20949621, PubMed:39809765). Activates MAPK1/MAPK3 resulting in phosphorylation and ultimately degradation of GJA1 (By similarity). Plays a role in promoting oncogenic events by inducing transcriptional silencing of tumor suppressor genes (TSGs) in colorectal cancer (CRC) cells in a ZNF304-dependent manner (PubMed:24623306). Recognized by LZTR1 that mediates its ubiquitination by a BCR (BTB-CUL3-RBX1) E3 ubiquitin-protein ligase complex (PubMed:40934300)

Subcellular location

Cell membraneEndomembrane systemCytoplasm
Domains and Gene Ontology detail (33)

Gene Ontology

  • Ccytoplasm
  • Ccytoplasmic side of plasma membrane
  • Ccytosol
  • Cendoplasmic reticulum membrane
  • Cfocal adhesion
  • CGolgi membrane
  • Cmembrane
  • Cmitochondrial outer membrane
  • Cplasma membrane
  • FG protein activity
  • FGDP binding
  • FGMP binding

189 aa · 22 kDa · 2 isoforms

Biological roles

Reactome v97

What this protein does, drawn together from its UniProt function, Gene Ontology terms and Reactome pathways.

Oncogenic signallingUniProt · ReactomeReceptor tyrosine kinase signallingReactomeGrowth-factor signallingReactomeCell proliferation & survivalGOImmune signallingGO · ReactomeTranscriptional regulationUniProt · GO
View supporting evidence

Oncogenic signalling

  • ·Signal transducer in the Ras-MAPK signaling pathway that regulates cell proliferation an…
  • ·Constitutive Signaling by Ligand-Responsive EGFR Cancer Variants

Receptor tyrosine kinase signalling

  • ·SHC1 events in ERBB2 signaling
  • ·SHC1 events in ERBB4 signaling
  • ·GRB2 events in ERBB2 signaling

Growth-factor signalling

  • ·Constitutive Signaling by EGFRvIII

Cell proliferation & survival

  • ·positive regulation of cell population proliferation

Immune signalling

  • ·cytokine-mediated signaling pathway
  • ·Activation of RAS in B cells

Transcriptional regulation

  • ·Signal transducer in the Ras-MAPK signaling pathway that regulates cell proliferation an…
  • ·positive regulation of gene expression
View underlying pathways (25)

Concepts derived from UniProt GO Reactome — each badge above shows which sources supported that role.

Interaction neighbourhood

STRING v12.0

Proteins with the strongest functional or physical association. Node size and line weight reflect STRING confidence; hover or select a partner to inspect one association.

RALGDSBRAFSOS1RAF1CALML5CALML3CALM3CALML6CALML4PIK3CAKRAS

10 strongest partners — larger node and heavier line mean higher confidence

Functional and physical associations from STRING v12.0. Only associations with this protein are drawn — partner-to-partner links are not part of this evidence.

Approved medicines with mapped indications

2 medicines · 2 areas

Approved therapies targeting this protein, grouped by what they are approved to treat — the disease-first view of the medicines below. Relationships come from the canonical approved-indication graph (ChEMBL phase-4), the same source as the drug cards.

Carcinoma, Non-Small-Cell Lung2 medicines
Broader indication categories (1)
Neoplasms2 medicines

Broad umbrella indications (e.g. “Neoplasms”). Shown here because every medicine also appears under a more specific disease above — kept for completeness, de-emphasised for clarity.

Approved indications from ChEMBL (phase-4), via the canonical drug→disease graph.

Drugs targeting this protein

2

How approved and investigational drugs engage this protein — mechanism and action type, direct vs complex targeting, and how broadly each acts across other targets. A drug-first view (the section above groups the approved ones disease-first); direct binders with few recorded targets are listed first.

adagrasib
Narrow target profileApprovedInhibitor

GTPase KRas inhibitor

Indicated for Carcinoma, Non-Small-Cell Lung, Neoplasms

Direct interaction with this protein · Only this protein recorded as a target

sotorasib
Narrow target profileApprovedInhibitor

GTPase KRas inhibitor

Indicated for Carcinoma, Non-Small-Cell Lung, Neoplasms

Direct interaction with this protein · Only this protein recorded as a target

ChEMBL mechanism, action type, target identity and approved indications. Open Targets clinical status.

Translational evidence

Open Targets 26

Why this target matters therapeutically, strongest evidence first. Disease associations are gene-level (via the gene that encodes this protein) and open into the full confidence synthesis; the development universe, tractability and safety annotations are target-level, from Open Targets.

Strongest disease associations · via encoding gene KRAS

Gene-level evidence surfaced through the gene KRASthat encodes this protein — not a direct protein–disease relationship. Ranked by Forefront's causal-directness weighting, so genetically- and clinically-evidenced diseases lead over ones that merely share the literature.

Stomach Neoplasms
0.95Well supported

Genetic evidence dominant · Open Targets 0.77

Leukemia, Myeloid, Acute
0.95Well supported

Genetic evidence dominant · Open Targets 0.75

Noonan syndrome 3
0.95Well supported

Genetic evidence dominant · Open Targets 0.83

Toriello-Lacassie-Droste syndrome
0.94Well supported

Genetic evidence dominant · Open Targets 0.74

Noonan syndrome
0.93Well supported

Genetic evidence dominant · Open Targets 0.83

View evidence synthesis (5)
Stomach NeoplasmsWell supported
0.95
agreement 0.841.00
Genetic61%Somatic mutation30%Literature10%Genetic literaturedup

Open Targets aggregate 0.77 · 3 independent evidence families · 1 not counted as duplicate

Leukemia, Myeloid, AcuteWell supported
0.95
agreement 0.861.00
Genetic42%Somatic mutation27%Animal model13%Pathway12%Literature7%Genetic literaturedup

Open Targets aggregate 0.75 · 5 independent evidence families · 1 not counted as duplicate

Noonan syndrome 3Well supported
0.95
agreement 0.831.00
Genetic89%Animal model10%Literature0%Genetic literaturedup

Open Targets aggregate 0.83 · 3 independent evidence families · 1 not counted as duplicate

Toriello-Lacassie-Droste syndromeWell supported
0.94
agreement 0.831.00
Genetic62%Somatic mutation36%Literature2%Genetic literaturedup

Open Targets aggregate 0.74 · 3 independent evidence families · 1 not counted as duplicate

Noonan syndromeWell supported
0.93
agreement 0.821.00
Genetic61%Pathway26%Animal model12%Literature2%Genetic literaturedup

Open Targets aggregate 0.83 · 4 independent evidence families · 1 not counted as duplicate

This ranking differs from Open Targets' own: re-weighting moves genetically-evidenced diseases above more heavily co-mentioned ones. The evidence agreement range shows how closely the independent evidence families agree — it is not a statistical confidence interval, and nothing here is fitted to outcome data. Derived from Open Targets evidence types under Forefront weighting; the per-type scores above show the calculation.

Show all associations
Noonan syndrome0.83
Noonan syndrome 30.83
Cardiofaciocutaneous syndrome 20.82
Cardiofaciocutaneous syndrome0.82
Carcinoma, Non-Small-Cell Lung0.80
Stomach Neoplasms0.77
Leukemia, Myeloid, Acute0.75
Linear nevus sebaceous syndrome0.74
Toriello-Lacassie-Droste syndrome0.74
Linear nevus sebaceus syndrome0.73

Drug development

3 compounds recorded · 2 approved · 1 in clinical development

Open Targets' development universe — every compound recorded against the target at any stage, not all approved medicines. Distinct from the 2 drugs that target this protein in Forefront's canonical graph (2 with a mapped approved indication, shown above): these count different sets and are not a subset relation.

View all recorded compounds (3)
SOTORASIBApproval
ADAGRASIBApproval
SALIRASIBPhase 2

Open Targets known-drugs universe. Drug name and highest clinical stage only — the disease relationship is NOT read from this slice (it carries trial-context noise); approved indications come from the canonical graph above.

Tractability

Small moleculesStrong

Approved Drug and Structure with Ligand support this modality.

AntibodiesEmerging

Feasibility evidence (uniprot loc high conf and go cc high conf) — no clinical-stage drug of this modality recorded.

Protein degradersEmerging

Feasibility evidence (literature and uniprot ubiquitination) — no clinical-stage drug of this modality recorded.

View underlying tractability evidence (10)
SM · Approved DrugSM · Structure with LigandSM · High-Quality LigandAB · UniProt loc high confAB · GO CC high confPR · LiteraturePR · UniProt UbiquitinationPR · Database UbiquitinationPR · Half-life DataPR · Small Molecule Binder

Raw Open Targets tractability assessment buckets, by modality.

Clinical trials

30

Trials of drugs that target this protein — reached indirectly through those drugs, so a trial listed here studies the drug, not the protein. Ranked by active status, then clinical phase and recency, and spread across the targeting drugs.

View all trials (26)

RECRUITING · via sotorasib · NCT05564377

ACTIVE_NOT_RECRUITING · via adagrasib · NCT03994796

RECRUITING · via sotorasib · NCT06807619

ClinicalTrials.gov via the drug-target graph.

What's happening now

6

Recent therapeutic activity around this target — regulatory actions, clinical trials and safety signals for 2 drugs that target this protein, plus publications where such a drug is a genuine subject. Every item is reached indirectly through the drug, not the protein itself; incidental mentions (a paper that merely measures a drug) and press items are excluded.

  1. New publication2024-06-01
    Efficacy and Safety of Adagrasib plus Cetuximab in Patients with KRASG12C-Mutated Metastatic Colorectal Cancer.

    Cancer discovery · 2024 · 81 citations · Europe PMC · via adagrasib

  2. Regulatory approval2024-01-05

    Approval: Krazati (EMA)

    ema · regulatory · ema · via adagrasib

  3. New publication2022-12-21
    Adagrasib with or without Cetuximab in Colorectal Cancer with Mutated <i>KRAS</i> G12C.

    The New England journal of medicine · 2023 · 394 citations · Europe PMC · via adagrasib

  4. New publication2022-12-21
    Sotorasib in <i>KRAS</i> p.G12C-Mutated Advanced Pancreatic Cancer.

    The New England journal of medicine · 2023 · 391 citations · Europe PMC · via sotorasib

  5. New publication2022-06-03
    Adagrasib in Non-Small-Cell Lung Cancer Harboring a <i>KRAS<sup>G12C</sup></i> Mutation.

    The New England journal of medicine · 2022 · 696 citations · Europe PMC · via adagrasib

  6. Regulatory approval2022-01-06

    Approval: Lumykras (EMA)

    ema · regulatory · ema · via sotorasib

Objective event titles are shown unmodified; the event kind and significance line are derived from structured fields. Forefront AttentionEvent stream aggregating Europe PMC Regulatory filings ClinicalTrials.gov.