Back to discover

Protein / target

Macrophage-stimulating protein receptor

Encoded byMST1RQ04912Homo sapiensSwiss-Prot
Clinically validated
Therapeutic maturity
1
Approved medicines
Open Targets target-level
View by indication →
30
Clinical trials
Small-molecule tractable
Druggability
Phase 1 Clinical

Protein at a glance

Biological role

Transmembrane receptor protein tyrosine kinase

Strongest disease association

Nasopharyngeal Neoplasms

Via encoding gene MST1R · Genetic evidence · score 0.87

Therapeutic position

Established drug target

Small molecules and antibodies

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

Receptor tyrosine kinase that transduces signals from the extracellular matrix into the cytoplasm by binding to MST1 ligand.

View complete UniProt function annotation

Receptor tyrosine kinase that transduces signals from the extracellular matrix into the cytoplasm by binding to MST1 ligand. Regulates many physiological processes including cell survival, migration and differentiation. Ligand binding at the cell surface induces autophosphorylation of RON on its intracellular domain that provides docking sites for downstream signaling molecules. Following activation by ligand, interacts with the PI3-kinase subunit PIK3R1, PLCG1 or the adapter GAB1. Recruitment of these downstream effectors by RON leads to the activation of several signaling cascades including the RAS-ERK, PI3 kinase-AKT, or PLCgamma-PKC. RON signaling activates the wound healing response by promoting epithelial cell migration, proliferation as well as survival at the wound site. Also plays a role in the innate immune response by regulating the migration and phagocytic activity of macrophages. Alternatively, RON can also promote signals such as cell migration and proliferation in response to growth factors other than MST1 ligand

Subcellular location

Membrane
Domains and Gene Ontology detail (26)

Domains & features

SemaIPT/TIG 1IPT/TIG 2IPT/TIG 3Protein kinase

Gene Ontology

  • Ccell surface
  • Cplasma membrane
  • Creceptor complex
  • Cstress fiber
  • Cvacuole
  • FATP binding
  • Fenzyme binding
  • Fmacrophage colony-stimulating factor receptor activity
  • Ftransmembrane receptor protein tyrosine kinase activity
  • Pcell migration
  • Pcell surface receptor protein tyrosine kinase signaling pathway
  • Pdefense response

1400 aa · 152 kDa · 7 isoforms

Biological roles

Reactome v97

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

Receptor tyrosine kinase signallingUniProt · GOCell proliferation & survivalUniProt · GOCell migrationUniProt · GOImmune signallingUniProt · GO
View supporting evidence

Receptor tyrosine kinase signalling

  • ·Receptor tyrosine kinase that transduces signals from the extracellular matrix into the…
  • ·transmembrane receptor protein tyrosine kinase activity
  • ·cell surface receptor protein tyrosine kinase signaling pathway

Cell proliferation & survival

  • ·Receptor tyrosine kinase that transduces signals from the extracellular matrix into the…
  • ·positive regulation of cell population proliferation

Cell migration

  • ·Receptor tyrosine kinase that transduces signals from the extracellular matrix into the…
  • ·cell migration

Immune signalling

  • ·Receptor tyrosine kinase that transduces signals from the extracellular matrix into the…
  • ·innate immune response
View underlying pathways (1)

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.

MST1HGFHYAL2CBLSRSF1SPAM1EGFRCTNNB1GRB2PLXNB1MST1R

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

1 medicine · 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 Lung1 medicine
Broader indication categories (1)
Neoplasms1 medicine

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

1

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.

crizotinib
ApprovedInhibitor

Macrophage-stimulating protein receptor inhibitor

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

Direct interaction with this protein · 1 of 6 recorded protein targets

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 MST1R

Gene-level evidence surfaced through the gene MST1Rthat 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.

Nasopharyngeal Neoplasms
0.86Well supported

Genetic evidence dominant · Open Targets 0.62

Carcinoma, Non-Small-Cell Lung
0.74Moderately supported

Clinical evidence dominant · Open Targets 0.59

Neoplasms
0.54Moderately supported

Clinical evidence dominant · Open Targets 0.41

Nasopharyngeal Carcinoma
0.39Limited support

Genetic evidence dominant · Open Targets 0.23

Inflammatory myofibroblastic tumor
0.25Limited support

Clinical evidence dominant · Open Targets 0.20

View evidence synthesis (5)
Nasopharyngeal NeoplasmsWell supported
0.86
agreement 0.740.98
Genetic100%Genetic literaturedup

Open Targets aggregate 0.62 · 1 independent evidence family · 1 not counted as duplicate

Carcinoma, Non-Small-Cell LungModerately supported
0.74
agreement 0.580.89
Clinical89%Literature11%

Open Targets aggregate 0.59 · 2 independent evidence families

NeoplasmsModerately supported
0.54
agreement 0.390.70
Clinical76%Literature24%

Open Targets aggregate 0.41 · 2 independent evidence families

Nasopharyngeal CarcinomaLimited support
0.39
agreement 0.250.53
Genetic87%Literature13%

Open Targets aggregate 0.23 · 2 independent evidence families

Inflammatory myofibroblastic tumorLimited support
0.25
agreement 0.100.41
Clinical99%Literature1%

Open Targets aggregate 0.20 · 2 independent evidence families

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
Nasopharyngeal Neoplasms0.62
Carcinoma, Non-Small-Cell Lung0.59
Neoplasms0.41
Nasopharyngeal Carcinoma0.23
Inflammatory myofibroblastic tumor0.20
Diabetes Mellitus0.15

Drug development

4 compounds recorded · 1 approved · 3 in clinical development

Open Targets' development universe — every compound recorded against the target at any stage, not all approved medicines. Distinct from the 1 drug that targets this protein in Forefront's canonical graph (1 with a mapped approved indication, shown above): these count different sets and are not a subset relation.

View all recorded compounds (4)
NARNATUMABPhase 1
CRIZOTINIBApproval
GLESATINIBPhase 2
MK-8033Phase 1

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 moleculesSupported

Phase 1 Clinical and Structure with Ligand support this modality.

AntibodiesStrong

Advanced Clinical and GO CC high conf support this modality.

Protein degradersEmerging

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

View underlying tractability evidence (10)
SM · Phase 1 ClinicalSM · Structure with LigandSM · High-Quality LigandSM · Druggable FamilyAB · Advanced ClinicalAB · GO CC high confAB · UniProt SigP or TMHMMPR · UniProt UbiquitinationPR · Database UbiquitinationPR · 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)

ACTIVE_NOT_RECRUITING · via crizotinib · NCT06357975

ACTIVE_NOT_RECRUITING · via crizotinib · NCT02465060

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 a drug that targets 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 publication2024-05-31
    Lorlatinib Versus Crizotinib in Patients With Advanced <i>ALK</i>-Positive Non-Small Cell Lung Cancer: 5-Year Outcomes From the Phase III CROWN Study.

    Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2024 · 254 citations · Europe PMC · via crizotinib

  2. New publication2021-09-16
    Brigatinib Versus Crizotinib in ALK Inhibitor-Naive Advanced ALK-Positive NSCLC: Final Results of Phase 3 ALTA-1L Trial.

    Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2021 · 300 citations · Europe PMC · via crizotinib

  3. Safety communication2015-11-12

    Drug Safety Update: Crizotinib (Xalkori▼): risk of cardiac failure

    mhra · safety · mhra · via crizotinib

  4. New publication2014-12-01
    First-line crizotinib versus chemotherapy in ALK-positive lung cancer.

    The New England journal of medicine · 2014 · 2,470 citations · Europe PMC · via crizotinib

  5. Regulatory approval2012-10-23

    Approval: Xalkori (EMA)

    ema · regulatory · ema · via crizotinib

  6. New publication2012-01-03
    ROS1 rearrangements define a unique molecular class of lung cancers.

    Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2012 · 1,121 citations · Europe PMC · via crizotinib

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.