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Protein / target

Plasminogen

Encoded byPLGP00747Homo sapiensSwiss-Prot
Clinically validated
Therapeutic maturity
7
Approved medicines
Open Targets target-level
20
Clinical trials
Small-molecule tractable
Druggability
Approved Drug

Protein at a glance

Biological role

Serine-type endopeptidase

Strongest disease association

Angioedemas, Hereditary

Via encoding gene PLG · Genetic evidence · score 0.87

Therapeutic position

Established drug target

Small molecules

Research activity

Emerging research

1 papers · latest 2023

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

Protease which primary function is to degrade fibrin, the main component of blood clots.

View complete UniProt function annotation

Protease which primary function is to degrade fibrin, the main component of blood clots (PubMed:6094526, PubMed:6919539). Also cleaves other components of blood clots like thrombospondin-1/THBS1 and von Willebrand factor/VWF (PubMed:24449821, PubMed:7679575). Can also directly and/or through the activation of other proteases degrade the various components of the extracellular matrix including collagen, fibronectin and laminin (PubMed:14699093, PubMed:28849762, PubMed:9171346). Thereby, regulates a variety of biological processes including embryonic development, tissue remodeling, and inflammation (PubMed:9171346). In ovulation, weakens the walls of the Graafian follicle (By similarity). In vitro, it is also able to cleave several complement zymogens, such as C1, C4 and C5 (PubMed:6447255)

Subcellular location

Secreted
Domains and Gene Ontology detail (42)

Domains & features

PANKringle 1Kringle 2Kringle 3Kringle 4Kringle 5Peptidase S1

Gene Ontology

  • Cblood microparticle
  • Ccell surface
  • Cexternal side of plasma membrane
  • Cextracellular exosome
  • Cextracellular matrix
  • Cextracellular region
  • Cextracellular space
  • Cglutamatergic synapse
  • Cplasma membrane
  • Cplatelet alpha granule lumen
  • CSchaffer collateral - CA1 synapse
  • Fapolipoprotein binding

810 aa · 91 kDa

Biological roles

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

Synaptic signallingGOCell migrationGOCell adhesionUniProt · GOProteolysisUniProt · GOHaemostasisUniProt · GO
View supporting evidence

Synaptic signalling

  • ·glutamatergic synapse
  • ·Schaffer collateral - CA1 synapse
  • ·trans-synaptic signaling by BDNF, modulating synaptic transmission

Cell migration

  • ·positive regulation of blood vessel endothelial cell migration

Cell adhesion

  • ·Protease which primary function is to degrade fibrin, the main component of blood clots…
  • ·extracellular matrix
  • ·extracellular matrix disassembly
  • ·negative regulation of cell-cell adhesion mediated by cadherin

Proteolysis

  • ·Protease which primary function is to degrade fibrin, the main component of blood clots…
  • ·endopeptidase activity
  • ·protease binding
  • ·serine-type endopeptidase activity

Haemostasis

  • ·Protease which primary function is to degrade fibrin, the main component of blood clots…
  • ·platelet alpha granule lumen
  • ·blood coagulation
  • ·fibrinolysis

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

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.

defibrotide
ApprovedActivator

Plasminogen activator

Direct interaction with this protein · 1 of 5 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 PLG

Gene-level evidence surfaced through the gene PLG that 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.

Angioedemas, Hereditary
0.93Well supported

Genetic evidence dominant · Open Targets 0.74

Myocardial Infarction
0.88Well supported

Genetic evidence dominant · Open Targets 0.56

Coronary Artery Disease
0.82Well supported

Genetic evidence dominant · Open Targets 0.51

Atrial Fibrillation
0.80Well supported

Genetic evidence dominant · Open Targets 0.49

Hepatic veno-occlusive disease
0.74Moderately supported

Clinical evidence dominant · Open Targets 0.58

View evidence synthesis (5)
Angioedemas, HereditaryWell supported
0.93
agreement 0.831.00
Genetic60%Clinical22%Animal model10%Literature7%Genetic literaturedup

Open Targets aggregate 0.74 · 4 independent evidence families · 1 not counted as duplicate

Myocardial InfarctionWell supported
0.88
agreement 0.770.98
Genetic58%Clinical35%Literature7%

Open Targets aggregate 0.56 · 3 independent evidence families

Coronary Artery DiseaseWell supported
0.82
agreement 0.680.96
Genetic91%Literature9%

Open Targets aggregate 0.51 · 2 independent evidence families

Atrial FibrillationWell supported
0.80
agreement 0.660.94
Genetic90%Literature10%

Open Targets aggregate 0.49 · 2 independent evidence families

Hepatic veno-occlusive diseaseModerately supported
0.74
agreement 0.610.87
Clinical84%Animal model16%Literature0%

Open Targets aggregate 0.58 · 3 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
Angioedemas, Hereditary0.74
Hepatic veno-occlusive disease0.58
Myocardial Infarction0.56
Coronary Artery Disease0.51
Atrial Fibrillation0.49

Drug development

9 compounds recorded · 7 approved · 2 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: these count different sets and are not a subset relation.

View all recorded compounds (9)
AMINOCAPROIC ACIDApproval
AMEDIPLASEPhase 3
DESMOTEPLASEPhase 3
TRANEXAMIC ACIDApproval
DEFIBROTIDEApproval
STREPTOKINASEApproval
ANISTREPLASEApproval
DEFIBROTIDE SODIUMApproval
APROTININApproval

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 (half-life data and small molecule binder) — no clinical-stage drug of this modality recorded.

Other modalitiesStrong

Approved Drug support this modality.

View underlying tractability evidence (11)
SM · Approved DrugSM · Structure with LigandSM · High-Quality LigandSM · Med-Quality PocketSM · Druggable FamilyAB · UniProt loc high confAB · GO CC high confAB · UniProt SigP or TMHMMPR · Half-life DataPR · Small Molecule BinderOC · Approved Drug

Raw Open Targets tractability assessment buckets, by modality.

Clinical trials

20

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 (16)

ClinicalTrials.gov via the drug-target graph.

What's happening now

2

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. Regulatory approval2013-10-18

    Approval: Defitelio (EMA)

    ema · regulatory · ema · via defibrotide

  2. New publication2002-08-01
    Multi-institutional use of defibrotide in 88 patients after stem cell transplantation with severe veno-occlusive disease and multisystem organ failure: response without significant toxicity in a high-risk population and factors predictive of outcome.

    Blood · 2002 · 194 citations · Europe PMC · via defibrotide

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.

Research activity

1 papers · to 2023

Papers linked directly to this protein. This is the protein's own literature — descriptor-derived papers are kept separate below.

Most cited

Vinci P · International journal of environmental research and public health · 2023

Recent

Lipoprotein(a) as a Risk Factor for Cardiovascular Diseases: Pathophysiology and Treatment Perspectives.

Vinci P · International journal of environmental research and public health · 2023

Europe PMC papers linked directly to this protein.

Related family literature

1

Papers about “Serine Proteases” — a broader family this protein belongs to. Shown as context; not counted as papers specifically about this protein.

Lipoprotein(a) as a Risk Factor for Cardiovascular Diseases: Pathophysiology and Treatment Perspectives.

Vinci P · International journal of environmental research and public health · 2023

via Serine Proteases

Europe PMC literature, reached through curated HGNC family membership. Membership is a taxonomic relationship — it does not imply this protein participates in every mechanism these papers discuss.