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Protein / target

Renin

Encoded byRENP00797Homo sapiensSwiss-Prot
Clinically validated
Therapeutic maturity
2
Approved medicines
Open Targets target-level
Small-molecule tractable
Druggability
Approved Drug
1
Research papers

Protein at a glance

Biological role

Insulin-like growth factor receptor binding

Strongest disease association

Renal tubular dysgenesis

Via encoding gene REN · Genetic literature evidence · score 0.83

Therapeutic position

Established drug target

Small molecules

Research activity

Emerging research

1 papers · latest 2024

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

Renin is a highly specific endopeptidase, whose only known function is to generate angiotensin I from angiotensinogen in the plasma, initiating a cascade of reactions that produce an elevation of blood pressure and increased sodium retention by the kidney

Subcellular location

SecretedMembrane
Domains and Gene Ontology detail (22)

Domains & features

Peptidase A1

Gene Ontology

  • Capical part of cell
  • Cextracellular region
  • Cextracellular space
  • Cplasma membrane
  • Faspartic-type endopeptidase activity
  • Finsulin-like growth factor receptor binding
  • Fpeptidase activity
  • Fsignaling receptor binding
  • Pangiotensin maturation
  • Pcellular response to xenobiotic stimulus
  • Pjuxtaglomerular apparatus development
  • Pkidney development

406 aa · 45 kDa · 2 isoforms

Biological roles

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

ProteolysisGO
View supporting evidence

Proteolysis

  • ·aspartic-type endopeptidase activity
  • ·peptidase activity
  • ·proteolysis

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

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 REN

Gene-level evidence surfaced through the gene REN 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.

Renal tubular dysgenesis
0.85Well supported

Genetic evidence dominant · Open Targets 0.74

Hypertension
0.83Well supported

Clinical evidence dominant · Open Targets 0.64

Renal tubular dysgenesis of genetic origin
0.83Well supported

Genetic evidence dominant · Open Targets 0.73

Genetic Diseases, Inborn
0.68Moderately supported

Genetic evidence dominant · Open Targets 0.42

Stroke
0.59Moderately supported

Clinical evidence dominant · Open Targets 0.47

View evidence synthesis (5)
Renal tubular dysgenesisWell supported
0.85
agreement 0.730.97
Genetic82%Animal model17%Literature1%Genetic literaturedup

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

HypertensionWell supported
0.83
agreement 0.730.94
Clinical63%Genetic25%Literature12%

Open Targets aggregate 0.64 · 3 independent evidence families

Renal tubular dysgenesis of genetic originWell supported
0.83
agreement 0.710.95
Genetic81%Animal model18%Literature2%Genetic literaturedup

Open Targets aggregate 0.73 · 3 independent evidence families · 1 not counted as duplicate

Genetic Diseases, InbornModerately supported
0.68
agreement 0.550.82
Genetic99%Literature1%

Open Targets aggregate 0.42 · 2 independent evidence families

StrokeModerately supported
0.59
agreement 0.430.74
Clinical94%Literature6%

Open Targets aggregate 0.47 · 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
Renal tubular dysgenesis0.74
Renal tubular dysgenesis of genetic origin0.73
Hypertension0.64
Stroke0.47
Essential Hypertension0.43
Genetic Diseases, Inborn0.42
Cardiovascular Diseases0.38

Drug development

4 compounds recorded · 2 approved · 2 in clinical development

Open Targets' development universe — every compound recorded against the target at any stage, not all approved medicines.

View all recorded compounds (4)
ALISKIREN FUMARATEApproval
ALISKIRENApproval
SITOKIRENPhase 3
IMARIKIREN HYDROCHLORIDEPhase 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 (small molecule binder) — no clinical-stage drug of this modality recorded.

View underlying tractability evidence (9)
SM · Approved DrugSM · Structure with LigandSM · High-Quality LigandSM · High-Quality PocketSM · Druggable FamilyAB · UniProt loc high confAB · GO CC high confAB · UniProt SigP or TMHMMPR · Small Molecule Binder

Raw Open Targets tractability assessment buckets, by modality.

Safety-related annotations

edemaClinPGx

Terms indexed against this target in Open Targets' safety data, with their datasource. These are annotations, not causal claims: the direction of effect (whether activation or inhibition is implicated), species and evidence strength are not captured here, so an entry does not mean that modulating this target is known to cause that condition.

Research activity

1 papers · to 2024

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

Most cited

Recent

Europe PMC papers linked directly to this protein.