Protein / target

Angiotensin-converting enzyme

ACEP12821Homo sapiensSwiss-Prot
Clinically validated
Therapeutic maturity
22
Approved medicines
30
Clinical trials
Small-molecule tractable
Druggability
Approved Drug

Protein at a glance

Biological role

Mitogen-activated protein kinase kinase binding

Primary system

Nervous system

Strongest disease association

renal tubular dysgenesis

Genetic evidence · score 0.89

Therapeutic maturity

Clinically validated target

22 approved medicines against this target

Druggability

Small molecule

Open Targets tractability · Approved Drug

Clinical development

22 approved · 2 in clinical development

30 linked trials

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

Dipeptidyl carboxypeptidase that removes dipeptides from the C-terminus of a variety of circulating hormones, such as angiotensin I, bradykinin or enkephalins, thereby playing a key role in the regulation of blood pressure, electrolyte homeostasis or synaptic plasticity (PubMed:15615692, PubMed:20826823, PubMed:2558109, PubMed:4322742, PubMed:7523412, PubMed:7683654). Composed of two similar catalytic domains, each possessing a functional active site, with different selectivity for substrates (PubMed:10913258, PubMed:1320019, PubMed:1851160, PubMed:19773553, PubMed:7683654, PubMed:7876104). Plays a major role in the angiotensin-renin system that regulates blood pressure and sodium retention by the kidney by converting angiotensin I to angiotensin II, resulting in an increase of the vasoconstrictor activity of angiotensin (PubMed:11432860, PubMed:1851160, PubMed:19773553, PubMed:23056909, PubMed:4322742). Also able to inactivate bradykinin, a potent vasodilator, and therefore enhance the blood pressure response (PubMed:15615692, PubMed:2558109, PubMed:4322742, PubMed:6055465, PubMed:6270633, PubMed:7683654). Acts as a regulator of synaptic transmission by mediating cleavage of neuropeptide hormones, such as substance P, neurotensin or enkephalins (PubMed:15615692, PubMed:6208535, PubMed:6270633, PubMed:656131). Catalyzes degradation of different enkephalin neuropeptides (Met-enkephalin, Leu-enkephalin, Met-enkephalin-Arg-Phe and possibly Met-enkephalin-Arg-Gly-Leu) (PubMed:2982830, PubMed:6270633, PubMed:656131). Acts as a regulator of synaptic plasticity in the nucleus accumbens of the brain by mediating cleavage of Met-enkephalin-Arg-Phe, a strong ligand of Mu-type opioid receptor OPRM1, into Met-enkephalin (By similarity). Met-enkephalin-Arg-Phe cleavage by ACE decreases activation of OPRM1, leading to long-term synaptic potentiation of glutamate release (By similarity). Also acts as a regulator of hematopoietic stem cell differentiation by mediating degradation of hemoregulatory peptide N-acetyl-SDKP (AcSDKP) (PubMed:26403559, PubMed:7876104, PubMed:8257427, PubMed:8609242). Acts as a regulator of cannabinoid signaling pathway by mediating degradation of hemopressin, an antagonist peptide of the cannabinoid receptor CNR1 (PubMed:18077343). Involved in amyloid-beta metabolism by catalyzing degradation of Amyloid-beta protein 40 and Amyloid-beta protein 42 peptides, thereby preventing plaque formation (PubMed:11604391, PubMed:16154999, PubMed:19773553). Catalyzes cleavage of cholecystokinin (maturation of Cholecystokinin-8 and Cholecystokinin-5) and Gonadoliberin-1 (both maturation and degradation) hormones (PubMed:10336644, PubMed:2983326, PubMed:7683654, PubMed:9371719). Degradation of hemoregulatory peptide N-acetyl-SDKP (AcSDKP) and amyloid-beta proteins is mediated by the N-terminal catalytic domain, while angiotensin I and cholecystokinin cleavage is mediated by the C-terminal catalytic region (PubMed:10336644, PubMed:19773553, PubMed:7876104)

Subcellular location

Cell membraneCytoplasmSecreted
Domains and Gene Ontology detail (59)

Domains & features

Peptidase M2 1Peptidase M2 2

Gene Ontology

  • Cendosome
  • Cexternal side of plasma membrane
  • Cextracellular exosome
  • Cextracellular region
  • Cextracellular space
  • Clysosome
  • Cplasma membrane
  • Factin binding
  • Fbradykinin receptor binding
  • Fcalmodulin binding
  • Fchloride ion binding
  • Fendopeptidase activity

1306 aa · 150 kDa · 4 isoforms

Biological roles

Reactome v97

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

ProteolysisGOMetabolic enzyme activityGOKinase signallingGOTranscriptional regulationGOSynaptic signallingUniProtChloride transportGO
View supporting evidence

Proteolysis

  • ·endopeptidase activity
  • ·exopeptidase activity
  • ·metallocarboxypeptidase activity
  • ·metallodipeptidase activity

Metabolic enzyme activity

  • ·amyloid-beta metabolic process
  • ·hormone metabolic process
  • ·regulation of angiotensin metabolic process

Kinase signalling

  • ·mitogen-activated protein kinase binding
  • ·mitogen-activated protein kinase kinase binding

Transcriptional regulation

  • ·negative regulation of gene expression
  • ·post-transcriptional regulation of gene expression

Synaptic signalling

  • ·Dipeptidyl carboxypeptidase that removes dipeptides from the C-terminus of a variety of…

Chloride transport

  • ·chloride ion binding
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.

AGTKNG1RENAGTR1ACE2AGTR2BDKRB2ALBNR3C2MMEL1ACE

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.

Drugs targeting this protein

2

Whether each drug engages this protein directly or through a complex, and how many other targets are recorded for it. Direct binders with few recorded targets are listed first.

Captopril
Narrow target profileApprovedInhibitor

Angiotensin-converting enzyme inhibitor

Appears in clinical studies involving hypertensive disorder, myocardial infarction, congestive heart failure, diabetic kidney disease

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

Lisinopril
Narrow target profileApprovedInhibitor

Angiotensin-converting enzyme inhibitor

Appears in clinical studies involving hypertensive disorder, heart failure, stroke disorder, diabetes mellitus

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

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

Translational evidence

Open Targets 26

Why this target matters therapeutically — disease associations, drugs in development, tractability and safety, from Open Targets.

Strongest genetic associations

Human genetic evidence — the most direct causal link between this target and a disease.

renal tubular dysgenesis0.89

Genetic · overall 0.72

renal tubular dysgenesis of genetic origin0.84

Genetic · overall 0.72

hypertensive disorder0.81

Genetic · overall 0.74

cardiovascular disorder0.65

Genetic · overall 0.69

diabetic kidney disease0.61

Genetic literature · overall 0.69

Highest-confidence therapeutic associations

Diseases where a drug acting on this target has already reached clinical development.

Hypertension0.98

Clinical · overall 0.62

heart failure0.97

Clinical · overall 0.62

myocardial infarction0.97

Clinical · overall 0.61

congestive heart failure0.97

Clinical · overall 0.61

diabetes mellitus0.92

Clinical · overall 0.66

Show all associations
hypertensive disorder0.74
renal tubular dysgenesis0.72
renal tubular dysgenesis of genetic origin0.72
cardiovascular disorder0.69
diabetic kidney disease0.69
diabetes mellitus0.66
Hypertension0.62
heart failure0.62
congestive heart failure0.61
myocardial infarction0.61

Open Targets ranks 2,523 associations for this target and we store the top 10 by aggregated score. The long tail is largely literature co-mention and RNA-expression evidence, not evidence that this target drives those diseases.

Known drugs · 24 total

CILAZAPRILApproval

cardiovascular disorder · congestive heart failure

ENALAPRIL MALEATEApproval

hypertensive disorder · heart failure · congestive heart failure

PERINDOPRIL ARGININEApproval

hypertensive disorder · essential hypertension · Hypertension

ENALAPRILATApproval

Hypertension · hypertensive disorder · dilated cardiomyopathy

CAPTOPRILApproval

hypertensive disorder · myocardial infarction · congestive heart failure

DELAPRILApproval

cardiovascular disorder · hypertensive disorder

BENAZEPRIL HYDROCHLORIDEApproval

hypertensive disorder · diabetes mellitus · stroke disorder

MOEXIPRIL HYDROCHLORIDEApproval

hypertensive disorder

LISINOPRIL ANHYDROUSPhase 3

Stroke · coronary artery disorder · hypertensive disorder

IMIDAPRILApproval

cardiovascular disorder · Hypertension · type 2 diabetes mellitus

Tractability

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 · Database UbiquitinationPR · Half-life DataPR · Small Molecule Binder

Safety liabilities

proximal tubular degenerationincreased urine excretiongastrointestinal hemorrhagic erosion/ulcerdiabetes mellitusinterstitial cell infiltrationincreased risk spontaneous abortiondecreased blood pressureincreased urinary sodium excretionaspirin intolerancejuxtaglomerular cell hyperplasiahepatocytic vacuolar degenerationdecreased bone marrow erythropoiesis

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.

Show remaining trials (24)

WITHDRAWN · via Captopril · NCT01399424

COMPLETED · via Lisinopril · NCT01885559

COMPLETED · via Lisinopril · NCT00661895

ClinicalTrials.gov via the drug-target graph.

Forefront confidence

Synthesis

Our own weighting of the evidence behind each disease association. Human genetics and clinical evidence count for most; literature co-mention counts for little, because two entities sharing an abstract is not evidence that one drives the other.

hypertensive disorderWell supported
0.96
agreement 0.851.00
Genetic48%Clinical44%Literature8%

Open Targets aggregate 0.74 · 3 independent evidence families

renal tubular dysgenesisWell supported
0.91
agreement 0.791.00
Genetic84%Animal model15%Literature1%Genetic literaturedup

Open Targets aggregate 0.72 · 3 independent evidence families · 1 not counted as duplicate

cardiovascular disorderWell supported
0.91
agreement 0.801.00
Clinical51%Genetic45%Literature4%

Open Targets aggregate 0.69 · 3 independent evidence families

diabetes mellitusWell supported
0.90
agreement 0.800.99
Clinical46%Genetic37%Animal model10%Literature8%

Open Targets aggregate 0.66 · 4 independent evidence families

diabetic kidney diseaseWell supported
0.88
agreement 0.760.99
Clinical54%Genetic literature36%Literature10%

Open Targets aggregate 0.69 · 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 underlying per-type scores are shown above so the calculation can be checked.

What's happening now

3

Recent activity around this target, drawn from one canonical event stream. Every item is reached through 2 drugs that target this protein, so each event is news about that drug rather than about the protein directly.

  1. New publication2004-09-01
    Relation between renal dysfunction and cardiovascular outcomes after myocardial infarction.

    The New England journal of medicine · 2004 · 1,345 citations · Europe PMC · via Captopril

  2. New publication2003-11-10
    Valsartan, captopril, or both in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both.

    The New England journal of medicine · 2003 · 1,589 citations · Europe PMC · via Captopril

  3. New publication2000-09-01
    A novel angiotensin-converting enzyme-related carboxypeptidase (ACE2) converts angiotensin I to angiotensin 1-9.

    Circulation research · 2000 · 2,163 citations · Europe PMC · via Lisinopril

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.