Protein / target

Carbonic anhydrase 9

Encoded byCA9Q16790Homo sapiensSwiss-Prot

UniProt: Q16790 Ensembl: ENSG00000107159 HGNC: HGNC:1383 NCBI Gene: 768

Clinically validated

Therapeutic maturity

Approved medicines

Open Targets target-level

Small-molecule tractable

Druggability

Approved Drug

Research papers

Protein at a glance

Biological role

Molecular function activator

Strongest disease association

Epilepsy

Via encoding gene CA9 · Clinical evidence · score 0.37

Therapeutic position

Established drug target

Small molecules and antibodies

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

Catalyzes the interconversion between carbon dioxide and water and the dissociated ions of carbonic acid (i.e.

View complete UniProt function annotation

Catalyzes the interconversion between carbon dioxide and water and the dissociated ions of carbonic acid (i.e. bicarbonate and hydrogen ions)

Subcellular location

NucleusNucleus, nucleolusCell membraneCell projection, microvillus membrane

Domains and Gene Ontology detail (12)

Domains & features

Alpha-carbonic anhydrase

Gene Ontology

Cbasolateral plasma membrane
Cmembrane
Cmicrovillus membrane
Cnucleolus
Cplasma membrane
Fcarbonate dehydratase activity
Fmolecular function activator activity
Fzinc ion binding
Presponse to hypoxia
Presponse to testosterone
Presponse to xenobiotic stimulus

459 aa · 50 kDa

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 CA9

Gene-level evidence surfaced through the gene CA9 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.

Carcinoma, Renal Cell

0.61Moderately supported

Clinical evidence dominant · Open Targets 0.30

Epilepsy

0.46Limited support

Clinical evidence dominant · Open Targets 0.37

Neurodegenerative Diseases

0.24Preliminary

Pathway evidence dominant · Open Targets 0.36 · no direct causal or clinical evidence

Carcinoma, Non-Small-Cell Lung

0.21Preliminary

Literature evidence dominant · Open Targets 0.12 · no direct causal or clinical evidence

Neoplasms

0.15Preliminary

Literature evidence dominant · Open Targets 0.12 · no direct causal or clinical evidence

View evidence synthesis (5)

Carcinoma, Renal CellModerately supported

0.61

agreement 0.50–0.73

Clinical44%Pathway30%Literature18%RNA expression9%

Open Targets aggregate 0.30 · 4 independent evidence families

EpilepsyLimited support

0.46

agreement 0.30–0.61

Clinical99%Literature1%

Open Targets aggregate 0.37 · 2 independent evidence families

Neurodegenerative DiseasesPreliminary

0.24

agreement 0.06–0.42

Pathway99%Literature1%

Open Targets aggregate 0.36 · 2 independent evidence families · no direct causal or clinical evidence

Carcinoma, Non-Small-Cell LungPreliminary

0.21

agreement 0.02–0.40

Literature57%RNA expression43%

Open Targets aggregate 0.12 · 2 independent evidence families · no direct causal or clinical evidence

NeoplasmsPreliminary

0.15

agreement 0.00–0.42

Literature100%

Open Targets aggregate 0.12 · 1 independent evidence family · no direct causal or clinical evidence

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

Epilepsy0.37

Neurodegenerative Diseases0.36

Carcinoma, Renal Cell0.30

Neoplasms0.12

Carcinoma, Non-Small-Cell Lung0.12

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)

ETHOXZOLAMIDEApproval

GIRENTUXIMABPhase 3

IODINE I 124 GIRENTUXIMABPhase 2

SULTHIAMEApproval

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 molecules — Strong

Approved Drug and Structure with Ligand support this modality.

Antibodies — Strong

Advanced Clinical and UniProt loc high conf support this modality.

Protein degraders — Emerging

Feasibility evidence (small molecule binder) — no clinical-stage drug of this modality recorded.

View underlying tractability evidence (11)

SM · Approved DrugSM · Structure with LigandSM · High-Quality LigandSM · Med-Quality PocketSM · Druggable FamilyAB · Advanced ClinicalAB · UniProt loc high confAB · GO CC high confAB · UniProt SigP or TMHMMAB · Human Protein Atlas locPR · Small Molecule Binder

Raw Open Targets tractability assessment buckets, by modality.

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

Carbonic anhydrase IX: An atypical target for innovative therapies in cancer.54 cites

Ronca R · Biochimica et biophysica acta. Reviews on cancer · 2024

Recent

Carbonic anhydrase IX: An atypical target for innovative therapies in cancer.

Ronca R · Biochimica et biophysica acta. Reviews on cancer · 2024

Europe PMC papers linked directly to this protein.

Related family literature

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

Multiple binding modes of inhibitors to carbonic anhydrases: how to design specific drugs targeting 15 different isoforms?

Alterio V · Chemical reviews · 2012

via Carbonic Anhydrases

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.