Protein / target

Heme oxygenase 1

Encoded byHMOX1P09601Homo sapiensSwiss-Prot

UniProt: P09601 Ensembl: ENSG00000100292 HGNC: HGNC:5013 NCBI Gene: 3162

Small-molecule tractable

Druggability

Structure with Ligand

Research papers

Protein at a glance

Biological role

Heme oxygenase (decyclizing)

Strongest disease association

Amyloidosis

Via encoding gene HMOX1 · Genetic literature evidence · score 0.76

Research activity

Emerging research

4 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

View complete UniProt function annotation

Catalyzes the oxidative cleavage of heme at the alpha-methene bridge carbon, released as carbon monoxide (CO), to generate biliverdin IXalpha, while releasing the central heme iron chelate as ferrous iron (PubMed:11121422, PubMed:19556236, PubMed:7703255). Affords protection against programmed cell death and this cytoprotective effect relies on its ability to catabolize free heme and prevent it from sensitizing cells to undergo apoptosis (PubMed:20055707)

Subcellular location

Endoplasmic reticulum membrane

Domains and Gene Ontology detail (46)

Gene Ontology

Ccytosol
Cendoplasmic reticulum
Cendoplasmic reticulum membrane
Cextracellular space
Cmembrane
Cmitochondrial outer membrane
Cnucleoplasm
Cnucleus
Cperinuclear region of cytoplasm
Cplasma membrane
Fenzyme binding
Fheme binding

288 aa · 33 kDa

Biological roles

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

Cell migrationGOLipid & lipoprotein metabolismGOApoptosis & cell deathUniProt · GOImmune signallingGO

View supporting evidence

Cell migration

·positive regulation of cell migration involved in sprouting angiogenesis

Lipid & lipoprotein metabolism

·low-density lipoprotein particle clearance

Apoptosis & cell death

·Catalyzes the oxidative cleavage of heme at the alpha-methene bridge carbon, released as…
·apoptotic process

Immune signalling

·negative regulation of cytokine production involved in inflammatory response
·wound healing involved in inflammatory response

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 HMOX1

Gene-level evidence surfaced through the gene HMOX1that 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.

Cystic Fibrosis

0.69Moderately supported

Genetic evidence dominant · Open Targets 0.39

Amyloidosis

0.61Moderately supported

Genetic literature evidence dominant · Open Targets 0.47

Pulmonary Disease, Chronic Obstructive

0.61Moderately supported

Genetic evidence dominant · Open Targets 0.36

Gastrointestinal Diseases

0.47Limited support

Genetic evidence dominant · Open Targets 0.28

Neurodegenerative Diseases

0.32Preliminary

Pathway evidence dominant · Open Targets 0.46 · no direct causal or clinical evidence

View evidence synthesis (5)

Cystic FibrosisModerately supported

0.69

agreement 0.57–0.80

Genetic74%Animal model13%Literature11%RNA expression2%

Open Targets aggregate 0.39 · 4 independent evidence families

AmyloidosisModerately supported

0.61

agreement 0.46–0.77

Genetic literature98%Literature3%

Open Targets aggregate 0.47 · 2 independent evidence families

Pulmonary Disease, Chronic ObstructiveModerately supported

0.61

agreement 0.47–0.75

Genetic80%Literature20%

Open Targets aggregate 0.36 · 2 independent evidence families

Gastrointestinal DiseasesLimited support

0.47

agreement 0.33–0.60

Genetic99%Literature1%

Open Targets aggregate 0.28 · 2 independent evidence families

Neurodegenerative DiseasesPreliminary

0.32

agreement 0.14–0.49

Pathway92%Literature8%

Open Targets aggregate 0.46 · 2 independent evidence families · 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

Amyloidosis0.47

Neurodegenerative Diseases0.46

Cystic Fibrosis0.39

Pulmonary Disease, Chronic Obstructive0.36

Gastrointestinal Diseases0.28

Neoplasms0.12

Acute Kidney Injury0.12

Alzheimer's Disease0.12

Carcinoma, Hepatocellular0.12

Tractability

Small molecules — Emerging

Feasibility evidence (structure with ligand and high-quality ligand) — no clinical-stage drug of this modality recorded.

Antibodies — Emerging

Feasibility evidence (uniprot sigp or tmhmm) — no clinical-stage drug of this modality recorded.

Protein degraders — Emerging

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

View underlying tractability evidence (7)

SM · Structure with LigandSM · High-Quality LigandSM · High-Quality PocketAB · UniProt SigP or TMHMMPR · Database UbiquitinationPR · Half-life DataPR · Small Molecule Binder

Raw Open Targets tractability assessment buckets, by modality.