Protein / target

Spermine synthase

Encoded bySMSP52788Homo sapiensSwiss-Prot

UniProt: P52788 Ensembl: ENSG00000102172 HGNC: HGNC:11123 NCBI Gene: 6611

Small-molecule tractable

Druggability

Structure with Ligand

Research papers

Protein at a glance

Biological role

Spermine synthase

Strongest disease association

Genetic Diseases, Inborn

Via encoding gene SMS · Genetic evidence · score 0.79

Research activity

Emerging research

1 papers · latest 1986

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 production of spermine from spermidine and decarboxylated S-adenosylmethionine (dcSAM)

Domains and Gene Ontology detail (7)

Domains & features

PABS

Gene Ontology

Ccytosol
Cextracellular exosome
Fspermine synthase activity
Pmethionine metabolic process
Ppolyamine metabolic process
Pspermine biosynthetic process

366 aa · 41 kDa · 2 isoforms

Biological roles

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

Metabolic enzyme activityGO

View supporting evidence

Metabolic enzyme activity

·methionine metabolic process
·polyamine metabolic process

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 SMS

Gene-level evidence surfaced through the gene SMSthat 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.

Genetic Diseases, Inborn

0.80Well supported

Genetic evidence dominant · Open Targets 0.48

Autoimmune disorder of central nervous system

0.22Preliminary

Pathway evidence dominant · Open Targets 0.34 · no direct causal or clinical evidence

Neurodegenerative Diseases

0.22Preliminary

Pathway evidence dominant · Open Targets 0.33 · no direct causal or clinical evidence

Developmental Disabilities

0.20Preliminary

Genetic evidence dominant · Open Targets 0.12

Colorectal Neoplasms

0.10Preliminary

Literature evidence dominant · Open Targets 0.08 · no direct causal or clinical evidence

View evidence synthesis (5)

Genetic Diseases, InbornWell supported

0.80

agreement 0.66–0.93

Genetic99%Literature1%

Open Targets aggregate 0.48 · 2 independent evidence families

Autoimmune disorder of central nervous systemPreliminary

0.22

agreement 0.00–0.45

Pathway100%

Open Targets aggregate 0.34 · 1 independent evidence family · no direct causal or clinical evidence

Neurodegenerative DiseasesPreliminary

0.22

agreement 0.00–0.45

Pathway100%

Open Targets aggregate 0.33 · 1 independent evidence family · no direct causal or clinical evidence

Developmental DisabilitiesPreliminary

0.20

agreement 0.07–0.32

Genetic100%

Open Targets aggregate 0.12 · 1 independent evidence family

Colorectal NeoplasmsPreliminary

0.10

agreement 0.00–0.37

Literature100%

Open Targets aggregate 0.08 · 1 independent evidence family · no direct causal or clinical evidence

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

Genetic Diseases, Inborn0.48

Autoimmune disorder of central nervous system0.34

Neurodegenerative Diseases0.33

Developmental Disabilities0.12

Colorectal Neoplasms0.08

Pancreatic Neoplasms0.08

Tractability

Small molecules — Emerging

Feasibility evidence (structure with ligand and high-quality pocket) — 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 (6)

SM · Structure with LigandSM · High-Quality PocketSM · Druggable FamilyPR · Database UbiquitinationPR · Half-life DataPR · Small Molecule Binder

Raw Open Targets tractability assessment buckets, by modality.

Research activity

1 papers · to 1986

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

Most cited

Recent advances in the biochemistry of polyamines in eukaryotes.1,096 cites

Pegg AE · The Biochemical journal · 1986

Recent

Recent advances in the biochemistry of polyamines in eukaryotes.

Pegg AE · The Biochemical journal · 1986

Europe PMC papers linked directly to this protein.