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Protein / target

Nicotinamide phosphoribosyltransferase

Encoded byNAMPTP43490Homo sapiensSwiss-Prot
Clinical-stage
Therapeutic maturity
3
Clinical candidates
Small-molecule tractable
Druggability
Advanced Clinical
1
Research papers

Protein at a glance

Biological role

Nicotinamide phosphoribosyltransferase

Strongest disease association

Eosinophilic Esophagitis

Via encoding gene NAMPT · Genetic evidence · score 0.39

Therapeutic position

Clinically advancing target

Small molecules

Research activity

Emerging research

1 papers · latest 2021

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 condensation of nicotinamide with 5-phosphoribosyl-1-pyrophosphate to yield nicotinamide mononucleotide, an intermediate in the biosynthesis of NAD.

View complete UniProt function annotation

Catalyzes the condensation of nicotinamide with 5-phosphoribosyl-1-pyrophosphate to yield nicotinamide mononucleotide, an intermediate in the biosynthesis of NAD. It is the rate limiting component in the mammalian NAD biosynthesis pathway. The secreted form behaves both as a cytokine with immunomodulating properties and an adipokine with anti-diabetic properties, it has no enzymatic activity, partly because of lack of activation by ATP, which has a low level in extracellular space and plasma. Plays a role in the modulation of circadian clock function. NAMPT-dependent oscillatory production of NAD regulates oscillation of clock target gene expression by releasing the core clock component: CLOCK-BMAL1 heterodimer from NAD-dependent SIRT1-mediated suppression (By similarity)

Subcellular location

NucleusCytoplasmSecreted
Domains and Gene Ontology detail (20)

Gene Ontology

  • Ccytosol
  • Cextracellular exosome
  • Cmitochondrial matrix
  • Cnucleus
  • Fcytokine activity
  • Fidentical protein binding
  • Fnicotinamide phosphoribosyltransferase activity
  • Pcell-cell signaling
  • Pcircadian regulation of gene expression
  • Pinflammatory response
  • PNAD+ biosynthetic process
  • PNAD+ biosynthetic process via the salvage pathway

491 aa · 56 kDa

Biological roles

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

Cell proliferation & survivalGOTranscriptional regulationUniProt · GOImmune signallingUniProt · GOMetabolic enzyme activityGO
View supporting evidence

Cell proliferation & survival

  • ·positive regulation of cell population proliferation

Transcriptional regulation

  • ·Catalyzes the condensation of nicotinamide with 5-phosphoribosyl-1-pyrophosphate to yiel…
  • ·circadian regulation of gene expression
  • ·positive regulation of gene expression
  • ·positive regulation of transcription by RNA polymerase II

Immune signalling

  • ·Catalyzes the condensation of nicotinamide with 5-phosphoribosyl-1-pyrophosphate to yiel…
  • ·cytokine activity
  • ·inflammatory response

Metabolic enzyme activity

  • ·nicotinamide phosphoribosyltransferase activity
  • ·nicotinate 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 NAMPT

Gene-level evidence surfaced through the gene NAMPT 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.

Asthma
0.39Limited support

Genetic evidence dominant · Open Targets 0.23

Eosinophilic Esophagitis
0.39Limited support

Genetic evidence dominant · Open Targets 0.24

Nutritional deficiency disease
0.34Limited support

Genetic evidence dominant · Open Targets 0.20

Neurodegenerative Diseases
0.23Preliminary

Pathway evidence dominant · Open Targets 0.32 · no direct causal or clinical evidence

Melanoma
0.21Preliminary

Literature evidence dominant · Open Targets 0.12

View evidence synthesis (5)
AsthmaLimited support
0.39
agreement 0.26–0.53
Genetic92%Literature8%

Open Targets aggregate 0.23 · 2 independent evidence families

Eosinophilic EsophagitisLimited support
0.39
agreement 0.27–0.51
Genetic100%

Open Targets aggregate 0.24 · 1 independent evidence family

Nutritional deficiency diseaseLimited support
0.34
agreement 0.20–0.47
Genetic98%Literature2%

Open Targets aggregate 0.20 · 2 independent evidence families

Neurodegenerative DiseasesPreliminary
0.23
agreement 0.06–0.41
Pathway86%Literature14%

Open Targets aggregate 0.32 · 2 independent evidence families · no direct causal or clinical evidence

MelanomaPreliminary
0.21
agreement 0.05–0.36
Literature58%Clinical42%

Open Targets aggregate 0.12 · 2 independent evidence families

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
Neurodegenerative Diseases0.32
Eosinophilic Esophagitis0.24
Asthma0.23
Nutritional deficiency disease0.20
Esophageal Squamous Cell Carcinoma0.17
Melanoma0.12

Drug development

3 compounds recorded · 3 in clinical development

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

View all recorded compounds (3)
TEGLARINADPhase 1
TEGLARINAD CHLORIDEPhase 1
DAPORINADPhase 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 molecules — Strong

Advanced Clinical and Structure with Ligand support this modality.

Antibodies — Emerging

Feasibility evidence (uniprot loc high conf and go cc med conf) — 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 (10)
SM · Advanced ClinicalSM · Structure with LigandSM · High-Quality LigandSM · High-Quality PocketSM · Druggable FamilyAB · UniProt loc high confAB · GO CC med confPR · Database UbiquitinationPR · Half-life DataPR · Small Molecule Binder

Raw Open Targets tractability assessment buckets, by modality.

Research activity

1 papers · to 2021

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

Most cited

Navas LE · Signal transduction and targeted therapy · 2021

Recent

NAD<sup>+</sup> metabolism, stemness, the immune response, and cancer.

Navas LE · Signal transduction and targeted therapy · 2021

Europe PMC papers linked directly to this protein.