Back to discover

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 NAMPTthat 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 0.260.53
Genetic92%Literature8%

Open Targets aggregate 0.23 · 2 independent evidence families

Eosinophilic EsophagitisLimited support
0.39
agreement 0.270.51
Genetic100%

Open Targets aggregate 0.24 · 1 independent evidence family

Nutritional deficiency diseaseLimited support
0.34
agreement 0.200.47
Genetic98%Literature2%

Open Targets aggregate 0.20 · 2 independent evidence families

Neurodegenerative DiseasesPreliminary
0.23
agreement 0.060.41
Pathway86%Literature14%

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

MelanomaPreliminary
0.21
agreement 0.050.36
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
Colorectal Neoplasms0.12
Breast Neoplasms0.11

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 moleculesStrong

Advanced Clinical and Structure with Ligand support this modality.

AntibodiesEmerging

Feasibility evidence (uniprot loc high conf and go cc med conf) — no clinical-stage drug of this modality recorded.

Protein degradersEmerging

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.