Protein / target

Islet amyloid polypeptide

Encoded byIAPPP10997Homo sapiensSwiss-Prot

UniProt: P10997 Ensembl: ENSG00000121351 HGNC: HGNC:5329 NCBI Gene: 3375

Small-molecule tractable

Druggability

Structure with Ligand

Research papers

Protein at a glance

Biological role

Signaling receptor binding

Strongest disease association

Gout

Via encoding gene IAPP · Genetic evidence · score 0.14

Research activity

Emerging research

3 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

Amylin/IAPP is a glucoregulatory peptide hormone that plays an important role in the regulation of energy homeostasis.

View complete UniProt function annotation

Amylin/IAPP is a glucoregulatory peptide hormone that plays an important role in the regulation of energy homeostasis (PubMed:2690069). Selectively inhibits insulin-stimulated glucose utilization and glycogen deposition in muscle, while not affecting adipocyte glucose metabolism. IAPP function is mediated by the CALCR-RAMPs (AMYRs) receptor complexes (By similarity). Amylin can also bind CALCR receptor in the absence of RAMPs, although it is more selective for AMYRs (By similarity)

Subcellular location

Secreted

Domains and Gene Ontology detail (23)

Gene Ontology

Cextracellular region
Cextracellular space
Cneuronal cell body
Famyloid-beta binding
Fhormone activity
Fidentical protein binding
Flipid binding
Freceptor ligand activity
Fsignaling receptor binding
Pamylin receptor 1 signaling pathway
Pamylin receptor 2 signaling pathway
Pamylin receptor 3 signaling pathway

89 aa · 10 kDa

Biological roles

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

Apoptosis & cell deathGO

View supporting evidence

Apoptosis & cell death

·apoptotic process
·positive regulation of apoptotic 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 IAPP

Gene-level evidence surfaced through the gene IAPPthat 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.

Immunoglobulin Light-chain Amyloidosis

0.31Preliminary

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

Obesity due to melanocortin 4 receptor deficiency

0.28Preliminary

Animal model evidence dominant · Open Targets 0.08 · no direct causal or clinical evidence

Metabolic Syndrome

0.19Preliminary

Animal model evidence dominant · Open Targets 0.09 · no direct causal or clinical evidence

Hypertension

0.16Preliminary

Literature evidence dominant · Open Targets 0.09

Gout

0.15Preliminary

Genetic evidence dominant · Open Targets 0.09

View evidence synthesis (5)

Immunoglobulin Light-chain AmyloidosisPreliminary

0.31

agreement 0.13–0.48

Pathway98%Literature2%

Open Targets aggregate 0.46 · 2 independent evidence families · no direct causal or clinical evidence

Obesity due to melanocortin 4 receptor deficiencyPreliminary

0.28

agreement 0.10–0.46

Animal model79%Literature21%

Open Targets aggregate 0.08 · 2 independent evidence families · no direct causal or clinical evidence

Metabolic SyndromePreliminary

0.19

agreement 0.01–0.37

Animal model50%Literature50%

Open Targets aggregate 0.09 · 2 independent evidence families · no direct causal or clinical evidence

HypertensionPreliminary

0.16

agreement 0.02–0.29

Literature58%Genetic42%

Open Targets aggregate 0.09 · 2 independent evidence families

GoutPreliminary

0.15

agreement 0.01–0.29

Genetic96%Literature4%

Open Targets aggregate 0.09 · 2 independent evidence families

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

Immunoglobulin Light-chain Amyloidosis0.46

Alzheimer's Disease0.12

Diabetes Mellitus0.11

Diabetes Mellitus, Type 20.10

Metabolic Syndrome0.09

Gout0.09

Hypertension0.09

Hydrops fetalis0.09

Obesity due to melanocortin 4 receptor deficiency0.08

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 loc high conf and go cc high conf) — no clinical-stage drug of this modality recorded.

Protein degraders — Emerging

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

View underlying tractability evidence (7)

SM · Structure with LigandSM · High-Quality LigandSM · High-Quality PocketAB · UniProt loc high confAB · GO CC high confAB · UniProt SigP or TMHMMPR · Small Molecule Binder

Raw Open Targets tractability assessment buckets, by modality.