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Protein / target

Dystrophin

Encoded byDMDP11532Homo sapiensSwiss-Prot
Clinically validated
Therapeutic maturity
5
Approved medicines
Open Targets target-level
View by indication →
2
Clinical trials
Antibody-tractable
Druggability
GO CC high conf

Protein at a glance

Biological role

Structural constituent of cytoskeleton

Strongest disease association

Neuromuscular disease caused by qualitative or quantitative defects of dystrophin

Via encoding gene DMD · Genetic evidence · score 0.93

Therapeutic position

Established drug target

Research activity

Emerging research

3 papers · latest 2025

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

Anchors the extracellular matrix to the cytoskeleton via F-actin.

View complete UniProt function annotation

Anchors the extracellular matrix to the cytoskeleton via F-actin. Ligand for dystroglycan. Component of the dystrophin-associated glycoprotein complex which accumulates at the neuromuscular junction (NMJ) and at a variety of synapses in the peripheral and central nervous systems and has a structural function in stabilizing the sarcolemma. Also implicated in signaling events and synaptic transmission

Subcellular location

Cell membrane, sarcolemmaCytoplasm, cytoskeletonPostsynaptic cell membrane
Domains and Gene Ontology detail (55)

Domains & features

Calponin-homology (CH) 1Calponin-homology (CH) 2WW

Gene Ontology

  • Ccell surface
  • Ccell-substrate junction
  • Ccostamere
  • Ccytoskeleton
  • Ccytosol
  • Cdystrophin-associated glycoprotein complex
  • Cfilopodium
  • Cfilopodium membrane
  • Cmembrane raft
  • Cneuron projection terminus
  • Cnucleus
  • Cplasma membrane

3685 aa · 427 kDa · 17 isoforms

Biological roles

Reactome v97

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

Synaptic signallingUniProt · GOIon channel gatingGOMuscle contractionGO · Reactome
View supporting evidence

Synaptic signalling

  • ·Anchors the extracellular matrix to the cytoskeleton via F-actin. Ligand for dystroglyca…
  • ·Postsynaptic cell membrane
  • ·postsynaptic membrane
  • ·synapse

Ion channel gating

  • ·regulation of calcium ion transmembrane transport
  • ·regulation of sodium ion transmembrane transport

Muscle contraction

  • ·cardiac muscle contraction
  • ·regulation of cardiac muscle contraction by regulation of the release of sequestered cal…
  • ·regulation of skeletal muscle contraction
  • ·regulation of skeletal muscle contraction by regulation of release of sequestered calciu…
View underlying pathways (3)

Concepts derived from UniProt GO Reactome — each badge above shows which sources supported that role.

Interaction neighbourhood

STRING v12.0

Proteins with the strongest functional or physical association. Node size and line weight reflect STRING confidence; hover or select a partner to inspect one association.

DAG1SSPNSNTA1SNTB1SGCDSGCAUTRNSNTG1SGCBCAV3DMD

10 strongest partners — larger node and heavier line mean higher confidence

Functional and physical associations from STRING v12.0. Only associations with this protein are drawn — partner-to-partner links are not part of this evidence.

Approved medicines with mapped indications

1 medicine · 1 area

Approved therapies targeting this protein, grouped by what they are approved to treat — the disease-first view of the medicines below. Relationships come from the canonical approved-indication graph (ChEMBL phase-4), the same source as the drug cards.

Muscular Dystrophy, Duchenne1 medicine

5 medicines meet Open Targets' target-level approved-medicine definition; the 1 shown here are those on this page with a canonical approved disease indication in the graph. Approved indications from ChEMBL (phase-4), via the canonical drug→disease graph.

Drugs targeting this protein

1

How approved and investigational drugs engage this protein — mechanism and action type, direct vs complex targeting, and how broadly each acts across other targets. A drug-first view (the section above groups the approved ones disease-first); direct binders with few recorded targets are listed first.

delandistrogene moxeparvovec
Narrow target profileApprovedExogenous gene

Dystrophin exogenous gene

Indicated for Muscular Dystrophy, Duchenne

Direct interaction with this protein · Only this protein recorded as a target

ChEMBL mechanism, action type, target identity and approved indications. Open Targets clinical status.

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 DMD

Gene-level evidence surfaced through the gene DMDthat 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.

Muscular Dystrophy, Duchenne
0.99Well supported

Genetic evidence dominant · Open Targets 0.87

Muscular dystrophy
0.95Well supported

Genetic evidence dominant · Open Targets 0.66

Neuromuscular disease caused by qualitative or quantitative defects of dystrophin
0.94Well supported

Genetic evidence dominant · Open Targets 0.59

dilated cardiomyopathy 3B
0.94Well supported

Genetic evidence dominant · Open Targets 0.79

Cardiomyopathies
0.89Well supported

Genetic evidence dominant · Open Targets 0.55

View evidence synthesis (5)
Muscular Dystrophy, DuchenneWell supported
0.99
agreement 0.911.00
Genetic36%Clinical29%Somatic mutation16%Animal model12%Literature6%RNA expression1%Genetic literaturedup

Open Targets aggregate 0.87 · 6 independent evidence families · 1 not counted as duplicate

Muscular dystrophyWell supported
0.95
agreement 0.841.00
Genetic55%Clinical42%Literature3%

Open Targets aggregate 0.66 · 3 independent evidence families

Neuromuscular disease caused by qualitative or quantitative defects of dystrophinWell supported
0.94
agreement 0.801.00
Genetic90%Literature10%

Open Targets aggregate 0.59 · 2 independent evidence families

dilated cardiomyopathy 3BWell supported
0.94
agreement 0.821.00
Genetic77%Animal model21%Literature2%Genetic literaturedup

Open Targets aggregate 0.79 · 3 independent evidence families · 1 not counted as duplicate

CardiomyopathiesWell supported
0.89
agreement 0.761.00
Genetic96%Literature4%

Open Targets aggregate 0.55 · 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
Muscular Dystrophy, Duchenne0.87
dilated cardiomyopathy 3B0.79
Muscular dystrophy0.66
Familial isolated dilated cardiomyopathy0.63
Progressive muscular dystrophy0.62
Neuromuscular disease caused by qualitative or quantitative defects of dystrophin0.59
Cardiomyopathies0.55

Drug development

8 compounds recorded · 5 approved · 2 in clinical development · 1 earlier-stage

Open Targets' development universe — every compound recorded against the target at any stage, not all approved medicines. Distinct from the 1 drug that targets this protein in Forefront's canonical graph (1 with a mapped approved indication, shown above): these count different sets and are not a subset relation.

View all recorded compounds (8)
DELANDISTROGENE MOXEPARVOVECApproval
SUVODIRSEN SODIUMUnknown
SUVODIRSENPhase 2 3
ETEPLIRSENApproval
VILTOLARSENApproval
GOLODIRSENApproval
DRISAPERSENPhase 3
CASIMERSENApproval

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

AntibodiesEmerging

Feasibility evidence (go cc high conf and uniprot loc 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 (4)
AB · GO CC high confAB · UniProt loc med confPR · Database UbiquitinationPR · Half-life Data

Raw Open Targets tractability assessment buckets, by modality.

Clinical trials

2

Trials of drugs that target this protein — reached indirectly through those drugs, so a trial listed here studies the drug, not the protein. Ranked by active status, then clinical phase and recency, and spread across the targeting drugs.

ClinicalTrials.gov via the drug-target graph.

What's happening now

1

Recent therapeutic activity around this target — regulatory actions, clinical trials and safety signals for a drug that targets this protein, plus publications where such a drug is a genuine subject. Every item is reached indirectly through the drug, not the protein itself; incidental mentions (a paper that merely measures a drug) and press items are excluded.

  1. New publication2024-10-09
    AAV gene therapy for Duchenne muscular dystrophy: the EMBARK phase 3 randomized trial.

    Nature medicine · 2025 · 107 citations · Europe PMC · via delandistrogene moxeparvovec

Objective event titles are shown unmodified; the event kind and significance line are derived from structured fields. Forefront AttentionEvent stream aggregating Europe PMC Regulatory filings ClinicalTrials.gov.

Research activity

3 papers · to 2025

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

Most cited

Recent

Europe PMC papers linked directly to this protein.