Protein / target

Activin receptor type-2B

ACVR2BQ13705Homo sapiensSwiss-Prot
Clinically validated
Therapeutic maturity
1
Approved medicines
9
Clinical trials
Small-molecule tractable
Druggability
Structure with Ligand

Protein at a glance

Biological role

Protein serine/threonine/tyrosine kinase activity

Primary system

Nervous system

Strongest disease association

Heterotaxia

Genetic literature evidence · score 0.78

Therapeutic maturity

Clinically validated target

1 approved medicine against this target

Druggability

Small molecule

Open Targets tractability · Structure with Ligand

Clinical development

1 approved · 1 in clinical development

9 linked trials

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

Transmembrane serine/threonine kinase activin type-2 receptor forming an activin receptor complex with activin type-1 serine/threonine kinase receptors (ACVR1, ACVR1B or ACVR1c). Transduces the activin signal from the cell surface to the cytoplasm and is thus regulating many physiological and pathological processes including neuronal differentiation and neuronal survival, hair follicle development and cycling, FSH production by the pituitary gland, wound healing, extracellular matrix production, immunosuppression and carcinogenesis. Activin is also thought to have a paracrine or autocrine role in follicular development in the ovary. Within the receptor complex, the type-2 receptors act as a primary activin receptors (binds activin-A/INHBA, activin-B/INHBB as well as inhibin-A/INHA-INHBA). The type-1 receptors like ACVR1B act as downstream transducers of activin signals. Activin binds to type-2 receptor at the plasma membrane and activates its serine-threonine kinase. The activated receptor type-2 then phosphorylates and activates the type-1 receptor. Once activated, the type-1 receptor binds and phosphorylates the SMAD proteins SMAD2 and SMAD3, on serine residues of the C-terminal tail. Soon after their association with the activin receptor and subsequent phosphorylation, SMAD2 and SMAD3 are released into the cytoplasm where they interact with the common partner SMAD4. This SMAD complex translocates into the nucleus where it mediates activin-induced transcription. Inhibitory SMAD7, which is recruited to ACVR1B through FKBP1A, can prevent the association of SMAD2 and SMAD3 with the activin receptor complex, thereby blocking the activin signal. Activin signal transduction is also antagonized by the binding to the receptor of inhibin-B via the IGSF1 inhibin coreceptor

Subcellular location

Cell membrane
Domains and Gene Ontology detail (38)

Domains & features

Protein kinase

Gene Ontology

  • Cactivin receptor complex
  • Ccytoplasm
  • Cplasma membrane
  • Cprotein-containing complex
  • Creceptor complex
  • Factivin binding
  • Factivin receptor activity
  • Factivin receptor activity, type II
  • FATP binding
  • Fgrowth factor binding
  • Fkinase activator activity
  • Fmetal ion binding

512 aa · 58 kDa · 2 isoforms

Biological roles

Reactome v97

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

Kinase signallingUniProt · GOTranscriptional regulationUniProt · GOImmune signallingGOCell adhesionUniProt
View supporting evidence

Kinase signalling

  • ·Transmembrane serine/threonine kinase activin type-2 receptor forming an activin recepto…
  • ·protein serine/threonine kinase activity
  • ·protein serine/threonine/tyrosine kinase activity

Transcriptional regulation

  • ·Transmembrane serine/threonine kinase activin type-2 receptor forming an activin recepto…
  • ·negative regulation of transcription by RNA polymerase II
  • ·regulation of DNA-templated transcription

Immune signalling

  • ·trophoblast cell migration

Cell adhesion

  • ·Transmembrane serine/threonine kinase activin type-2 receptor forming an activin recepto…
View underlying pathways (4)

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.

MSTNACVR1BINHBAGDF11TGFBR1BMP2BMP7ACVR2AACVR1CGDF2ACVR2B

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.

Drugs targeting this protein

1

Whether each drug engages this protein directly or through a complex, and how many other targets are recorded for it. Direct binders with few recorded targets are listed first.

bimagrumab
Narrow target profilePhase 3Antagonist

Activin receptor type-2B antagonist

Appears in clinical studies involving inclusion body myositis, acute myeloid leukemia by FAB classification, inclusion body myositis, muscle atrophy

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

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

Translational evidence

Open Targets 26

Why this target matters therapeutically — disease associations, drugs in development, tractability and safety, from Open Targets.

Strongest genetic associations

Human genetic evidence — the most direct causal link between this target and a disease.

Heterotaxia0.78

Genetic literature · overall 0.73

visceral heterotaxy0.61

Genetic literature · overall 0.47

Abnormality of the skeletal system0.58

Genetic · overall 0.35

disorder of pilosebaceous unit0.47

Genetic · overall 0.29

Highest-confidence therapeutic associations

Diseases where a drug acting on this target has already reached clinical development.

bone disorder0.61

Clinical · overall 0.37

spinal fusion0.61

Clinical · overall 0.37

inclusion body myositis0.59

Clinical · overall 0.36

Highest overall evidence

Remaining associations by Open Targets' aggregated evidence score.

autoimmune disorder of central nervous system0.35

Pathway

neurodegenerative disease0.33

Pathway

multiple sclerosis0.29

Pathway

Show all associations
Heterotaxia0.73
visceral heterotaxy0.47
bone disorder0.37
spinal fusion0.37
inclusion body myositis0.36
Abnormality of the skeletal system0.35
autoimmune disorder of central nervous system0.35
neurodegenerative disease0.33
disorder of pilosebaceous unit0.29
multiple sclerosis0.29

Open Targets ranks 1,338 associations for this target and we store the top 10 by aggregated score. The long tail is largely literature co-mention and RNA-expression evidence, not evidence that this target drives those diseases.

Known drugs · 2 total

BIMAGRUMABPhase 3

inclusion body myositis · acute myeloid leukemia by FAB classification · inclusion body myositis

DIBOTERMIN ALFAApproval

spinal fusion · bone disorder · osteoporosis

Tractability

SM · Structure with LigandSM · High-Quality LigandSM · Med-Quality PocketSM · Druggable FamilyAB · Advanced ClinicalAB · UniProt loc high confAB · GO CC high confAB · UniProt SigP or TMHMMPR · Database UbiquitinationPR · Small Molecule BinderOC · Approved Drug

Clinical trials

9

Trials of drugs that target this protein — reached indirectly through those drugs, so a trial listed here studies the drug, not the protein.

ClinicalTrials.gov via the drug-target graph.

Forefront confidence

Synthesis

Our own weighting of the evidence behind each disease association. Human genetics and clinical evidence count for most; literature co-mention counts for little, because two entities sharing an abstract is not evidence that one drives the other.

HeterotaxiaWell supported
0.80
agreement 0.680.92
Genetic76%Animal model24%Genetic literaturedup

Open Targets aggregate 0.73 · 2 independent evidence families · 1 not counted as duplicate

Abnormality of the skeletal systemModerately supported
0.58
agreement 0.460.70
Genetic100%

Open Targets aggregate 0.35 · 1 independent evidence family

visceral heterotaxyModerately supported
0.57
agreement 0.430.70
Genetic literature76%Animal model24%

Open Targets aggregate 0.47 · 2 independent evidence families

disorder of pilosebaceous unitLimited support
0.47
agreement 0.350.59
Genetic100%

Open Targets aggregate 0.29 · 1 independent evidence family

bone disorderLimited support
0.46
agreement 0.300.61
Clinical99%Literature1%

Open Targets aggregate 0.37 · 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 underlying per-type scores are shown above so the calculation can be checked.

What's happening now

2

Recent activity around this target, drawn from one canonical event stream. Every item is reached through a drug that targets this protein, so each event is news about that drug rather than about the protein directly.

  1. New publication2026-03-02
    Bimagrumab plus semaglutide alone or in combination for the treatment of obesity: a randomized phase 2 trial.

    Nature medicine · 2026 · 10 citations · Europe PMC · via bimagrumab

  2. New publication2024-01-11
    Antibody blockade of activin type II receptors preserves skeletal muscle mass and enhances fat loss during GLP-1 receptor agonism.

    Molecular metabolism · 2024 · 79 citations · Europe PMC · via bimagrumab

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.