Protein / target
Interferon alpha/beta receptor 2
Protein at a glance
Biological role
JAK pathway signal transduction adaptor
Strongest disease association
COVID-19
Therapeutic position
Established drug target
Derived from structured UniProt, Open Targets and literature data on this page.
Protein profile
Canonical identity and biological annotation from UniProt.
Function overview
Together with IFNAR1, forms the heterodimeric receptor for type I interferons (including interferons alpha, beta, epsilon, omega and kappa).
View complete UniProt function annotationHide complete annotation
Together with IFNAR1, forms the heterodimeric receptor for type I interferons (including interferons alpha, beta, epsilon, omega and kappa) (PubMed:10049744, PubMed:10556041, PubMed:21854986, PubMed:26424569, PubMed:28165510, PubMed:32972995, PubMed:7665574, PubMed:7759950, PubMed:8181059, PubMed:8798579, PubMed:8969169). Type I interferon binding activates the JAK-STAT signaling cascade, resulting in transcriptional activation or repression of interferon-regulated genes that encode the effectors of the interferon response (PubMed:10049744, PubMed:17517919, PubMed:21854986, PubMed:26424569, PubMed:28165510, PubMed:32972995, PubMed:7665574, PubMed:7759950, PubMed:8181059, PubMed:8798579, PubMed:8969169). Mechanistically, type I interferon-binding brings the IFNAR1 and IFNAR2 subunits into close proximity with one another, driving their associated Janus kinases (JAKs) (TYK2 bound to IFNAR1 and JAK1 bound to IFNAR2) to cross-phosphorylate one another (PubMed:10556041, PubMed:11682488, PubMed:12105218, PubMed:21854986, PubMed:32972995). The activated kinases phosphorylate specific tyrosine residues on the intracellular domains of IFNAR1 and IFNAR2, forming docking sites for the STAT transcription factors (STAT1, STAT2 and STAT) (PubMed:11682488, PubMed:12105218, PubMed:21854986, PubMed:32972995). STAT proteins are then phosphorylated by the JAKs, promoting their translocation into the nucleus to regulate expression of interferon-regulated genes (PubMed:12105218, PubMed:28165510, PubMed:9121453)
Subcellular location
Domains and Gene Ontology detail (17)Hide
Gene Ontology
- Cextracellular region
- Cextracellular space
- Cplasma membrane
- Fcytokine binding
- FJAK pathway signal transduction adaptor activity
- Fprotein kinase binding
- Ftype I interferon binding
- Ftype I interferon receptor activity
- Pcell surface receptor signaling pathway
- Pcell surface receptor signaling pathway via JAK-STAT
- Pcellular response to interferon-beta
- Pcellular response to virus
Approved medicines with mapped indications
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.
11 medicines meet Open Targets' target-level approved-medicine definition; the 7 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
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.
Interferon alpha/beta receptor agonist
Indicated for Multiple Sclerosis, Neoplasms
Interferon alpha/beta receptor agonist
Indicated for Multiple Sclerosis, Neoplasms
Interferon alpha/beta receptor agonist
Indicated for Multiple Sclerosis, Neoplasms
Interferon alpha/beta receptor agonist
Indicated for Hepatitis B, Hepatitis B, Chronic, Hepatitis C, Chronic, Neoplasms
Interferon alpha/beta receptor positive modulator
Indicated for Neoplasms
Interferon alpha/beta receptor agonist
Indicated for Hepatitis C, Chronic, Melanoma, Neoplasms
View all 7 targeting drugsHide
Interferon alpha/beta receptor agonist
Indicated for Carcinoid Tumor, Hepatitis B, Chronic, Hepatitis C, Chronic, Leukemia, Myelogenous, Chronic, BCR-ABL Positive
ChEMBL mechanism, action type, target identity and approved indications. Open Targets clinical status.
Translational evidence
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 IFNAR2
Gene-level evidence surfaced through the gene IFNAR2that 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.
View evidence synthesis (5)Hide
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.
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Drug development
11 compounds recorded · 11 approved
View all recorded compounds (10)Hide
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 — Emerging
Antibodies — Emerging
Protein degraders — Emerging
Other modalities — Strong
View underlying tractability evidence (6)Hide
Raw Open Targets tractability assessment buckets, by modality.
Clinical trials
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.
View all trials (26)Hide
ClinicalTrials.gov via the drug-target graph.
What's happening now
Recent therapeutic activity around this target — regulatory actions, clinical trials and safety signals for 3 drugs that target 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.
- Trial status changed
A Randomized, Double-Blind, Placebo-Controlled Multicenter Phase III Study to Assess Efficacy and Safety of Ropeginterferon Alfa-2b (P1101) in Adult Patients With Pre-fibrotic/Early Primary Myelofibrosis (PMF) or Overt PMF at Low or Intermediate-1 Risk According to DIPSS Plus (HOPE-PMF): The Core Study and Its Extension Study
- Label change
Label change: ROPEGINTERFERON ALFA-2B (BLA761166)
- Withdrawn from market
Market withdrawal: Extavia (EMA)
- Label change
Label change: ROPEGINTERFERON ALFA-2B (BLA761166)
- Regulatory approval
Approval: ROPEGINTERFERON ALFA-2B (BLA761166)
- New publicationSafety and efficacy of ozanimod versus interferon beta-1a in relapsing multiple sclerosis (RADIANCE): a multicentre, randomised, 24-month, phase 3 trial.
- Regulatory approval
Approval: Besremi (EMA)
- New publicationAlemtuzumab improves contrast sensitivity in patients with relapsing-remitting multiple sclerosis.
- New publicationAlemtuzumab versus interferon β-1a in early relapsing-remitting multiple sclerosis: post-hoc and subset analyses of clinical efficacy outcomes.
- New publicationAlemtuzumab vs. interferon beta-1a in early multiple sclerosis.
- Regulatory approval
Approval: Avonex (EMA)
- Regulatory approval
Approval: Betaferon (EMA)
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.
Related family literature
Papers about “Receptor, Interferon alpha-beta” — a broader family this protein belongs to. Shown as context; not counted as papers specifically about this protein.
via Receptor, Interferon alpha-beta
via Receptor, Interferon alpha-beta
via Receptor, Interferon alpha-beta
via Receptor, Interferon alpha-beta
Europe PMC literature, reached through curated HGNC family membership. Membership is a taxonomic relationship — it does not imply this protein participates in every mechanism these papers discuss.