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interferon (BetaJect / BetaJect Light / Extavia)

✓ Approved

Warner Chilcott PLC · IFNAR2 · Recombinant Proteins

What is interferon?

interferon is a recombinant proteins developed by Warner Chilcott PLC. It is approved for therapeutic indications via injectable (others) or subcutaneous injection.

Drug Profile

Brand NamesBetaJect, BetaJect Light, Extavia
CompanyWarner Chilcott PLC
Drug ClassRecombinant Proteins
Molecular TargetIFNAR2
RouteInjectable (Others), Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, Warner Chilcott PLC

Mechanism of Action

Molecular Targets

interferon acts on 1 molecular target:

IFNAR2interferon alpha and beta receptor subunit 2 (IFNARB, IFN-alpha-REC)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

interferon is developed for 4 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Nervous system disordersRelapsing-remitting multiple sclerosis✓ Approved
Nervous system disordersSecondary progressive multiple sclerosis✓ Approved
Nervous system disordersPrimary progressive multiple sclerosisPhase II
Infections and infestationsAcquired immunodeficiency syndromePreclinical

Related Research Articles

PubMedFrontiers in artificial intelligence2026-10-22

scTIME: single-cell-informed interpretable modeling of immunotherapy-associated immune states in non-small cell lung cancer.

Chen Guozhi G, You Chenqiu C, Gao Hong H, Xu Chengjie C

Immune checkpoint inhibitor response in non-small cell lung cancer (NSCLC) reflects coordinated tumor and immune states that are not fully captured by single biomarkers. We developed scTIME, an interpretable model that translates single-cell immune programs into bulk transcriptomic scores, and integrated public single-cell, T-cell receptor, transcriptomic, survival, and proteogenomic cohorts. Response modeling used two cohorts with different endpoints (40 patients) and compared six algorithms. ElasticNet was selected as a sparse reporting model, achieving a pooled five-fold out-of-fold ROC-AUC of 0.810; nested model selection yielded 0.772. Matched held-out stratification identified response-enriched scTIME groups in a direct descriptive comparison with CD274, while the fitted score emphasized cytotoxic CD8, natural killer, SPP1 macrophage, interferon-response, and antigen-presentation programs. Single-cell analyses and external projections linked these programs to CXCL10-CXCR3 recruitment, exclusion-associated states, and T-cell receptor ecology across molecular contexts. Exploratory survival and cross-omics analyses extended the framework beyond the response cohorts but were interpreted as projection rather than independent validation. Together, the results show how cell-resolved immune biology can support transparent, multi-omic biomarker development without reducing response to a single pathway. scTIME remains exploratory because model choice was post hoc, cohorts were small and clinically heterogeneous, and endpoint-matched external validation was unavailable.

PMID 42903172
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PubMedAging cell2026-10-22

Cellular Senescence Dysregulates Antiviral Interferon Responses in Idiopathic Pulmonary Fibrosis.

Hughes Jun-Wei B JB, Reisser Yasmina Y, Hornung Franziska F, Hilsabeck Tyler A U TAU et al.

Patients with idiopathic pulmonary fibrosis (IPF) are highly vulnerable to respiratory virus infections, but the cellular mechanisms linking fibrotic remodeling to impaired local antiviral defense remain unclear. Here, we investigated how cellular senescence shapes the response of patient-derived healthy (HLF) and IPF primary lung fibroblasts to influenza A virus (IAV) infection. Transcriptomic profiling identified infection as the driver of gene expression in both DNA damage-induced senescent HLF and IPF fibroblasts and revealed induction of canonical antiviral pathways in both cell states. However, senescent IPF fibroblasts adopted a distinct antiviral response state characterized by a broader set of uniquely induced genes and differential coordination of antiviral transcriptional networks. Functionally, senescence increased viral titers in HLF and IPF fibroblasts, while senescent IPF fibroblasts displayed an altered inflammatory response. Network analysis linked viral response- and cell cycle-associated modules specifically to the senescent HLF infected state, whereas these programs were weaker in senescent IPF fibroblasts. Transcription factor inference identified IRF3 and STAT1 as candidate regulators of this altered antiviral state in both senescent HLF and IPF fibroblasts. Consistent with the network and transcription factor analyses, siRNA-mediated depletion of IRF3 or STAT1 significantly reduced IFN-β secretion in senescent HLF fibroblasts, whereas IPF fibroblasts showed only milder effects, indicating a disease-specific dependence on these pathways for antiviral control. Together, these findings show that the combination of cellular senescence and fibrotic fibroblast identity creates a dysfunctional antiviral state that may help explain the high susceptibility of IPF patients to virus-associated acute exacerbations and disease worsening.

PMID 42902866
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PubMedMolecular oral microbiology2026-10-22

Th17 Cells Impair Epithelial Defense Against Intracellular Bacteria in Part Through TGF-β.

Kang Mingyu M, Kim Hyeong-Jin HJ, Song Jieun J, Acharya Sabin S et al.

While Th1 and Th17 cells are well known for their distinct roles in host defense, how these effector CD4+ T-cell subsets influence epithelial responses to intracellular bacteria remains unclear. Here, we investigated whether Th1 or Th17 cells modulate the intracellular survival of Escherichia coli 7.2 (Ec7.2), a clinical isolate from oral lichen planus (OLP) tissue, in oral keratinocytes. To assess antigen-specific and antigen-independent T-cell effects, we established a co-culture system using IFN-γ-pretreated, Ec7.2-infected immortalized murine oral keratinocytes (IMOK) and Th1 or Th17 cells differentiated from OT-II-restricted CD4+ T cells, in the absence or presence of cognate peptide. Th1 cells reduced intracellular Ec7.2 in an antigen-dependent manner, whereas Th17 cells consistently increased bacterial persistence through largely antigen-independent and contact-independent mechanisms. Transcriptomic analysis of infected IMOK cells revealed that Th17-associated soluble signals broadly attenuated epithelial innate immune and antibacterial responses, including pathways related to type II interferon signaling, chemokine production, and defense response to bacterium. Among these, Nos2 expression was significantly reduced upon Th17 co-culture and was accompanied by decreased nitric oxide (NO) production. Th17 cells expressed higher levels of Tgfb1 than Th1 cells, and elevated TGF-β concentrations were consistently observed under Th17 co-culture conditions associated with increased bacterial persistence. Neutralization of TGF-β was associated with a trend toward increased NO production and reduced intracellular Ec7.2 recovery relative to isotype-treated controls. Together, these findings identify a previously underappreciated role for Th17-associated signals in modulating epithelial defense against intracellular bacteria, in part through TGF-β-associated suppression of NO-associated antimicrobial responses, which may contribute to bacterial persistence in Th17-dominated mucosal environments.

PMID 42902863
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PubMedJournal of hematology & oncology2026-10-21

Nanoengineered STING agonists for cancer therapy: toward immunodynamic control.

Liu Naimeng N, Wang Xiangyu X, Zhang Wenxiang W, Kan Yonemori Y et al.

Activation of the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway is a mechanistically compelling strategy for cancer immunotherapy, but first-generation STING agonists have shown limited clinical activity despite clear pharmacodynamic induction of interferon-related signals. This translational gap suggests that therapeutic benefit depends not only on pathway engagement but also on where, in which cells, at what amplitude, and for how long STING is activated. In this review, we summarize the cellular context of cGAS-STING signaling, the pharmacological evolution and clinical experience of STING agonists, and the major barriers imposed by route, species differences, biological heterogeneity, and systemic inflammatory toxicity. We then examine how nanoengineering may improve agonist protection, cytosolic access, tissue and cell-type selectivity, and temporal exposure. Importantly, we distinguish improved delivery or tumor accumulation from direct evidence of altered signaling kinetics or a wider therapeutic window. Representative lipid, polymeric, inorganic, biogenic, biomimetic, antibody-directed, and prodrug-based platforms are evaluated together with mechanism-based combination sequencing, hematologic malignancy-specific considerations, biomarker-guided patient selection, repeated-dose safety, and manufacturability. Overall, nano-STING therapy should be developed toward immunodynamic control rather than simple delivery enhancement, with benefit judged by the relationship among delivery, cell-resolved pharmacodynamics, antitumor efficacy, and toxicity.

PMID 42902412
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PubMedSignal transduction and targeted therapy2026-10-21

Nanotherapeutic macrophage reprogramming through immunometabolic and microbial modulation for sepsis treatment.

Lu Xintong X, Wang Wenhui W, Zhang Bingjie B, Li Qian Q et al.

Sepsis is a life-threatening syndrome characterized by dysregulated immune responses and metabolic dysfunction, and remains a major cause of global mortality. While nanomedicine offers new opportunities for sepsis therapy, current strategies rarely achieve comprehensive modulation of macrophage immunometabolism and microenvironmental signaling. Here, we develop a glutathione-responsive nanotherapeutic platform (EONPs) by conjugating the stimulator of interferon genes (STING) inhibitor 4-octyl itaconate to polyethylene glycol, followed by encapsulation of the dihydroorotate dehydrogenase (DHODH) inhibitor EA6. Integrated transcriptomic, metabolomic, and metagenomic analyses combined with pharmacological assessments reveal that EONPs suppress systemic hyperinflammation, reprogram macrophages toward an anti-inflammatory phenotype, restore gut microbial homeostasis, and protect against multi-organ injury in septic models. Notably, EONPs enhance the production of the microbiota-derived metabolite 5-hydroxyindoleacetic acid (5-HIAA), which is functionally linked to the anti-inflammatory response and may further support macrophage reprogramming. Our findings establish a previously unrecognized strategy for precise metabolic and microbiota-driven modulation of macrophages, offering a conceptual framework for further investigation of macrophage-targeted nanotherapeutics in sepsis.

PMID 42901916
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PubMedNature communications2026-10-21

Type I IFN promotes ILC2-to-ILC1 plasticity in pre-clinical radiation-induced lung injury.

Kim Jaeho J, Li Haiqing H, Mannan Rifat R, Doherty Taylor A TA et al.

Radiation-induced lung injury (RILI) is a common dose-limiting toxicity after radiotherapy for lung cancer, but the immunological mechanisms contributing to RILI pathogenesis remain poorly understood. Here we analyze a RILI mouse model using high-dose, restricted-field irradiation to the left lung. Flow cytometry and cytokine profiling analysis of innate lymphoid cells (ILC) reveals a radiation-induced shift from lung-resident type 2 ILCs (ILC2) toward pro-inflammatory type 1 ILCs (ILC1). Single-cell RNA-sequencing analysis of mouse lung ILC populations after radiation suggests that type I interferon (IFN) promotes radiation-induced ILC2-to-ILC1 plasticity. In vitro, IFN-β stimulation of mouse ILC2s leads to increased expression of the ILC1 markers T-bet and IFN-γ, while IFN-β stimulation of human peripheral blood mononuclear cells increases the ILC1-to-ILC2 ratio. In vivo, inhibition of type I IFN signaling attenuates lung damage after irradiation in our RILI model. Thus, our findings indicate that radiation-induced type I IFN induces ILC2-to-ILC1 plasticity to contribute to RILI pathogenesis, and suggest that targeting type I IFN signaling may be a therapeutic strategy to mitigate radiation-induced lung injury.

PMID 42901893
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