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interferon (IFNß Mochida)

✓ Approved

Mochida · IFNAR2

What is interferon?

interferon is a therapeutic agent developed by Mochida. It is approved for therapeutic indications via injectable (others) or intravenous (iv).

Drug Profile

Brand NamesIFNß Mochida
CompanyMochida
Molecular TargetIFNAR2
RouteInjectable (Others), Intravenous (IV)
StatusApproved

Mechanism of Action

Molecular Targets

interferon acts on 1 molecular target:

IFNAR2interferon alpha and beta receptor subunit 2 (IFNARB, IFN-alpha-REC)
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Therapeutic Indications

interferon is developed for 5 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Brain neoplasm malignant✓ Approved
Infections and infestationsHepatitis B✓ Approved
Infections and infestationsHepatitis C✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Skin cancer✓ Approved
Infections and infestationsSalmonellosisPhase III

Related Research Articles

PubMedNature metabolism2026-10-16

IRF7 signalling in tanycytes controls brain-body-immune response across the ovarian cycle.

Nampoothiri Sreekala S, Fernandois Daniela D, Journiac Nathalie N, Delahaye Fabien F et al.

Sex-specific differences in metabolic and immune function are shaped by endocrine-immune interactions, yet the complexity of this relationship remains poorly understood. Here, we identify an immune cell-like state of tanycytes, an ependymoglial cell type lining the third ventricle that mediates brain-body communication1,2 in both mice and humans. Using single-cell transcriptomics, we provide a high-resolution cellular map of the mouse and human mediobasal hypothalamus with cross-species comparison of tanycytes. We capture dynamic sex-, oestrous cycle- and high-fat diet-dependent transcriptomic changes in tanycytes, including a cyclic interferon response in tanycytes during the physiological oestrous cycle in female mice. We found that the oestrous cycle, with its changing hormonal milieu, especially oestradiol, affected the brain's immune responses, characterized by the temporal and cyclic expression of interferon regulatory factor 7 (Irf7) gene, as well as downstream interferon-stimulated genes such as Cxcl10 in tanycytes of female mice, which are associated with increased infiltration of leukocytes and cytokine responses. Irf7 expression in tanycytes of physiological males remained stable and markedly lower, suggesting a distinct immune activation pattern in the brains of cycling females. By targeting oestrogen and interferon signaling in tanycytes, we show that balanced, cyclic leukocyte infiltration into the median eminence may have a role in oestrous cycle maintenance, whereas Irf7 in tanycytes modulates circulating monocyte proportions, revealing brain-immune system communication through tanycytes. Our findings reveal an immune-associated role for tanycytes, with potential implications for understanding the endocrine and immunological mechanisms underlying sex-biased diseases.

PubMedInternational journal of molecular sciences2026-10-16

ISG15 Is a Key Multidirectional Regulator of Cytosolic RNA- and DNA-Sensing Pathways and Type I Interferon Feedback Loops.

White Maleana G MG, Iordanskiy Sergey S

Activation of cytosolic RNA and DNA sensing pathways that normally recognize viral nucleic acids triggers the expression and release of type I interferons (IFN-I). This release drives the expression of interferon-stimulated genes (ISGs) that activate acute inflammation and counteract viral replication at various stages. Recent studies have highlighted how interferon-stimulated gene 15 (ISG15), a small, ubiquitin-like modifier, regulates cytosolic RNA and DNA sensing pathway proteins to control the antiviral response and inflammation. ISG15 is a multifunctional protein that acts as a secreted cytokine, binds freely to intracellular proteins, and covalently modifies proteins in a reversible process termed ISGylation. A dual regulatory molecule, ISG15 can both stabilize and destabilize proteins that promote and inhibit IFN-I signaling. Conversely, viruses have evolved strategies to disrupt and exploit ISG15-dependent antiviral responses to evade the host immune system. In this review, we examine how ISG15 regulates cytosolic RNA and DNA sensing pathway proteins to control IFN-I signaling and the antiviral response, highlighting it as a master regulator that fine-tunes IFN-I signaling and feedback. Recognizing the multifaceted action of ISG15 is essential for designing balanced therapeutic strategies across antiviral drug development, cancer immunotherapy, and chronic inflammatory disease management.

PubMedEMBO reports2026-10-16

TREX1 limits anti-tumor immunity by degrading short cytosolic DNA molecules.

Yang Chun-Yen CY, Chami Bayan B, Ursino Chiara C, Johnson Silpa Mary SM et al.

TREX1 has recently emerged as a promising therapeutic target in cancer owing to its role in degrading cytosolic DNA and suppressing type I interferon signaling. However, the nature of the immunostimulatory DNA species degraded by TREX1 remains elusive. Here, we show that TREX1 deficiency in murine lung and melanoma tumor cells leads to a substantial, MRE11-dependent increase in short cytosolic DNA fragments that originate preferentially from transcriptionally active regions of the genome, without a corresponding increase in micronuclei. These fragments robustly activate interferon-stimulated genes and drive differentiation of pro-inflammatory macrophages. In syngeneic mice, tumors derived from Trex1-knockout cells exhibit delayed growth, increased sensitivity to anti-PD-1 immune checkpoint blockade, and extended survival. These effects depend on an intact immune system and foster durable anti-tumor memory. Together, our results reveal that short, transcription-derived cytosolic DNA fragments are key TREX1 substrates mediating immune activation in cancer, establishing TREX1 inhibition as a compelling strategy to enhance tumor immunogenicity.

PubMedInternational journal of molecular sciences2026-10-16

Integrated Assessment of Humoral and Cellular SARS-CoV-2 Immunity Using ELISA and a Gold Nanoparticle-Based IGRA.

Todorović Aleksandra A, Ćujić Danica D, Knežević Jugović Zorica Z, Uskoković Petar P et al.

Although SARS-CoV-2 immunity has been widely investigated, the relationship between antibody levels and cellular immune responses following different routes of exposure to SARS-CoV-2 remains not fully revealed. In this study, cellular immunity was assessed using a newly developed whole-blood interferon-gamma release assay (nano-IGRA) based on gold nanoparticle (AuNP)-conjugated SARS-CoV-2 antigens. AuNP-conjugated and soluble antigens were compared regarding interferon gamma (IFN-γ) responses and intra- and interassay reproducibility in 112 individuals with immunity acquired through infection, vaccination, or both. Humoral immunity was evaluated by enzyme-linked immunosorbent assay (ELISA). Overall, 88% of participants were seropositive. AuNP-conjugated Spike (S) and Nucleocapsid (N) SARS-CoV-2 antigens induced significantly higher IFN-γ responses than soluble antigens in all exposure groups (p < 0.001). AuNP conjugation reduced intraassay variability by 62.4% and 61.4% for S and N, respectively, and interassay variability by 71.7% and 68.3%, respectively. Antibody levels correlated significantly with IFN-γ responses to S (ρ = 0.358, p < 0.001) and N (ρ = 0.309, p < 0.001). An interesting finding is that cellular responses were also detected in some seronegative individuals. Nano-IGRA, based on a novel AuNP-based approach, provides antigen-specific cellular immune assessment, combining enhanced IFN-γ responses with improved reproducibility. Further studies should establish diagnostic cut-offs, sensitivity, specificity, and clinical performance.

PubMedInternational journal of molecular sciences2026-10-16

Flipons, Noncoding Transcripts and Retroelements: A Universal Host Defense.

Herbert Alan A

Encoding genetic information involves both structure and sequence. Non-protein-coding (NCR) RNAs modulate host immune responses by guiding and assembling stress-specific protein effectors, with flipons enabling dynamic transitions between states. Small NCRs transcribed by both RNA Polymerases 2 and 3 normally modulate these pathways. The miRNAs, tRNA fragments, mitrons, piRNAs, and endo-small-interfering RNA products target the guide effector complexes to their targets. These NCRs filter the subset of RNAs that are translated, a process modulated by other NCRs that fine-tune RNA stability, localization, and kinetics through the modifications they direct. When these RNAs, or their targets, are dysregulated, host interferon responses are activated through the accumulation of uncapped triphosphorylated RNAs, dsRNAs, or flipon-encoded Z-RNAs. These responses are initially suppressed to avoid attacks on self-RNAs, but above a threshold, highly immunogenic pathways are unleashed. These same responses resist viral and other infections without pathogen-specific effectors or prior exposure. They also eliminate dysfunctional cells. These universal responses, when unresolved, contribute to a range of pathologies, increasing cancer, inflammatory diseases, and senescence. The review focuses on recent findings showing how these integrated host responses are driven by, and exploit, the retrotransposon invasion of animal genomes.

PubMedCells2026-10-16

Antigen-Presentation Competence in Gynecologic Cancers: Mechanisms, Evidence and Translational Priorities.

Xu Zihao Z, Liu Yifan Y, Xu Jun J, Xiong Mengxin M

Immune-checkpoint biomarkers in gynecologic cancers primarily estimate antigenic potential or characterize an inhibited immune response. However, they do not establish whether malignant cells are visible to antigen-specific lymphocytes. We define antigen-presentation competence as the capacity of the tumor-immune ecosystem to generate antigenic peptides, display them through functional human leukocyte antigen molecules, prime cognate T cells through professional antigen-presenting cells, and permit recognition of malignant cells by effector lymphocytes. Recurrent defects have been reported at each step in cervical, endometrial, and ovarian cancers, but the evidence is not equally mature across these diseases. Cervical studies emphasize human papillomavirus-associated immune selection and antigen-processing machinery abnormalities; endometrial cancer provides relatively direct treatment-linked evidence for major histocompatibility complex class I and interferon-pathway defects; and ovarian cancer offers direct immunopeptidomic and multiregion evidence that antigen availability, presentation, and immune recognition can diverge. Taken together, the literature makes antigen-presentation competence a testable functional framework. It does not yet justify a biomarker or clinical score. Prospective work will need spatial and longitudinal measurements of tumor presentation, dendritic-cell priming, and T-cell recognition. A key test is whether these measurements improve prediction beyond mismatch repair, polymerase epsilon, programmed death-ligand 1, and tumor mutational burden.

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