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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
Sources: ClinicalTrials.gov, Mochida

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 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

PubMedCellular and molecular life sciences : CMLS2026-11-12

GBP2 counteracts interferon therapy by stabilizing HBx to promote HBV replication and progression.

Wang Fei F, Song Hongxiao H, Xu Fengchao F, Li Xiaolu X et al.

Type I interferon (IFN-I) is widely used for the treatment of hepatitis B virus (HBV) infection, yet its therapeutic efficacy remains limited. Here, we identify guanylate-binding protein 2 (GBP2), an interferon-stimulated gene, as a host factor that paradoxically promotes HBV replication. GBP2 overexpression stabilized the viral regulatory protein HBx and markedly prolonged its half-life, whereas GBP2 knockdown facilitated HBx degradation. Mechanistically, GBP2 recruited the E3 ligase HUWE1 to induce K29-linked ubiquitination of HBx at lysine 95, which in turn suppressed K48-linked ubiquitination and proteasomal degradation. Functionally, GBP2-mediated HBx stabilization enhanced HBV replication and promoted hepatoma cell migration and invasion. Importantly, GBP2 expression was elevated in PBMCs of HBV-infected patients and further induced by IFN-I treatment, while HBV delayed early IFN-mediated GBP2 induction in HBV-containing hepatocyte-derived cells. Together, these findings reveal a novel mechanism by which GBP2 antagonizes the antiviral activity of IFN-I by stabilizing HBx, thereby facilitating HBV replication and potentially contributing to hepatocarcinogenesis. In brief, IFN activates ISGF3 via the JAK-STAT signaling pathway to produce the IFN-stimulating gene, GBP2, which promotes the K29 chain ubiquitination of HBx protein on the K95 site, which in turn competitively inhibits the K48 chain ubiquitination of HBx, thereby inhibiting HBx protein degradation.

PMID 43015458
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PubMedFrontiers in cell and developmental biology2026-11-12

The role of the cGAS-STING-mediated inflammatory amplification loop in osteoarthritis: from danger-associated DNA sensing to whole-joint remodeling and precision therapy.

Yang Xuxu X, Zhang Lin L, Yu Yang Y, Wu Shuhong S et al.

Osteoarthritis (OA) is a heterogeneous disorder of the entire joint in which mechanical overload, aging, metabolic disturbance, and dysregulated immunity converge. Growing evidence places the cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS)-stimulator of interferon genes (STING) pathway at the interface between cellular damage and sterile inflammation because this pathway detects self-deoxyribonucleic acid (DNA) that escapes its normal intracellular compartments. This review interprets current findings through a danger-signal amplification framework rather than treating cGAS-STING as an isolated inflammatory pathway. Mechanical and metabolic stress, oxidative injury, and aging can compromise mitochondrial and nuclear integrity; among the resulting DNA species, cytosolic mitochondrial DNA (mtDNA) currently has the strongest experimental support as an endogenous activator of cGAS in OA. cGAS-generated 2'3'-cyclic guanosine monophosphate-adenosine monophosphate (2'3'-cGAMP) activates STING and engages TANK-binding kinase 1 (TBK1)-interferon regulatory factor 3 (IRF3)/type I interferon (IFN-I) and nuclear factor kappa B (NF-κB) programs. These responses intersect with inflammasomes, pyroptosis, cellular senescence, and the senescence-associated secretory phenotype (SASP), thereby linking DNA exposure to renewed tissue injury. Extracellular vesicles (EVs), including vesicles carrying mtDNA, can extend this process across cartilage, synovium, the infrapatellar fat pad, and subchondral bone and help convert focal cellular stress into whole-joint remodeling. Potential interventions therefore span several levels: preventing mtDNA damage or escape, restoring mitochondrial quality control, directly modulating cGAS or STING, attenuating downstream inflammatory and cell-death programs, and improving tissue-selective local delivery. A major translational priority is to define when and in which OA endotypes cGAS-STING activity is sufficiently dominant to justify pathway-directed treatment. Combining temporal analysis, cell-specific models, and mechanism-linked biomarkers may ultimately support stage-adapted therapy that controls danger signals while preserving physiological innate immune function.

PMID 43017468
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PubMedMicrobiology spectrum2026-11-12

m6A coordinates mumps virus replication and innate immune sensing.

Wang Shixuan S, Zhang Yifei Y, Hu Qing Q, Ping Tongyu T et al.

In this study, we test the hypothesis that N6-methyladenosine (m6A) coordinates a functional trade-off between viral replication and innate immune sensing during mumps virus (MuV) infection. Using single-base resolution GLORI-seq, we identified widespread and non-canonically distributed m6A sites across MuV genomic, antigenomic, and messenger RNAs. Functional analyses revealed that depletion of the m6A methyltransferase METTL3 enhances viral RNA synthesis and nucleocapsid encapsidation in interferon-deficient cells, indicating an intrinsic suppressive role of m6A in viral replication. In contrast, in immune-competent epithelial and dendritic cells, host m6A enhances antiviral signaling, as METTL3 deficiency reduces infection-induced interferon and cytokine responses. Mechanistically, m6A-deficient MuV RNA exhibited increased binding to multiple pattern recognition receptors, including RIG-I-like and toll-like receptors, resulting in enhanced innate immune activation. Additionally, MuV infection extensively remodels the host m6A epitranscriptome in a cell type-dependent manner, with m6A enrichment positively correlating with the expression of immune-related transcripts. Together, these findings demonstrate that m6A acts as a bidirectional regulator during MuV infection by simultaneously restricting viral replication and modulating host immune recognition, providing new insight into epitranscriptomic control of paramyxovirus-host interactions.IMPORTANCEN6-methyladenosine (m6A) modification has emerged as a key regulator of RNA virus infection, yet its role in mumps virus (MuV) remains undefined. Here, we map the single-base resolution m6A landscape of a recombinant MuV and demonstrate that viral m6A restricts genome encapsidation and replication while attenuating innate immune sensing. MuV infection extensively remodels host m6A profiles in epithelial and dendritic cells, preferentially enhancing methylation of innate immune transcripts. Strikingly, m6A-deficient MuV RNA exhibits increased affinity for RIG-I-like and toll-like receptors, eliciting stronger interferon and proinflammatory responses. Our findings identify m6A as a bidirectional regulator of MuV replication and immunity and suggest an epitranscriptomic strategy to optimize live-attenuated vaccine design.

PMID 43018140
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PubMedJournal of human immunity2026-11-12

Severe dengue: Are type I interferon autoantibodies involved?

Tran Vu Le-Huy VL, Borghesi Alessandro A, Casanova Jean-Laurent JL, Zhang Shen-Ying SY

Dengue virus (DENV) is the most rapidly disseminating arbovirus worldwide. A new study by Yang et al. (https://doi.org/10.70962/jhi.20260072) shows that autoantibodies neutralizing type I IFNs (AAN-I-IFN) may underlie severe dengue in ∼14% (7/49) of cases in a cohort of Chinese patients. Further studies of children and adults of different ancestries with silent, benign, and severe DENV infection are warranted.

PMID 43018474
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PubMedACS applied materials & interfaces2026-11-12

A Biomimetic Cell Membrane-Coated Nanoreactor Reshapes ROS Homeostasis and Activates STING Pathway for Synergistic Chemodynamic-Immunotherapy.

Ahmad Waqas W, Ashraf Ghazala G, Sajjad Wasim W, Shams Saira S et al.

The combination of chemodynamic therapy (CDT) and immunotherapy offers a promising therapeutic paradigm for advanced cancer treatment, yet its translation is largely hindered by inadequate intratumoral reactive oxygen species (ROS) production and the lack of a robust link between ROS-induced cytotoxicity and durable immune activation. To address these challenges, we herein engineer a multifunctional biomimetic nanoplatform (ZMGM) by encapsulating Mn2+ and glucose oxidase (GOX) within zeolitic imidazolate framework-8 (ZIF-8), followed by surface functionalization with 4T1 breast cancer cell membranes. This design integrates three synergistic functions: (1) GOX depletes glucose and generates hydrogen peroxide (H2O2) within the acidic tumor microenvironment; (2) the produced H2O2 fuels the Mn2+-mediated Fenton-like reaction to amplify ROS production; and (3) Mn2+ simultaneously serves as a potent stimulator of interferon genes (STING) agonist, triggering type-I interferon responses and promoting dendritic cell maturation. Meanwhile, the homologous cancer cell membrane coating endows ZMGM with specific tumor homing and enhanced tumor localization. Both in vitro and in vivo findings demonstrate that ZMGM not only efficiently eradicates primary tumors but also induces a systemic antitumor immune response, characterized by increased CD8+ T cell infiltration, that effectively suppresses distant metastatic lesions. Notably, the synergistic CDT-STING immunotherapy achieves a primary tumor inhibition rate of 84.22% without obvious systemic toxicity. This work provides a paradigm for rationally designing a single nanoplatform that bridges ROS-mediated cell killing and innate immune activation, offering a promising avenue for combating metastatic triple-negative breast cancer.

PMID 43016149
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PubMedRevue medicale suisse2026-11-12

[Tuberculosis continuum: new definitions and clinical implications].

Amato Lorenzo L, Rodrigues Bandeira Joyce J, Opota Onya O, Mazza-Stalder Jesica J et al.

In 2026, tuberculosis remains a major global public health challenge and the deadliest infectious disease in the world. The concept of the tuberculosis continuum is progressively replacing the traditional distinction between latent tuberculosis infection and tuberculosis disease. It describes Mycobacterium tuberculosis infection as a dynamic spectrum that includes incipient and subclinical stages, which may benefit from early diagnosis and treatment. Interferon-Gamma Release Assays remain the reference tests for screening for tuberculosis infection, although their ability to predict progression to disease is limited. The microbiological diagnosis relies on sputum analysis and rapid molecular assays. This review summarizes current knowledge and emerging diagnostic tools.

PMID 43016218
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