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interferon (IFNß Mochida)

✓ Approved

Mochida · IFNAR2

什么是 interferon？

interferon 是一种治疗药物，由Mochida研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Intravenous (IV)。

药物档案

商品名IFNß Mochida
公司Mochida
分子靶点IFNAR2
给药途径Injectable (Others), Intravenous (IV)
状态Approved
来源： ClinicalTrials.gov, Mochida

作用机制

分子靶点

interferon 作用于 1 个分子靶点：

IFNAR2interferon alpha and beta receptor subunit 2 (IFNARB, IFN-alpha-REC)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

interferon 针对 5 个适应症，涉及 2 个治疗领域。

治疗领域疾病/病症分期
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

相关研究文献

PubMedGenes, chromosomes & cancer2026-09-10

IRF8 Suppresses Hepatocellular Carcinoma Progression Through LIAS-Dependent IFN Production and Cuproptosis Activation.

Zhu Li L, Hu Zhaoxia Z, Wu Bei B, Duan Meng M et al.

Hepatocellular carcinoma (HCC) is one of the most lethal malignancies worldwide. Cuproptosis is a novel form of regulated cell death closely linked to tumor progression. Although interferon regulatory factors (IRFs) exert tumor-suppressive effects in various cancers, its precise regulatory mechanisms concerning cuproptosis in HCC remain largely elusive. IRF8 expression was evaluated in clinical HCC specimens and cell lines. Gain- and loss-of-function assays were conducted. Underlying transcriptional mechanisms were elucidated using ChIP-qPCR and dual-luciferase reporter assays. Subcutaneous nude mouse xenograft models were utilized to validate in vivo phenotypes. IRF8 was significantly downregulated in HCC. IRF8 overexpression induced oxidative stress and cuproptosis, as evidenced by excessive intracellular copper accumulation, elevated reactive oxygen species (ROS), and lipid peroxidation. Mechanistically, IRF8 directly bound to the promoter region of lipoyl synthase (LIAS) to activate its transcription. Phenotypic rescue assays confirmed that LIAS is indispensable for IRF8-induced interferon (IFN-α/β) production, copper engorgement, and cuproptosis. Furthermore, in vivo xenograft models demonstrated that IRF8 profoundly impeded tumor growth, an effect that was effectively abrogated by LIAS silencing. IRF8 inhibits HCC progression by directly upregulating LIAS to instigate lethal cuproptosis and interferon responses. The IRF8/LIAS axis may serve as a potential mechanistic basis and candidate axis for developing HCC therapeutic strategies.

PMID 42717274
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PubMedFrontiers in immunology2026-09-10

Cathepsin L potentiates autoimmunity by inhibiting lysosome-mediated STING degradation.

Xing Jia-Qing JQ, Zhang Zhi-Hao ZH, Guo Zeng-Lin ZL, Cai Hong H et al.

The stimulator of interferon genes (STING) orchestrates type I interferon (IFN) production in response to cytosolic DNA and plays essential roles in antiviral defense and autoimmune pathogenesis. The stability of STING determines the activation intensity of the pathway. Therefore, identifying proteins that govern its homeostatic regulation is needed. Here, we uncover the lysosomal protease cathepsin L (CTSL) as a critical stabilizer of STING in cells. CTSL deficiency selectively impairs STING-induced IFN responses without compromising overall lysosomal digestive function. Mechanistically, CTSL interacts with AP1B1 to prevent AP1B1-mediated lysosomal degradation of STING, thereby enhancing IFN signaling. Furthermore, CTSL expression is elevated in cells from systemic lupus erythematosus (SLE) patients and positively correlates with disease activity. Together, our findings establish an important role of CTSL in innate immunity by regulating STING homeostasis.

PMID 42718669
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PubMedFrontiers in physiology2026-09-10

Post-translational control of MAVS signaling: linking mitochondrial antiviral immunity to metabolic and cellular stress contexts.

Morimoto Nao N, Okazaki Tomohiko T

Mitochondria function not only as metabolic and bioenergetic centers but also as critical signaling hubs that integrate cellular context with innate immune response. The mitochondrial antiviral-signaling protein (MAVS), anchored to the outer mitochondrial membrane, is a central adaptor in the RIG-I-like receptor (RLR) pathway, orchestrating type I interferon (IFN) production and apoptosis. Although long regarded as a docking platform for RLR-derived signals, recent advances, particularly concerning its diverse post-translational modifications (PTMs), reveal MAVS as a dynamic integrator that decodes cellular stress and metabolic cues to fine-tune antiviral immunity. Canonical PTMs such as ubiquitination and phosphorylation highlight the importance of precisely controlling both the initiation and downregulation of MAVS signaling, but recent discoveries substantially broaden this regulatory landscape. Stress-responsive phosphorylation mediated via the ASK1-p38 MAPK pathway enhances MAVS signaling capacity under oxidative and ER stress, linking cellular damage to amplified interferon production. In parallel, a newly identified vitamin K-dependent carboxylation of MAVS reshapes downstream signaling by promoting interferon induction while restraining apoptosis, introducing a regulatory layer that may reflect the metabolic context surrounding GGCX activity, including vitamin K availability. Understanding this multilayered regulatory network not only redefines MAVS as a stress-sensitive mitochondrial signaling hub responsive to cellular context but also highlights new avenues for therapeutic modulation of innate immunity and cell fate during viral infection. This review summarizes emerging insights into PTM-mediated regulation of MAVS and outlines their broader implications for mitochondrial antiviral signaling.

PMID 42719470
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PubMedMolecular and clinical oncology2026-09-10

Tumor microenvironment-mediated resistance to immune checkpoint inhibitors in non-small cell lung cancer: Mechanisms, combination strategies and clinical perspectives (Review).

Mu Jiange J, Xu Qiqi Q

Non-small cell lung cancer (NSCLC) is one of the leading causes of cancer-associated mortality worldwide. Immune checkpoint inhibitors targeting programmed cell death protein 1, programmed death-ligand 1 (PD-L1) and cytotoxic T lymphocyte-associated protein 4 have transformed the treatment landscape of NSCLC. However, primary and acquired resistance limit durable clinical benefit. The current review article aimed to summarize tumor microenvironment-mediated resistance as an interconnected biological process rather than a collection of isolated factors. Immunosuppressive myeloid populations, regulatory lymphocytes, cancer-associated fibroblasts, extracellular matrix remodeling, vascular endothelial growth factor-driven vascular dysfunction, hypoxia, transforming growth factor-β signaling and metabolic reprogramming cooperate with defects in antigen presentation, dysregulation of serine/threonine kinase 11/Kelch-like ECH-associated protein 1/nuclear factor erythroid 2-related factor 2/stimulator of interferon genes and oncogenic driver signaling to generate immune-desert (minimal immune cell infiltration), immune-excluded (immune cells retained outside tumors) or exhausted immune-inflamed (immune-cell infiltration with functional exhaustion) phenotypes. The present review also critically evaluated combination therapeutic strategies, distinguishing phase III-supported standards from early-phase clinical or preclinical approaches, while highlighting considerations associated with patient selection, toxicity and the evolving regulatory context. Finally, an operational biomarker framework integrating PD-L1 expression, tumor mutational burden, interferon γ-associated signatures, spatial profiling, circulating tumor DNA, exosomal biomarkers and microbiome features was proposed to guide precision immunotherapy in NSCLC.

PMID 42719683
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PubMedFrontiers in cellular and infection microbiology2026-09-10

Integrative transcriptomics and hypothesis-driven transfer machine learning reveal conserved and species-specific host-parasite dynamics across Leishmania species in THP-1 cells: a systematic review and meta-analysis.

Al-Ghafli Hawra H, Alqurain Aymen A, Alzahrani Faisal M FM, Elhadi Nasreldin N et al.

Leishmaniasis is a vector-borne parasitic disease caused by protozoa of the genus Leishmania, characterized by clinical outcomes ranging from self-limiting cutaneous lesions to fatal visceral disease. Disease progression is multifactorial and is largely shaped by interactions between the parasite and host macrophages, as well as by other host- and pathogen-related factors. Although transcriptomic studies have provided insights into these interactions, differences in experimental design, parasite species, and analytical workflows have limited cross-study comparisons and the identification of conserved molecular responses. A systematic review was conducted following PRISMA guidelines to identify publicly available RNA-seq datasets of Leishmania-infected THP-1 macrophages. Raw sequencing data from eligible studies were reanalyzed using a unified bioinformatics pipeline incorporating standardized quality control, differential gene expression analysis, and batch-effect correction to enable robust cross-study integration. Comparative analyses were performed across infection stages and between L. infantum and L. amazonensis. The integrated transcriptomic dataset was subsequently used to develop a hypothesis-driven transfer learning framework to evaluate the feasibility of predicting L. amazonensis parasite gene expression at 96 hours post-infection (hpi) from experimentally generated 24 hpi transcriptomic profiles. Integrated analysis revealed a pronounced early induction of pro-inflammatory and interferon-stimulated genes, including CXCL10, IL1B, and IFIT1, followed by attenuation of inflammatory signalling at later infection stages. Comparative analyses identified a conserved interferon-driven host response shared between L. infantum and L. amazonensis, together with species-specific transcriptional adaptations. The transfer learning framework demonstrated the feasibility of predicting late-stage parasite gene expression from early transcriptomic data, highlighting the potential of machine learning approaches to leverage limited transcriptomic datasets. This study provides an integrated transcriptomic framework for investigating host-parasite interactions in Leishmania-infected macrophages and identifies conserved and species-specific transcriptional responses across infection. Furthermore, the proposed hypothesis-driven transfer learning approach demonstrates the potential to address transcriptomic data scarcity in neglected tropical disease research. Future in vitro studies and the availability of additional transcriptomic datasets will facilitate improved model training, validation, and generalizability.

PMID 42719152
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PubMedDiscover public health2026-09-10

Immunometabolic and RAAS determinants of circulating interferon gamma in an HIV and TB Zambian cohort.

Sidambi Dauyrinah D, Chisompola David D, Lwindi Propheria P, Kaango Arasidah A et al.

Tuberculosis (TB) and human immunodeficiency virus (HIV) remain major global health challenges, particularly in sub-Saharan Africa where co-infection and chronic immune activation are highly prevalent. Interferon-gamma (IFN-γ) plays a central role in host defense against Mycobacterium tuberculosis, yet its determinants in real-world, high-burden populations especially in the context of metabolic and systemic inflammation are not fully understood. This study investigated clinical, inflammatory, and metabolic factors associated with circulating IFN-γ levels in adults in a high HIV/TB burden setting. This was a cross-sectional study of 227 adults attending medical clinic at Livingstone University Teaching Hospital, Zambia. Circulating IFN-γ and a panel of inflammatory, metabolic, and renin-angiotensin-aldosterone system (RAAS) biomarkers were measured. Associations were assessed using simple and multivariable linear regression models, with log transformation applied to skewed variables. Statistical significance was defined as p < 0.05. Among participants (median age 50 years; 64.3% living with HIV), several variables were associated with IFN-γ in unadjusted analyses, including inflammatory cytokines, hs-CRP, angiotensin II, and fasting glucose. However, in multivariable analysis, only female sex (β = -0.440, p = 0.023), fasting glucose (β = 0.153, p = 0.042), angiotensin II (log-transformed) (β = 0.688, p = 0.022), and IL-17 A (log-transformed) (β = 0.332, p = 0.019) remained independently associated with IFN-γ levels. Notably, HIV status, prior tuberculosis infection, hs-CRP, and other inflammatory markers were not independently associated after adjustment. In this high HIV/TB burden population, circulating IFN-γ levels were independently associated with metabolic (fasting glucose), vascular-hormonal (angiotensin II), and immune (IL-17 A) factors, but not with HIV infection or prior TB after adjustment. These findings suggest that IFN-γ may reflect broader immunometabolic and inflammatory processes rather than infection-specific immune activation in treated populations. Longitudinal studies are needed to clarify the prognostic and clinical utility of IFN-γ in integrated chronic disease management. The online version contains supplementary material available at https://doi.org/10.1186/s12982-026-02839-5.

PMID 42718946
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