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interferon (Feron)

✓ Approved

Toray · IFNAR2

什么是 interferon？

interferon 是一种治疗药物，由Toray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Feron
公司Toray
分子靶点IFNAR2
给药途径Injectable (Others), Intravenous (IV)
状态Approved
来源： ClinicalTrials.gov, Toray

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 6 个适应症，涉及 5 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
Hepatobiliary disordersHepatic cirrhosis✓ Approved
Infections and infestationsHepatitis B✓ Approved
Infections and infestationsHepatitis C✓ Approved
Surgical and medical proceduresSkin neoplasm excision✓ Approved

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相关研究文献

PubMedClinics and practice2026-10-26

The Relationship Between Interferon Status and HPV Infection in Patients with Oral Epithelial Dysplasia: An Observational Study.

Khisamieva Guzel G, Sologova Diana D, Svitich Oxana O, Diachkova Ekaterina E et al.

Background/Objectives: Oral potentially malignant diseases (OPMDs) with signs of epithelial dysplasia are characterized by a high risk of malignancy. However, there are still no algorithms for their early diagnosis and prediction, due to the many possible predisposing factors, including human papillomavirus (HPV) infection and decreased immunity. There is a need to assess the relationship between the manifestations of oral epithelial dysplasia (OED), HPV invasion in the oral cavity, and interferon status to improve the identification and characterization of patients with different degrees of dysplasia. Methods: This study was designed and reported with reference to the STROBE checklist. The study aimed to assess the association between interferon status and HPV invasion in patients with OED. As per the inclusion and exclusion criteria, this observational study included 180 patients with histologically confirmed oral epithelial dysplasia associated with leukoplakia or oral lichen planus. Interferon (IFN) status was assessed by measuring serum interferon activity, spontaneous interferon production, IFN-α/β, and IFN-γ activity in peripheral blood. HPV DNA was detected and genotyped in biopsy specimens using polymerase chain reaction. Results: HPV-positive patients demonstrated significantly lower IFN-α/β and IFN-γ activity compared with HPV-negative patients (p < 0.001). Severe OED was more frequently observed in HPV-positive individuals, whereas mild dysplasia predominated among HPV-negative patients (p < 0.05). Interferon activity progressively decreased with increasing dysplasia severity, with the lowest IFN-α/β and IFN-γ activity detected in patients with severe dysplasia (p < 0.001 and p < 0.05, respectively). A significant positive correlation between IFN-α/β and IFN-γ activity was identified in patients with moderate dysplasia (p = 0.003). Multivariate binary logistic regression analysis demonstrated that HPV positivity (adjusted OR = 4.62, 95% CI: 2.18-9.79; p < 0.001) and reduced IFN-α/β activity (adjusted OR = 1.34 per 10-unit decrease, 95% CI: 1.14-1.58; p < 0.001) were independently associated with severe dysplasia. The multivariable model demonstrated acceptable discriminatory ability for identifying patients with severe dysplasia (AUC = 0.736), with a sensitivity of 89.4% and a specificity of 56.1%. Conclusions: The findings suggest that HPV-associated OED is linked to reduced interferon status, particularly lower IFN-α/β and IFN-γ activity in more severe dysplastic lesions. Combined assessment of interferon status and HPV detection may help identify patients at higher risk of severe OED.

PMID 42930365
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PubMedCells2026-10-26

Antagonistic TGR5 and FXR Signaling Shapes STAT1-Dependent Interferon Responses in Intestinal Epithelial Cells.

Jia Huilin H, Wu Nannan N, Yan Yufeng Y, Kong Fanzhi F

Bile acids function not only as digestive metabolites but also as signaling molecules that influence mucosal immunity. However, how the bile acid receptors Takeda G-protein-coupled receptor 5 (TGR5; also known as GPBAR1) and farnesoid X receptor (FXR) coordinate intestinal epithelial interferon (IFN) responses remains incompletely understood. Here, we investigated the impact of TGR5 and FXR on IFN signaling in porcine IPEC-J2 and murine MODE-K intestinal epithelial cells. Pharmacological activation of TGR5 with INT-777 induced type I and type III IFNs together with multiple interferon-stimulated genes (ISGs), among which IFNλ3 and ISG15 showed the most prominent responses. Mechanistically, TGR5 enhanced STAT1 phosphorylation and nuclear accumulation, and both STAT1 silencing and pharmacological blockade of STAT1 phosphorylation attenuated TGR5-driven IFNλ3 and ISG15 expression. Inhibition of adenylate cyclase or protein kinase A further placed a cAMP-PKA-STAT1 axis downstream of TGR5. By contrast, activation of FXR with GW4064 suppressed poly(I:C)-induced IFNλ3 and ISG15 transcription and antagonized TGR5-mediated STAT1 activation and downstream gene expression. Confocal imaging further suggested that FXR restrains STAT1 nuclear trafficking through cytoplasmic colocalization with STAT1. Collectively, our findings identify a bile acid receptor rheostat in which TGR5 amplifies, whereas FXR dampens, epithelial IFN signaling through STAT1. This work provides a mechanistic framework for understanding how bile acid sensing may tune antiviral readiness at the intestinal mucosa.

PMID 42929875
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PubMedAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026-10-26

Large Oncosomes Induce Pro-Metastatic Stromal-Myeloid Reprogramming.

Silva Taylon Felipe TF, Concato-Lopes Virginia Marcia VM, Bedier Fatima F, Newman Lauren L et al.

Bone metastasis can be facilitated by systemic remodeling, yet the tumor-derived signals that influence the bone marrow microenvironment remain incompletely understood. Large oncosomes (LOs) are atypically large (> 1 µm), tumor-derived extracellular vesicles shed by amoeboid cancer cells. Here, we demonstrate that LOs function as systemic mediators of metastatic niche formation by activating innate immune sensing in bone marrow mesenchymal stem cells (BM-MSCs). Systemic administration of LOs to immunocompetent tumor-bearing mice did not affect primary tumor growth but increased metastatic burden. LOs induced a robust, dose-dependent interferon-driven inflammatory program, characterized by interferon-stimulated genes and neutrophil chemokines. Mechanistically, this response was driven by LO-associated nucleic acids activating convergent cytosolic DNA- and RNA-sensing pathways in recipient stromal cells. LO-conditioned BM-MSCs promoted the accumulation and polarization of neutrophils toward an immunosuppressive, polymorphonuclear myeloid-derived suppressor cell (PMN-MDSC)-like phenotype. In vivo, genetic suppression of LO shedding in tumor cells reduced PMN-MDSC accumulation in the bone marrow, which was reversed by systemic LO administration. Together, these findings support a model in which LO-associated signals reprogram the bone marrow microenvironment to support metastatic colonization, identifying a previously unrecognized mechanism linking tumor vesiculation to immune remodeling at distant sites.

PMID 42928450
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PubMedCells2026-10-26

Cytokine-Mediated Plasticity in the Molecular Requirements for Peptide-Loading Complex Formation and Antigen Presentation.

Aranha Ritchlynn R, Dastpeyman Mohadeseh M, Pandey Kirti K, Dorvash Mohammadreza M et al.

HLA class I antigen presentation depends on coordinated peptide processing, transport and loading, yet inflammatory signalling may modify the consequences of defects in this machinery. We examined wild-type HAP1 cells and isogenic ERAP1-, TAP1- and TAP2-knockout cells before and after interferon-γ (IFNγ) treatment using flow cytometry, proteomics, and immunopeptidomics. IFNγ strongly induced residual antigen-processing machinery in all HAP1-genotypes, increased HLA-I surface expression and expanded peptide recovery, including peptides derived from cancer-associated antigens. However, repertoire restoration was incomplete and defect-specific. ERAP1-deficient cells retained enrichment of longer, terminally extended peptides, whereas TAP2-deficient cells retained alterations in peptide length, processing of peptide flanking regions and source-protein location of the peptide. TAP1-deficient cells showed the greatest convergence to wards wild-type immunopeptidome features upon IFNγ stimulation. Components of the peptide-loading and ER quality-control machinery remained associated with immature HLA-I heavy chains in TAP-deficient cells and were enhanced by exposure to IFNγ. These findings demonstrate that inflammatory signalling can quantitatively and partially qualitatively compensate for defects in HLA-I antigen processing by amplifying intact pathway components and alternative peptide supply, without recreating a fully wild-type immunopeptidome.

PMID 42929886
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PubMedJournal of virology2026-10-26

Early innate immune signatures correlate with Ad26.COV2.S vaccine immunogenicity and protective efficacy.

Colarusso Alessandro A, Stephenson Kathryn E KE, Collier Ai-Ris Y A-RY, Wegmann Frank F et al.

The innate immune system is rapidly activated following antigen exposure and plays a critical role in shaping the ensuing adaptive immune responses. In this study, we performed bulk RNA sequencing and proteomic profiling in a cohort of 25 rhesus macaques following Ad26.COV2.S immunization to characterize early innate correlates of vaccine immunogenicity and protection. Our results show that innate immune activation occurred as early as day 1 post-vaccination and demonstrated a systemic enrichment of antiviral interferon pathways, cytokine signaling, and activation of innate immune cell signatures. These early transcriptomic signatures correlated positively with humoral and cellular immune responses at 6 weeks following vaccination and correlated inversely with viral loads following SARS-CoV-2 challenge. Similar correlates of immunogenicity were observed in a cohort of 25 adult healthy participants vaccinated with Ad26.COV2.S. Taken together, these findings highlight the importance of early activation of the innate immune responses following Ad26.COV2.S vaccination in shaping the protective adaptive immune response.IMPORTANCEEarly innate immune responses may shape vaccine immunogenicity and protection. We evaluated responses to Ad26.COV2.S vaccination in rhesus macaques and humans and found that day 1 innate immune signatures correlated with subsequent adaptive responses. These findings suggest that early post-vaccination immune programming influences immunogenicity and protective efficacy months later.

PMID 42929544
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PubMedCells2026-10-26

Immune Evasion Strategies of Human Poxviruses: A Roadmap for Engineering Low-Immunogenic CAR-Based and iPSC-Derived Cell Products.

Antonov Daniil O DO, Loguinova Marina Yu MY, Fan Hui H, Sazonova Elena V EV et al.

Allogeneic chimeric antigen receptor (CAR)-based cell products and induced pluripotent stem cell (iPSC)-derived regenerative grafts increasingly use multilayer immune engineering. Current strategies are strongest against direct human leukocyte antigen (HLA)-dependent recognition but incompletely address natural killer (NK)-cell counter-pressure, priming by recipient antigen-presenting cells, humoral and complement-mediated injury, inflammatory remodeling, blood- and tissue-interface damage, and terminal cell killing. Poxvirus research has characterized diverse immunomodulatory mechanisms relevant to these barriers. We review poxviral control of interferon signaling, antigen processing and presentation, T-cell activation, NK-cell surveillance, cytokine and chemokine networks, complement, inflammatory signaling, and regulated cell death, integrating viral mechanisms with human perturbation, cell-engineering, and transplantation evidence. A qualitative Tier 1-3 framework distinguishes mechanisms close to current cell-therapy practice from those requiring greater product-specific validation or control. The resulting design rules favor graded antigen-presentation control with paired NK validation, local or transient inflammatory buffering, interface-restricted complement protection, and survival enhancement only when independent eliminability is preserved. Selected poxviral proteins can act autonomously outside productive infection, but direct viral-protein expression remains a selective rather than default option. We propose a conditional defense-in-depth framework in which modules are added only when a residual barrier is demonstrated in the final therapeutic product.

PMID 42929874
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