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interferon (Alfaferone)

✓ Approved

Johnson & Johnson Services, Inc. · IFNAR2

什么是 interferon?

interferon 是一种治疗药物,由Johnson & Johnson Services, Inc.研发。该药已获批,用于治疗相关适应症,给药途径:Others、Injectable (Others)、Subcutaneous Injection。

药物档案

商品名Alfaferone
公司Johnson & Johnson Services, Inc.
分子靶点IFNAR2
给药途径Others, Injectable (Others), Subcutaneous Injection
状态Approved

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 9 个适应症,涉及 3 个治疗领域。

治疗领域疾病/病症分期
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Hairy cell leukaemia✓ Approved
Infections and infestationsHepatitis B✓ Approved
Infections and infestationsHepatitis C✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Kaposi's sarcoma✓ Approved
Nervous system disordersMultiple sclerosis✓ 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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PubMedJournal of biochemical and molecular toxicology2026-10-26

Theranekron Attenuates Inflammation, Oxidative Stress Index, and Apoptosis in Lipopolysaccharide-Induced Cardiovascular Toxicity: Association With Hypoxia-Inducible Factor-1 Alpha-Related Gene Expression.

Savran Mehtap M, Asci Halil H, Imeci Orhan O, Oguzlar Furkan Cagri FC et al.

This study aimed to evaluate the possible protective effects of Theranekron, an extract derived from Tarantula cubensis venom, on cardiovascular damage induced by lipopolysaccharide (LPS) in an experimental rat model. A total of 32 male Wistar Albino rats were randomly divided into 4 groups: Control, Lipopolysaccharide, Lipopolysaccharide plus Theranekron, and Theranekron alone. Lipopolysaccharide administration caused pronounced histopathological changes in the heart and aorta, including endothelial sloughing, hyperemia, hemorrhage, and infiltration of inflammatory cells. These pathological findings were accompanied by elevated oxidative stress markers, increased tumor necrosis factor-alpha and inducible nitric oxide synthase immunoreactivity, and increased caspase-3 immunoreactivity. Additionally, genes associated with the hypoxia-inducible factor-1 alpha (HIF-1α) pathway-such as interleukin 6, signal transducer and activator of transcription 3 (STAT3), and vascular endothelial growth factor-were significantly upregulated in the lipopolysaccharide group. Theranekron pretreatment was associated with partial attenuation of oxidative stress imbalance, of inflammatory and apoptotic immunoreactivity, and of the upregulation of HIF-1α-related transcripts. Overall, these findings suggest that Theranekron may offer partial protection against early LPS-induced cardiovascular injury.

PMID 42929009
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PubMedEcology2026-10-26

Community history modifies how plant diversity shapes beta multifunctionality.

He Yan Y, Yang Rui R, Mao Lingfeng L

Research on ecosystem multifunctionality (EMF) has mainly quantified the magnitude of multiple functions within local communities (alpha multifunctionality [alpha-EMF]), whereas less is known about variation in function profiles among communities (beta multifunctionality [beta-EMF]). We asked how plant diversity affects variation in ecosystem function profiles among communities and whether this relationship depends on community history. We analyzed 5-year means of six ecosystem functions from 240 subplots in the DELTa-BEF, short for DEterminants of Long-Term Biodiversity Effects on Ecosystem Functioning Experiment, comparing new communities without experimental plant or soil history, resown communities retaining soil history, and old communities with continuous plant and soil histories. We adapted a variance-based beta diversity framework to quantify beta-EMF and partition it into local contributions to beta multifunctionality (LCBM) and function contributions to beta multifunctionality (FCBM). Plant diversity increased alpha-EMF in all treatments, with stronger increases in resown and old than in new communities. Richness was not detectably related to LCBM in new communities but was associated with lower LCBM in resown communities and higher LCBM in old communities, with the clearest contrast between the resown and old treatments. Leaf area index contributed more to beta-EMF than expected under equal contributions (20.2%), whereas basal respiration contributed less (13.2%); the other four functions did not differ from the equal-contribution expectation. Thus, similar gains in local multifunctionality can be accompanied by contrasting patterns of spatial functional heterogeneity, depending on community history. Partitioning beta-EMF into local and function contributions provides a practical way to identify which communities and functions contribute to spatial heterogeneity.

PMID 42928695
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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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