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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
来源： ClinicalTrials.gov, Johnson & Johnson Services, Inc.

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

PubMedThe Journal of dairy research2026-09-10

The public perception of animal welfare in dairy cow farming: a systematic literature review approach.

Masi Margherita M, Dolfi Emanuele E, Vecchio Yari Y, Zambianchi Lucia L et al.

Animal welfare (AW) in dairy farming has garnered significant public attention, driven by evolving societal values that prioritize ethical treatment and the expression of natural behaviours. This systematic literature review aims to map how the public perceives AW in dairy cow farming. Peer-reviewed publications addressing public perception of dairy cow welfare were retrieved from the Scopus database (searched in May 2025), yielding 107 studies that were examined through bibliometric and network analyses. They were then categorized, according to the perspective they addressed, into three stakeholder spheres: experts (those directly involved in the production chain), citizens and consumers. A dedicated content analysis of 73 documents further examined the citizen and consumer groups across three temporal phases: (i) the 'Lag phase' (up to 2012), marking the topic's emergence in scientific literature; (ii) the 'Naturalness phase' (2013-2019), characterized by consistent emphasis on dairy cows' and calves' right to express natural behaviours; and (iii) the 'Detailed phase' (from 2020), refining and broadening earlier themes. AW perceptions are intrinsically linked to the enabling of natural behaviours (e.g. pasture access, prolonged cow-calf contact), whereas routine practices (e.g. early separation, hormone use, male calf culling) are generally viewed as exploitative. From the consumer's side, a willingness to pay a premium for welfare-assured products emerges, yet an attitude-behaviour gap exists, as citizens' ethical stances may not fully translate into purchasing decisions due to price sensitivity. Notably, AW frequently supersedes environmental sustainability in consumer priorities, while evidence-based communication improves the acceptance of innovations (e.g. genetic modifications for welfare). Being based on a single database and excluding grey literature, the review nonetheless emphasizes the importance of stakeholder collaboration, transparent labelling and policy frameworks that align ethical expectations with farming realities and advocates targeted education to bridge knowledge gaps and support sustainable dairy systems.

PMID 42717465
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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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PubMedStress biology2026-09-10

Lycopene mitigates T-2 toxin-induced systemic inflammation and oxidative stress in association with gut microbiota and SCFAs regulation in mice.

Adam Saber Y SY, Ennab Wael W, Zhu Cuipeng C, Yuan Long L et al.

T-2 toxin is a trichothecene mycotoxin produced by Fusarium species and can cause disease after contaminated food or feed ingestion. This study aimed to investigate the impact of lycopene (Ly) on systemic inflammation, oxidative stress, and dysbiosis in mice exposed to T-2 toxin. A total of 20 male BALB/c mice (6 weeks old, weighing 23.5 ± 0.32 g) randomly divided into four groups (n = 5): Control (Cont), Ly, T-2, and T-2 + Ly groups. Findings revealed that Ly enhanced the body weight, feedd, and water intake that have been reduced by T-2. Ly increased the villus height (VH) and VH: crypt depth (CD) and decreased CD and villus width (VW) in ileum compared to the T-2 group. In alpha diversity, Staphylococcus and Corynebacterium were the most prevalent in Cont group; Staphylococcus, and Lactobacillus, were the most prevalent in T-2 group; Candidatus-Arthromitus and Staphylococcus were the most prevalent in T-2 + Ly group. Moreover, T-2 mice had significantly (p < 0.05) greater levels of interleukin-1 beta (IL-1β), interferon gamma (IFN-γ), Interleukin-17 (IL-17), and tumor necrosis factor-alpha (TNF-α) than Cont, while the Ly significantly (p < 0.05) lowered their concentration. The T-2 mice had significantly (p < 0.05) higher levels of reactive oxygen species (ROS) and malondialdehyde (MDA), while their catalase (CAT),, glutathione (GSH), adenosine triphosphate (ATP), and superoxide dismutase 1(SOD1) activities were significantly (p < 0.05) lower than Cont. Ly significantly (p < 0.05) restored their concentration. Moreover, there was a significant reduction (p < 0.05) of hexanoic, butyric, acetic, pentanoic, and Heptanoic acids in the T-2 mice compared to Cont. In contrast, treatment with Ly was found to significantly restore their levels compared to T-2 group. We conclude that Ly administration in the context of T-2-induced toxicity may help attenuate systemic oxidative stress and inflammation, possibly through modulation of gut microbiota and fecal short-chain fatty acids (SCFAs).

PMID 42720699
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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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PubMedBMC veterinary research2026-09-10

Development of an inactivated, oral immunogenic product against post-weaning colibacillosis caused by enterotoxigenic Escherichia coli in piglets.

Inglesi Alessia A, Filipe Joel J, Valli Giulia G, Riva Federica F et al.

Post-weaning diarrhea (PWD) caused by enterotoxigenic Escherichia coli (ETEC) expressing F4 and F18 fimbriae remains a major challenge in pig production, contributing to economic losses and increased antimicrobial use. This study aimed to preliminary evaluate the immunogenic potential of an orally administered formulation comprising heat-inactivated ETEC strains expressing F4 and F18 fimbriae, combined with low-dose recombinant human interferon-alpha (IFN-α) as a mucosal adjuvant, in piglets. Piglets from two different litters were allocated into two experimental groups: a treated group (T) receiving the inactivated ETEC formulation with IFN-α for 26 days, and a control group (C) receiving only IFN-α. According to the farmer, the sows had not been vaccinated. Immune responses were evaluated in the sows colostrum and piglet serum, saliva, and feces by ELISA. In mesenteric lymph nodes anti-F4/F18 IgA and IgG antibodies were quantified by ELISPOT. The inactivated product preserved fimbrial antigenicity and remained sterile. Colostrum from both sows displayed elevated levels of fimbriae-specific IgA and IgG despite neither sow being vaccinated against E. coli. Treated piglets showed a transient serum IgA increase against F4 whereas serum IgG levels were often comparable to the controls. Notably, elevated mucosal IgA responses were observed in saliva and feces against both F4 and F18 (P < 0.01) in T group, accompanied by enhanced IgA-secreting B-cell activity in mesenteric lymph nodes. ELISA validation confirmed high assay reproducibility (R² > 0.98; CV < 10%). ELISPOT analysis underscored the adjuvant role of F4 and IFN-α in stimulating mucosal immunity. Our preliminary findings may represent a promising strategy to control PWD and reduce antimicrobial use in pig production.

PMID 42717342
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