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interferon alpha 2b

✓ Approved

Helvetic Biopharma · IFNAR2 · 重组蛋白

什么是 interferon alpha 2b?

interferon alpha 2b 是一种重组蛋白,由Helvetic Biopharma研发。该药已获批,用于治疗相关适应症,给药途径:Injectable (Others)。

药物档案

公司Helvetic Biopharma
药物类别重组蛋白
分子靶点IFNAR2
给药途径Injectable (Others)
状态Approved

作用机制

分子靶点

interferon alpha 2b 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 alpha 2b 针对 10 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)Basal cell carcinoma✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Bladder cancer✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Hairy cell leukaemia✓ Approved
Infections and infestationsHepatitis B✓ Approved
Infections and infestationsHepatitis C✓ Approved

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相关研究文献

PubMedGastroenterology research and practice2026-10-27

Prevalence of Decisional Regret and Associated Risk Factors in Patients With Hepatitis B Undergoing Pegylated Interferon Alpha Therapy.

Lin Yufen Y, Xiong Huan H, Yi Shuanglian S, Xie Shanshan S

Pegylated interferon alpha has been shown to enhance the likelihood of achieving a functional cure in patients with hepatitis B. However, it was associated with a greater number of contraindications and adverse reactions compared with nucleotide analogs. Current research has placed comparatively less emphasis on the potential for this treatment to induce decision regret among patients. The aim of this study was to investigate the current status of decision regret in hepatitis B patients undergoing interferon therapy and to explore its influencing factors. A cross-sectional study was conducted in a comprehensive hospital in Xiamen, Fujian Province, China, from February 20 to June 13, 2024. The study recruited hepatitis B patients undergoing treatment with pegylated interferon alpha. The survey encompassed general information, the All Aspects of Health Literacy Scale, the Perceived Social Support Scale, the Control Preferences Scale, the Decisional Conflict Scale, and the Decision Regret Scale. A total of 130 questionnaires were analyzed. Only 13.85% of patients had no regrets at all about the decision, 34.60% experienced mild regret, and the proportion of patients with moderate to severe regrets reached 51.50%. Mild impact on life, active decision-making roles, passive decision-making roles, and decision conflict were the influencing factors of decisional regret in hepatitis B patients on pegylated interferon alpha therapy, which together explained 29.6% of the total variation. Hepatitis B patients undergoing pegylated interferon alpha therapy had a high percentage of decisional regret. Healthcare professionals should pay close attention to this phenomenon. In the future, they can investigate additional potential influencing factors and promptly develop intervention strategies to effectively reduce decision regret.

PMID 42936011
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PubMedPlants (Basel, Switzerland)2026-10-27

Determinants of the Nucleocytoplasmic Balance of the Cucumber Mosaic Virus and Peanut Stunt Virus 2b Proteins Regulate the Subcellular Localization and RNA Silencing Suppressor Activity.

Pinczés Dóra D, Sáray Réka R, Fábián Attila A, Almási Asztéria A et al.

The 2b protein of cucumoviruses is an RNA silencing suppressor (RSS), and its activity is associated with its nucleocytoplasmic localization. However, the contribution of nuclear localization signals (NLSs), nuclear export signals (NESs), and their sequence context remains poorly understood. Here, we compare cucumber mosaic virus (CMV) and peanut stunt virus (PSV) 2b proteins and their NLS- and NES-containing regions using recombinant proteins. The subcellular localization of PSV 2b has not been characterized, and no protein structural model has been reported previously. CMV 2b displayed a balanced nucleocytoplasmic distribution and strong RSS activity, whereas PSV 2b showed predominantly nuclear localization and weaker RSS activity. Exchange of the N-terminal region and NLSs resulted in pronounced changes in localization and RSS activity. PPC 2b, containing the CMV C-terminal region preceded by PSV sequence, showed the highest RSS activity, while the corresponding recombinant virus caused the most severe symptoms. AlphaFold analysis demonstrated lower structural confidence and higher predicted flexibility in the NES-containing C-terminal regions of CMV 2b and PPC 2b, compared with PSV 2b and CCP 2b, containing the PSV C-terminal region preceded by CMV sequence. These differences may influence NES accessibility and nuclear export.

PMID 42943032
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PubMedMolecules (Basel, Switzerland)2026-10-27

Contribution of the ROS/IRE1α Signaling Pathway to Arsenic Trioxide-Induced Apoptosis and Autophagy-Associated Responses in BEAS-2B Cells.

Yuan Jiaming J, Chen Yanhong Y, Yao Chenjuan C, Wei Haiyan H et al.

Inorganic arsenic primarily originates from geological processes and human activities. Exposure to high concentrations of inorganic arsenic can cause diverse health problems, with lung injury being one of the main hazards. The present study sought to elucidate the cytotoxicity and underlying mechanisms of inorganic arsenic in BEAS-2B cells. The results showed that exposure of BEAS-2B cells to arsenic trioxide (As2O3) for 24 h resulted in a dose-dependent decline in viability. As2O3 triggered reactive oxygen species (ROS) production in BEAS-2B cells, and ROS contributed to increased p-IRE1α and p-eIF2α abundance relative to β-actin, along with GRP78 protein expression. The autophagy-associated and apoptotic responses induced by As2O3 in BEAS-2B cells were likewise associated with ROS. Further analysis revealed that increased p-IRE1α abundance relative to β-actin is involved in As2O3-triggered autophagy-associated responses and apoptosis in BEAS-2B cells. The antioxidant N-acetylcysteine (NAC) markedly attenuated As2O3-induced apoptosis and autophagy-associated responses and reduced p-IRE1α abundance relative to β-actin. Collectively, these findings indicate that the ROS/IRE1α pathway contributes to As2O3-triggered autophagy-associated responses and apoptosis in BEAS-2B cells.

PMID 42943855
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PubMedTurkish journal of pharmaceutical sciences2026-10-27

Synthesis, Characterization, and In Vitro Anticancer Activity of Fe3O4-PEG-Quercetin Nanoparticles in a Non-Small Cell Lung Cancer (NSCLC) Model.

Sis Yeşim Y, Yerer Mükerrem Betül MB

Lung cancer is one of the leading causes of cancer-related mortality worldwide, with non-small cell lung cancer (NSCLC) accounting for the vast majority of cases. Conventional chemotherapeutic approaches are frequently limited by systemic toxicity, poor bioavailability, and non-selective biodistribution. Nanoparticle-based drug delivery systems have emerged as a promising strategy to overcome these limitations. The present study aimed to synthesize a novel PEGylated magnetite nanoparticle system containing quercetin (Fe3O4-PEG-QUER) and evaluate its effects on the impedance-based cellular responses of the A549 NSCLC cell line compared with non-tumorigenic bronchial epithelial cells (BEAS-2B). Nanoparticles were synthesized via the coprecipitation method. Quercetin was introduced during the preparation of the Fe3O4-PEG formulation, resulting in the Fe3O4-PEG-QUER formulation. All formulations Fe3O4, Fe3O4-QUER, Fe3O4-PEG, and Fe3O4-PEG-QUER were characterized using X-ray diffraction, fourier-transform infrared spectroscopy, Zeta-sizer, and nanoparticle tracking analysis. Impedance-based cellular responses were assessed in BEAS-2B and A549 cell lines using the xCELLigence real-time cell analysis system. Fe3O4-PEG-QUER showed apparent antiproliferative effects against A549 cells, with IC50 values of 289 μg/mL at 24 h and 160 μg/mL at 48 h. For BEAS-2B cells, the apparent IC50 values were above the highest tested concentration (> 400 μg/mL) at the evaluated time points. Fe3O4-PEG alone showed marked effects on the impedance-based cellular response of A549 cells, with apparent IC50 values of 27 and 19 μg/mL at 24 and 48 h, respectively. Because quercetin loading was not quantitatively determined, the nanoparticle concentrations represent total formulation mass and cannot be directly converted to quercetin-equivalent doses. Fe3O4-PEG-QUER nanoparticles altered the impedance-based cellular response in the A549 NSCLC cell line, with smaller changes observed in BEAS-2B cells at lower concentrations. These findings provide preliminary in vitro evidence supporting further investigation of Fe3O4-PEG-QUER in lung cancer models.

PMID 42937524
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PubMedFood science & nutrition2026-10-27

XuanBi Mitigates Rheumatoid Arthritis via Regulation of ECM-Receptor Interactions and IL-17 Signaling: Insights From Integrated Proteomic and Pharmacological Analyses.

Zhu Hao H, Pan Zhenfeng Z, Lu Ying Y, Xia Ping P et al.

Plant-derived polyphenols possess broad anti-inflammatory activities and may benefit chronic inflammatory diseases. XuanBi is a traditional Chinese medicine formula containing orally absorbable polyphenolic constituents and is used to treat rheumatoid arthritis (RA). This study investigated its absorbable components and potential mechanisms associated with synovial inflammatory hyperplasia. XuanBi was evaluated in collagen-induced arthritis (CIA) rats and rheumatoid arthritis synovial fibroblasts (RASFs). Constituents in the decoction and rat serum were characterized by high-performance liquid chromatography coupled with quadrupole-Orbitrap mass spectrometry (HPLC-Q-Orbitrap-MS). Predicted targets were intersected with synovial differentially expressed proteins (DEPs), followed by network pharmacology, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses, and experimental validation. Twenty-six absorbable constituents were identified, including catechin, quercetin, baicalein, and wogonin, together with 14 candidate proteins associated with RA synovial pathology. Enrichment analysis implicated extracellular matrix (ECM)-receptor interaction, focal adhesion, and interleukin-17 (IL-17) signaling. Medium- and high-dose XuanBi reduced joint swelling, synovial hyperplasia, and inflammatory infiltration in CIA rats. In RASFs, XuanBi inhibited proliferation, migration, and invasion. It also downregulated fibronectin 1 (FN1) and caveolin 1 (CAV1), reduced phosphorylation of SRC, focal adhesion kinase (FAK), and FYN, decreased integrin alpha 2b (ITGA2B)+/integrin beta 1 (ITGB1)+ cells, and reduced interleukin-1 beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), matrix metallopeptidase 3 (MMP3), and matrix metallopeptidase 9 (MMP9). Overall, XuanBi exerted anti-inflammatory and anti-synovial-hyperplasia effects in experimental RA, accompanied by changes in proteins associated with these pathways, supporting the potential involvement of these pathways and warranting further mechanistic and clinical investigation.

PMID 42936092
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PubMedBiology2026-10-27

A Biomimetic In Vitro Model of the Pro-Inflammatory Microenvironment Recapitulates Type I/II Interferon Signaling and Refractory Acute Monocytic Leukemia.

Krasnov Kirill K, Kobyakova Margarita M, Meshcheriakova Elena E, Lomovskaya Yana Y et al.

Preclinical drug development suffers from a persistent translational gap, as conventional animal models fail to reproduce the human immune response, contributing to high attrition rates of drug candidates in clinical trials. To address this, we previously established an in vitro high-density culture (HDC) model of acute monocytic leukemia (AML) cells that recapitulates an aseptic pro-inflammatory microenvironment using acute monocytic leukemia (AMoL) THP-1 cells. In the present study, using RNA-seq, quantitative RT-PCR, flow cytometry, Western blotting, and multiplex cytokine analysis, we characterized how this biomimetic microenvironment shapes Type I and II interferon signaling in THP-1 cells that acquire resistance to apoptosis under HDC conditions. The model revealed predominant activation of the Type II interferon pathway, marked by elevated interferon-gamma expression, STAT1 activation, and increased production of interferon-stimulated chemokines. Protein-protein interaction network analysis identified key interferon-induced hub genes and regulatory transcription factors driving this response. Notably, the interferon-stimulated gene profile generated by this in vitro platform, including the Interferon-Related DNA Damage Resistance Signature, closely resembled gene expression patterns observed in clinical samples from patients with refractory AMoL, supporting the relevance of the HDC biomimetic system as a research model of inflammatory adaptation in leukemia cells and associated resistance. These findings support further investigation of the HDC biomimetic system as a research model of inflammatory adaptation in leukemia cells and associated resistance.

PMID 42939477
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