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interferon (DS Sumiferon / Humoferon / Sumiferon)

✓ Approved

Pacific Pharmaceuticals · IFNAR2

什么是 interferon？

interferon 是一种治疗药物，由Pacific Pharmaceuticals研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Intramuscular (IM) Injection、Subcutaneous Injection。

药物档案

商品名DS Sumiferon, Humoferon, Sumiferon
公司Pacific Pharmaceuticals
分子靶点IFNAR2
给药途径Injectable (Others), Intramuscular (IM) Injection, Subcutaneous Injection
状态Approved
来源： ClinicalTrials.gov, Pacific Pharmaceuticals

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 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)Hairy cell leukaemia✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Respiratory papilloma✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Chronic myeloid leukaemia✓ Approved
Infections and infestationsHepatitis B✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Plasma cell myeloma✓ 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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PubMedAntioxidants (Basel, Switzerland)2026-10-27

Immunomodulatory Effects of Cistanche deserticola Polysaccharides on LPS-Induced Immune Damage in RAW264.7 Macrophages with Transcriptome Analysis.

Zhao Baotang B, Tao Faqin F, Wang Shengfang S, He Jing J et al.

Polysaccharides (CDP-D2-N1) were extracted from Cistanche deserticola and used as an immunomodulatory substance to control inflammation and cytokines. This article chose LPS-induced inflammation model in RAW264.7 as the study subject and discloses the immune-inflammatory responses of CDP-D2-N1for lipopolysaccharide (LPS)-stimulated RAW264.7 cells. We investigated the screening of immunomodulatory activity of CDP-D2-N1 on LPS-induced RAW264.7 and the study of its pathway of action. CCK-8, qPCR and other tests were used to screen the CDP-D2-N1 with repairing effects on RAW264.7. The results show that CDP-D2-N1 pretreatment for 12 h at a concentration of 62.5-250 μg/mL improved the phagocytosis of RAW264.7, activated the expression of the TLR4 receptor, inhibited the expression of proinflammatory factors (TNF-α, IL-1, and IL-6) and the creation of iNOS, and modulated the NO of cell signaling molecules in RAW264.7 cells, thus improving the immunity of RAW264.7 cells and the activity of immune injury RAW264.7 cells. The combination of transcriptomics and p38 inhibitor analysis showed that CDP-D2-N1 could attenuate LPS-induced RAW264.7 cells' immune injury by affecting the regulation of MAP3/6 expression in the TNF signaling pathway.

PMID 42939809
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PubMedCancers2026-10-27

Incremental Prognostic Information Beyond Nodal Positivity: The AJCC 8th Edition N1/N2 Subdivision and the Lymph Node Ratio in Resected Periampullary Adenocarcinoma.

Na Gun Hyung GH, Seo Changho C

Background/Objectives: The American Joint Committee on Cancer (AJCC) 8th edition subdivides node-positive periampullary adenocarcinoma into N1 and N2 by the number of positive nodes. We quantified how much this subdivision and the lymph node ratio (LNR) each add to nodal positivity, and how the nodal yield affects the comparison. Methods: This retrospective cohort comprised 147 consecutive pancreatoduodenectomies for pancreatic head (n = 49), distal bile duct (n = 63), ampullary (n = 31) or duodenal (n = 4) adenocarcinoma. In covariate-adjusted Cox models stratified by origin, the N1/N2 subdivision and the LNR were tested over nodal positivity and over each other with nested likelihood-ratio tests, overall, with the examined-node count in the model and by the period of resection. Results: The median nodal yield was 17 (10 in 2013-2016, 19 in 2017-2024). Beyond nodal positivity, the N1/N2 subdivision added χ2 0.25 (p = 0.61; adjusted N2-versus-N1 hazard ratio 1.21, 95% confidence interval [CI] 0.59-2.45) and the LNR added χ2 9.60 (p = 0.002; hazard ratio 1.41 per 0.1, 95% CI 1.22-1.62). The LNR added to the N category (p = 0.002; optimism-corrected C-index gain 0.020, 95% CI 0.002-0.041), whereas the N category did not add detectably to the LNR (p = 0.54). With the examined-node count in the model, the LNR increment was attenuated (p = 0.045) and the subdivision's increment rose (χ2 3.65, p = 0.056). From 2017 onward (n = 113), the LNR and the positive-node count were nearly collinear among the node-positive patients (ρ 0.90 versus -0.02 before 2017), and neither the subdivision (p = 0.49) nor the LNR (p = 0.17) added significantly to positivity. Conclusions: The N1/N2 subdivision added little beyond nodal positivity, although imprecisely estimated, and its increment rose when the examined-node count was in the model. The LNR added prognostic information mainly when the yield was low or variable; where the yield was higher and more uniform, the ratio and the count-based category conveyed nearly the same information, and no additional value of the ratio was demonstrated.

PMID 42938856
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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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PubMedACS nano2026-10-27

Drug-Loaded Bacterial Outer Membrane Vesicles Eradicate Intratumoral Fusobacterium nucleatum to Enhance Colorectal Cancer Treatment.

Xie Yajun Y, Hu Bo B, Li Puze P, Zhou Yi Y et al.

Colorectal cancer (CRC) represents one of the most commonly diagnosed malignancies in which Fusobacterium nucleatum (Fn) infiltration critically drives tumor progression by fostering an immunosuppressive tumor microenvironment (TME) that compromises immunotherapy efficacy. Outer membrane vesicles (OMVs) originating from Escherichia coli Nissle 1917 offer an attractive tumor-targeting drug delivery system, combining intrinsic immunostimulatory properties with drug-loading capacity. We therefore developed an OMV-based dual-function system coencapsulating 5-fluorouracil (5-Fu) and metronidazole (MTZ), designated 5-Fu/MTZ@OMVs. In vitro, this system effectively eliminated both CT26 cells and Fn while promoting DC maturation and driving repolarization of M2 macrophages toward M1 as well as N2 neutrophils toward N1. In vivo, upon administration to an Fn-colonized CT26 model, the system homed to tumors, reduced the Fn burden, and inhibited tumor growth, demonstrating its bactericidal and antitumor efficacy. Notably, it reversed immunosuppressive TME by promoting DC maturation, M1 macrophage, and N1 neutrophil polarization, which enhanced the recruitment and functional activation of CD4+ and CD8+ T cells within the tumor. Thus, by integrating bactericidal, antitumor, and immune remodeling activities into a single OMV platform, our strategy constitutes a viable therapeutic approach for Fn-associated CRC.

PMID 42937547
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PubMedViruses2026-10-27

The 3' UTR Pseudoknot-Containing Region of Arteriviruses Acts as a PAMP to Activate RIG-I- and TLR8-Dependent Type I Interferon Responses.

Xie Sha S, Zhang Lu L, Sun Yan-Gang YG, Shu Meixin M

Porcine reproductive and respiratory syndrome virus (PRRSV) and other members of the Arteriviridae family cause substantial economic losses in livestock. However, their pathogen-associated molecular patterns (PAMPs) remain poorly characterized. Here, we investigated whether the 3' untranslated region (UTR) pseudoknot structures of Arteriviruses act as PAMPs and explored the underlying innate immune recognition mechanisms. Bioinformatics predictions (RNAalifold, RNArtist, and RNAComposer) revealed that the 3' UTR pseudoknot structures are conserved across all four Arteriviruses. In vitro transcribed pseudoknot RNAs significantly upregulated the mRNA expression of type I interferons (IFNα/β) and interferon-stimulated genes (protein kinase R, PKR; interferon-stimulated gene 15, ISG15; interferon-stimulated gene 56, ISG56) in Marc145 cells. Screening of RNA-sensing pattern recognition receptors (retinoic acid-inducible gene I, RIG-I; melanoma differentiation-associated protein 5, MDA5; Toll-like receptor 3/7/8/9, TLR3/7/8/9) in pseudoknot RNA-stimulated cells showed that RIG-I and TLR8 were significantly upregulated, whereas MDA5, TLR3, TLR7, and TLR9 were not. Short hairpin RNA (shRNA)-mediated knockdown of RIG-I or TLR8 significantly reduced pseudoknot-induced expression of IFNβ, PKR, and ISG56, confirming that both receptors are functionally required for this response. Upregulation of myeloid differentiation primary response 88 (MyD88), interferon regulatory factor 7 (IRF7), and signal transducer and activator of transcription 2 (STAT2) suggested that IFNα/β and downstream interferon-stimulated genes (ISGs) were induced via the TLR8-MyD88-IRF7 and RIG-I-IRF7 signaling pathways. Moreover, small-angle X-ray scattering (SAXS) analysis of the PRRSV pseudoknot RNA complexed with the porcine RIG-I regulatory domain was consistent with the formation of a complex between the pseudoknot RNA and RIG-I. In conclusion, this study identified the 3' UTR pseudoknot-containing region of Arteriviruses as a conserved PAMP that activates RIG-I- and TLR8-dependent type I IFN responses, providing a mechanistic basis and potential targets for antiviral therapy and vaccine adjuvant development against Arterivirus infections.

PMID 42944037
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