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interferon (Shanferon)

✓ Approved

Sanofi S.A · IFNAR2 · 重组蛋白

什么是 interferon？

interferon 是一种重组蛋白，由Sanofi S.A研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Subcutaneous Injection。

药物档案

商品名Shanferon
公司Sanofi S.A
药物类别重组蛋白
分子靶点IFNAR2
给药途径Injectable (Others), Subcutaneous Injection
状态Approved
来源： ClinicalTrials.gov, Sanofi S.A

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 3 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)Chronic myeloid leukaemia✓ Approved
Infections and infestationsHepatitis B✓ Approved
Infections and infestationsHepatitis C✓ Approved

相关研究文献

PubMedFunctional & integrative genomics2026-08-05

IFI6 is associated with interferon activation and complement-associated immune responses in primary Sjögren's disease.

Han Yibing Y, Mei Yikun Y, Meng Xiaoqin X, Zhang Minjv M et al.

Primary Sjögren's disease (pSjD) is a systemic autoimmune disease characterized by chronic immune-mediated inflammation of exocrine glands and a prominent type I interferon (IFN-I) signature. However, the molecular mechanisms linking interferon signaling with downstream immune and inflammatory pathways in pSjD remain incompletely understood. In this study, we performed an integrative analysis combining public transcriptomic datasets, immune infiltration analysis, single-cell RNA sequencing, and experimental validation to investigate the potential involvement of interferon alpha-inducible protein 6 (IFI6) in pSjD. Differential expression and network analyses identified IFI6 as an upregulated interferon-stimulated gene associated with immune-related pathways. Immune infiltration analysis showed that IFI6 expression was associated with activated dendritic cells and CD4⁺ memory T cells. Single-cell RNA sequencing further indicated preferential expression of IFI6 in dendritic cell subsets. Clinical validation revealed increased serum IFI6 levels in patients with pSjD, which were negatively associated with salivary flow rate. In addition, immunoprecipitation coupled with proteomic analysis identified complement-related proteins within IFI6-associated complexes, and enrichment analysis suggested the involvement of complement activation pathways. Overall, these findings indicate that IFI6 expression is associated with interferon-related immune activation and complement-associated inflammatory pathways in pSjD. IFI6 may serve as a potential biomarker reflecting interferon-related immune activation and is associated with reduced salivary flow rate in pSjD, although further studies are required to clarify its precise functional role.

PMID 42552444
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PubMedProteomics2026-08-05

MODY Mutations in Transcription Factors HNF1A and HNF1B Affect the Production of Interferon Signaling Proteins: Evidence at the Proteome Level.

Kuznetsova Ksenia G KG, Vašíček Jakub J, Skiadopoulou Dafni D, Unger Lucas L et al.

This discovery study investigated the impact of MODY-associated mutations in hepatocyte nuclear factors HNF1A and HNF1B on the cellular proteome, aiming to identify affected pathways and advance understanding of diabetes pathogenesis. Human induced pluripotent stem cells (hiPSCs) carrying the HNF1A frameshift mutation (p.Pro291fsinsC) were differentiated into pancreatic progenitors, and renal proximal tubule epithelial cells (RPTECs) were engineered to overexpress HNF1B with the S148L point mutation. Label-free quantitative proteomics was performed using data-dependent and data-independent acquisition on Orbitrap and timsTOF mass spectrometers. Pathway enrichment was analyzed using Qiagen IPA, Hallmark gene sets, and STRING networks. Comprehensive proteome coverage (over 7000 proteins) revealed consistent downregulation of oxidative phosphorylation, mitochondrial function, and interferon signaling pathways. Both models exhibited suppression of innate immune responses, with overlapping downregulated proteins, including members of the OAS, IFIT, and MX1 families. Using label-free proteomics, we show that MODY-associated mutations in HNF1A and HNF1B suppress mitochondrial function and interferon signaling and are additionally associated with reduced abundance of predicted targets such as A1CF as well as diabetes-related proteins including SCGN, supporting their role in diabetes pathogenesis.

PMID 42554236
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PubMedExpert opinion on pharmacotherapy2026-08-05

Evaluating Zasocitinib as an oral therapy for moderate to severe plaque Psoriasis.

McGuirt Victoria V, Razler Dillon D, Moore Savannah G SG, Feldman Steven S

Psoriasis is a chronic inflammatory disease with significant physical and psychosocial burden. Although biologic therapies targeting IL-17 and IL-23 are highly effective, their cost, injection burden, and variable response highlight the need for convenient oral alternatives. TYK2, a key mediator of the IL-23/IL-17 axis, represents a promising therapeutic target. Our objective is to evaluate the pharmacology, clinical efficacy, safety, and potential role of zasocitinib in plaque psoriasis. We conducted a narrative review of preclinical and clinical studies of zasocitinib, focusing on early-phase trials and comparisons with existing therapies. Zasocitinib is a highly selective oral TYK2 inhibitor that targets IL-12, IL-23, and interferon signaling. Adverse events were generally mild to moderate, with no major safety signals or laboratory abnormalities. Psoriasis varies widely, but treatment is mainly based on whether topicals are enough or stronger therapy is needed. Although better treatment options are still needed, especially for mild disease, new drugs like zasocitinib may have a role, but could face challenges competing with existing highly effective and well-established therapies.

PMID 42552595
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PubMedFrontiers in immunology2026-08-05

Spatial mapping of Ethiopian cutaneous leishmaniasis lesions reveals distinct tissue level immune programs.

Dey Nidhi S NS, Pham Thao-Thy TT, Dey Shoumit S, Kassa Mekibib M et al.

Human cutaneous leishmaniasis (CL) is a prevalent but neglected tropical disease characterised by inflammatory lesions that are either restricted to the site of the infected sand fly bite or disseminate to mucosae or within the skin. Compared to well-studied pre-clinical models, the nature and diversity of the tissue response in humans remains to be fully appreciated. We conducted an exploratory study using spatial transcriptomics on paired lesional and non-lesional skin punch biopsies from five Ethiopian CL patients (two infected with L. aethiopica, one with L. tropica, and two with species unconfirmed). We used reference-free deconvolution, morphology-guided regional analyses, and immunohistochemistry-based validation to characterise the tissue responses. We identified spatially distinct immunopathological tissue responses including: i) epithelial hyperplasia with interferon-stimulated keratinocytes, ii) cytotoxicity with tertiary lymphoid structures, iii) granulomatous inflammation with proinflammatory response, iv) granulomatous inflammation with M2-polarised myeloid cell responses, and v) fibrotic remodelling with active collagen synthesis. Each patient in this case series exemplified one of these tissue responses, but immunopathological features were not mutually exclusive. This study extends our understanding of Ethiopian CL immunopathology and provides a molecular and cellular context that can be applied in larger clinical cohorts for testing hypotheses regarding the host and/or parasite determinants of CL disease diversity.

PMID 42553130
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PubMedAdvanced materials (Deerfield Beach, Fla.)2026-08-05

Spatiotemporally Controlled Lysosomal Membrane Permeabilization Amplifies STING-Driven Antitumor Immunity in Prostate Cancer.

Jiao Qishu Q, Zhang Jiaqi J, Wang Chunlu C, Liu Zhaohan Z et al.

Prostate cancer (PCa) remains a major clinical challenge due to therapeutic resistance and immunologically cold tumor microenvironment. Lysosomal membrane permeabilization (LMP)-induced lysosome-dependent cell death offers an alternative route to eliminate resistant tumor cells and initiate immunogenic cell death, yet its efficacy is often limited by insufficient spatiotemporal control and immune activation. Here, we report a spatiotemporally programmable supramolecular nanoplatform (Cu-P-MSA) that integrates lysosome-targeted sonodynamic therapy with tumor-confined innate immune activation for PCa treatment. Cu-P-MSA is a modular self-assembling peptide incorporating a PSMA-targeting ligand, morpholine moiety, and cathepsin B-cleavable linker, enabling tumor-selective uptake and in situ formation of fibrous sonosensitizer depots within lysosomes. Upon ultrasound irradiation, a glutathione-responsive open-shell sonosensitizer induces controlled LMP, simultaneously activating ferroptosis and pyroptosis and promoting immunogenic cell death. Meanwhile, tumor-specific release of a STING agonist MSA-2 elicits robust type I interferon responses, driving dendritic cell maturation and cytotoxic T-cell infiltration. This coordinated lysosomal disruption-immune amplification strategy effectively reprograms the tumor immune microenvironment and suppresses both primary and distant tumors, with inhibition rates reaching 84.3% and 77.5%, respectively. Overall, this work establishes a spatiotemporally controlled supramolecular approach that integrates lysosomal disruption with innate immune activation to overcome therapeutic resistance and immunosuppression in PCa.

PMID 42554093
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PubMedFrontiers in immunology2026-08-05

Mechanisms of Epstein-Barr virus-associated autoimmunity: a comparative overview.

Shabnam Fathima F, Khan Gulfaraz G

Epstein-Barr virus (EBV) is a ubiquitous herpesvirus, increasingly implicated in the pathogenesis of several autoimmune diseases, such as multiple sclerosis (MS), systemic lupus erythematosus (SLE), and rheumatoid arthritis (RA). These diseases have both, shared and disease-specific immunopathogenic pathways involving EBV. Shared mechanisms include the role of EBV latent proteins in triggering immune dysfunction, molecular mimicry between viral and self-antigens, infection of autoreactive B-cells, and dysfunction of type 1 interferon (IFN-1) responses. In MS, EBV is associated with a CNS-compartmentalized CD8+ T-cell responses, molecular mimicry with neural antigens, and formation of meningeal tertiary lymphoid structures. In SLE, EBV contributes to systemic autoimmunity through mimicry with multiple autoantigens, recurrent viral reactivation, and IFN-driven multi-organ inflammation. In RA, EBV promotes the formation of synovial ectopic lymphoid structures, enhances anti-citrullinated protein antibody production, and drives proinflammatory cytokine dysregulation. Host genetic variations, particularly in HLA alleles, further modulate susceptibility by influencing antigen presentation, viral control and autoreactive T-cell responses. Rather than acting as a uniform and consistent trigger, EBV appears to function as a context-dependent immunological modifier whose pathogenic effects are influenced by factors such as the timing of infection, tissue microenvironment, HLA-associated genetic background, and other environmental exposures. Unravelling the details of these mechanisms may inform targeted preventive and therapeutic strategies for EBV-associated autoimmune diseases.

PMID 42553300
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